View
387
Download
0
Category
Preview:
Citation preview
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What is an EKGbullThe electrocardiogram (EKG) is a representation of the electrical events of the cardiac cyclebullEach event has a distinctive waveform bullthe study of waveform can lead to greater insight into a patientrsquos cardiac pathophysiology
mclmal
V1
V1
V2
V2
V3
V3
V4
V4
V5V5
Horizontal plane - the six chest leads
V6
V6RA
LALV
RV
65
9
The 12-LeadsThe 12-leads include
ndash3 Limb leads (I II III)
ndash3 Augmented leads (aVR aVL aVF)
1942- Goldberger increased Wilsonrsquos Unipolar lead voltage by 50
ndash6 Precordial leads (V1- V6)
1938 -AHA and Cardiac society of great Britain
1906 - William Einthoven diagnoses some heart problems 1924 - the noble prize
60 ndash 100 times a minute
40 ndash 60 times a minute
20 ndash 40 times a minute
Pacemakers of the heart
1111
Cardiac Conduction
Impulse Conduction amp the ECGSinoatrial node
AV nodeBundle of His
Bundle BranchesPurkinje fibers
The ldquoPQRSTrdquo
Normal Components of the EKG Waveform
ECG RULES
bull Professor Chamberlains 10 rules of normal-
1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2 The width of the QRS complex should not exceed 110 ms less than 3 little squares
3 The QRS complex should be dominantly upright in leads I and II
4 QRS and T waves tend to have the same general direction in the limb leads
5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S
wave must grow from V1 to at least V3 and disappear in V6
7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less
than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6
11
Normal tracing
R1
R2R3
R4
R5R6
R7
R8
R9NO ABNORMAL Q
R10
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
What is an EKGbullThe electrocardiogram (EKG) is a representation of the electrical events of the cardiac cyclebullEach event has a distinctive waveform bullthe study of waveform can lead to greater insight into a patientrsquos cardiac pathophysiology
mclmal
V1
V1
V2
V2
V3
V3
V4
V4
V5V5
Horizontal plane - the six chest leads
V6
V6RA
LALV
RV
65
9
The 12-LeadsThe 12-leads include
ndash3 Limb leads (I II III)
ndash3 Augmented leads (aVR aVL aVF)
1942- Goldberger increased Wilsonrsquos Unipolar lead voltage by 50
ndash6 Precordial leads (V1- V6)
1938 -AHA and Cardiac society of great Britain
1906 - William Einthoven diagnoses some heart problems 1924 - the noble prize
60 ndash 100 times a minute
40 ndash 60 times a minute
20 ndash 40 times a minute
Pacemakers of the heart
1111
Cardiac Conduction
Impulse Conduction amp the ECGSinoatrial node
AV nodeBundle of His
Bundle BranchesPurkinje fibers
The ldquoPQRSTrdquo
Normal Components of the EKG Waveform
ECG RULES
bull Professor Chamberlains 10 rules of normal-
1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2 The width of the QRS complex should not exceed 110 ms less than 3 little squares
3 The QRS complex should be dominantly upright in leads I and II
4 QRS and T waves tend to have the same general direction in the limb leads
5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S
wave must grow from V1 to at least V3 and disappear in V6
7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less
than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6
11
Normal tracing
R1
R2R3
R4
R5R6
R7
R8
R9NO ABNORMAL Q
R10
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
mclmal
V1
V1
V2
V2
V3
V3
V4
V4
V5V5
Horizontal plane - the six chest leads
V6
V6RA
LALV
RV
65
9
The 12-LeadsThe 12-leads include
ndash3 Limb leads (I II III)
ndash3 Augmented leads (aVR aVL aVF)
1942- Goldberger increased Wilsonrsquos Unipolar lead voltage by 50
ndash6 Precordial leads (V1- V6)
1938 -AHA and Cardiac society of great Britain
1906 - William Einthoven diagnoses some heart problems 1924 - the noble prize
60 ndash 100 times a minute
40 ndash 60 times a minute
20 ndash 40 times a minute
Pacemakers of the heart
1111
Cardiac Conduction
Impulse Conduction amp the ECGSinoatrial node
AV nodeBundle of His
Bundle BranchesPurkinje fibers
The ldquoPQRSTrdquo
Normal Components of the EKG Waveform
ECG RULES
bull Professor Chamberlains 10 rules of normal-
1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2 The width of the QRS complex should not exceed 110 ms less than 3 little squares
3 The QRS complex should be dominantly upright in leads I and II
4 QRS and T waves tend to have the same general direction in the limb leads
5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S
wave must grow from V1 to at least V3 and disappear in V6
7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less
than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6
11
Normal tracing
R1
R2R3
R4
R5R6
R7
R8
R9NO ABNORMAL Q
R10
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
V1
V1
V2
V2
V3
V3
V4
V4
V5V5
Horizontal plane - the six chest leads
V6
V6RA
LALV
RV
65
9
The 12-LeadsThe 12-leads include
ndash3 Limb leads (I II III)
ndash3 Augmented leads (aVR aVL aVF)
1942- Goldberger increased Wilsonrsquos Unipolar lead voltage by 50
ndash6 Precordial leads (V1- V6)
1938 -AHA and Cardiac society of great Britain
1906 - William Einthoven diagnoses some heart problems 1924 - the noble prize
60 ndash 100 times a minute
40 ndash 60 times a minute
20 ndash 40 times a minute
Pacemakers of the heart
1111
Cardiac Conduction
Impulse Conduction amp the ECGSinoatrial node
AV nodeBundle of His
Bundle BranchesPurkinje fibers
The ldquoPQRSTrdquo
Normal Components of the EKG Waveform
ECG RULES
bull Professor Chamberlains 10 rules of normal-
1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2 The width of the QRS complex should not exceed 110 ms less than 3 little squares
3 The QRS complex should be dominantly upright in leads I and II
4 QRS and T waves tend to have the same general direction in the limb leads
5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S
wave must grow from V1 to at least V3 and disappear in V6
7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less
than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6
11
Normal tracing
R1
R2R3
R4
R5R6
R7
R8
R9NO ABNORMAL Q
R10
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
9
The 12-LeadsThe 12-leads include
ndash3 Limb leads (I II III)
ndash3 Augmented leads (aVR aVL aVF)
1942- Goldberger increased Wilsonrsquos Unipolar lead voltage by 50
ndash6 Precordial leads (V1- V6)
1938 -AHA and Cardiac society of great Britain
1906 - William Einthoven diagnoses some heart problems 1924 - the noble prize
60 ndash 100 times a minute
40 ndash 60 times a minute
20 ndash 40 times a minute
Pacemakers of the heart
1111
Cardiac Conduction
Impulse Conduction amp the ECGSinoatrial node
AV nodeBundle of His
Bundle BranchesPurkinje fibers
The ldquoPQRSTrdquo
Normal Components of the EKG Waveform
ECG RULES
bull Professor Chamberlains 10 rules of normal-
1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2 The width of the QRS complex should not exceed 110 ms less than 3 little squares
3 The QRS complex should be dominantly upright in leads I and II
4 QRS and T waves tend to have the same general direction in the limb leads
5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S
wave must grow from V1 to at least V3 and disappear in V6
7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less
than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6
11
Normal tracing
R1
R2R3
R4
R5R6
R7
R8
R9NO ABNORMAL Q
R10
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
60 ndash 100 times a minute
40 ndash 60 times a minute
20 ndash 40 times a minute
Pacemakers of the heart
1111
Cardiac Conduction
Impulse Conduction amp the ECGSinoatrial node
AV nodeBundle of His
Bundle BranchesPurkinje fibers
The ldquoPQRSTrdquo
Normal Components of the EKG Waveform
ECG RULES
bull Professor Chamberlains 10 rules of normal-
1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2 The width of the QRS complex should not exceed 110 ms less than 3 little squares
3 The QRS complex should be dominantly upright in leads I and II
4 QRS and T waves tend to have the same general direction in the limb leads
5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S
wave must grow from V1 to at least V3 and disappear in V6
7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less
than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6
11
Normal tracing
R1
R2R3
R4
R5R6
R7
R8
R9NO ABNORMAL Q
R10
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
1111
Cardiac Conduction
Impulse Conduction amp the ECGSinoatrial node
AV nodeBundle of His
Bundle BranchesPurkinje fibers
The ldquoPQRSTrdquo
Normal Components of the EKG Waveform
ECG RULES
bull Professor Chamberlains 10 rules of normal-
1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2 The width of the QRS complex should not exceed 110 ms less than 3 little squares
3 The QRS complex should be dominantly upright in leads I and II
4 QRS and T waves tend to have the same general direction in the limb leads
5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S
wave must grow from V1 to at least V3 and disappear in V6
7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less
than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6
11
Normal tracing
R1
R2R3
R4
R5R6
R7
R8
R9NO ABNORMAL Q
R10
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Impulse Conduction amp the ECGSinoatrial node
AV nodeBundle of His
Bundle BranchesPurkinje fibers
The ldquoPQRSTrdquo
Normal Components of the EKG Waveform
ECG RULES
bull Professor Chamberlains 10 rules of normal-
1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2 The width of the QRS complex should not exceed 110 ms less than 3 little squares
3 The QRS complex should be dominantly upright in leads I and II
4 QRS and T waves tend to have the same general direction in the limb leads
5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S
wave must grow from V1 to at least V3 and disappear in V6
7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less
than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6
11
Normal tracing
R1
R2R3
R4
R5R6
R7
R8
R9NO ABNORMAL Q
R10
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Normal Components of the EKG Waveform
ECG RULES
bull Professor Chamberlains 10 rules of normal-
1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2 The width of the QRS complex should not exceed 110 ms less than 3 little squares
3 The QRS complex should be dominantly upright in leads I and II
4 QRS and T waves tend to have the same general direction in the limb leads
5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S
wave must grow from V1 to at least V3 and disappear in V6
7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less
than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6
11
Normal tracing
R1
R2R3
R4
R5R6
R7
R8
R9NO ABNORMAL Q
R10
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
ECG RULES
bull Professor Chamberlains 10 rules of normal-
1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2 The width of the QRS complex should not exceed 110 ms less than 3 little squares
3 The QRS complex should be dominantly upright in leads I and II
4 QRS and T waves tend to have the same general direction in the limb leads
5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S
wave must grow from V1 to at least V3 and disappear in V6
7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less
than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6
11
Normal tracing
R1
R2R3
R4
R5R6
R7
R8
R9NO ABNORMAL Q
R10
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Normal tracing
R1
R2R3
R4
R5R6
R7
R8
R9NO ABNORMAL Q
R10
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
STANDARDISATION ECG amplitude scale
Normal amplitude
10 mmmV
Half amplitude
5 mmmV
Double amplitude
20 mmmV
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Why ldquo1500 Xrdquo
bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute
bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10
OR
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Step 1 Calculate Rate when rhythm is regular
ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval
R wave
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DRSHAFEI LASHEEN
HR if irregular rhythm
ndash Count the of R waves in a 6 second rhythm strip then multiply by 10
ndash Reminder all rhythm strips in the Modules are 6 seconds in length
Interpretation
9 x 10 = 90 bpm
3 sec 3 sec
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Step 2 Determine rhythm
bull Look at the R-R distances (using a caliper or markings on a pen or paper)
bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular
Interpretation Regular
R R
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Regularity of Rhythm
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Axis
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
True LAD
bull So again if lead I is positive and aVF is negative we suspect LAD
bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Extreme RAD
bull If lead I is negative AND aVF is also negative ndash extreme RAD
bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or
Pacemakersbull In general we should never have an axis over
here
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Right axis deviation
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
P-waveNormal values1 up in all leads except
AVR2 Duration
lt 25 mm3 Amplitude lt 25 mm
Extreme RT axis
Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
P Pulmonale
P Mitrale
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Slide 9
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Slide 15
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Step 3 Assess the P waves
bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P
wave for every QRS
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second
PR interval
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
PR interval
Definition the time interval between beginning of P-wave to beginning of QRS complex
Normal PR interval 3-5mm or 3-5
small squares on ECG graph (012-02 sec)
Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree
heart block
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Slide 17
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Slide 44
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Step 4 Determine PR interval
bull Normal 012 - 020 seconds (3 - 5 boxes)
Interpretation 012 seconds
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
QRS Complex
Represents complete ventricular depolarization
QRS complex
QRS Complex Variants
QRS Complex
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
QRS complex
Normal valuesbull Duration lt 25 mmbull Morphology
progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6
Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm
2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic
cardiomyopathybull Normal variant
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Small voltage QRS
bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads
bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy
bull Acute causes mdash pleural andor pericardial effusions
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Step 5 QRS duration
bull Normal 004 - 012 seconds (1 - 3 boxes)
Interpretation 008 seconds
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Q Wave
Represents the beginning of septaldepolarization
The first negative deflection off of the baseline
Q Wave
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Q WAVES
bull Q waves lt004 secondbull Thatrsquos is less than one small square
durationbull Height lt25 or lt 14 of R wave height
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Normal Q wave
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
61
61
Normal Q waves
Notice the small Normal Q in Lead I
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Abnormal Q waves
bull The duration or width of Q waves becomes more than one small square on ECG graph
bull The depth of Q wave becomes more than 25 of R wave
bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Q wave in MI
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
64
64Pathological Q wave
Notice the deep amp wide Infarction Q in Lead I
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Q wave in septal hypertrophy
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
R Wave
Indicates left ventricular depolarization
The first positive deflection off the baseline
R Wave
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Normal upward progression of R wave from V1 to V6
V1V2
V3V4
V5V6
The R wave in the precordial leads must grow from V1 to at least V4
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
T-waveNormal values1amplitude
lt 10mm in the chest leads
Abnormalities
1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant
2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
NORMAL ST- SEGMENT
its isoelectric [ie at same level of PR or PQ segment at
least in the beginning]
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Abnormalities
1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization
ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Abnormalities of ST- segment
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Slide 11
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Slide 12
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
QT- interval
Definition Time interval between beginning of
QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and
congenital long QT syndrome2 Short QT interval hypercalcemia
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec
lt 044 s gt 044 s
Normal Long QT
A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease
Torsades de Pointes
Long QT
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
EKG Intervals
1 P-wave lt 0110 sec (approximately 3 small boxes)
2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec
3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec
4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
U WaveRepresents the last phase of
repolarizationThe exact significance is
unknownCharacteristic of
hypokalemiaMay predispose to
ventricular arrhythmias
U Wave
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
1 Every QRS is preceded by a P-wave
2 P-waves appear normal that is they are of sinus node origin
A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm
B Normal Axis ndash upright P-waves in lead II
Sinus Rhythmhellipor Not
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Rhythm Summary
bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
NSR Parameters
bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s
Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN 2010
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DREL SHAFEI A-AZIZ LASHEEN
Public Health Administration HAIL
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
What types of pathology can we identify and study from EKGs
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
SA Node Problems
The SA Node canbull fire too slowbull fire too fast
SAN diseasesSinus Arrhythmia
Sinus BradycardiaSinus Tachycardia
(Sinus Tachycardia may be an appropriate response to stress)
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Rhythm 1
30 bpmbull Ratebull Regularity regular
normal
010 s
bull P wavesbull PR interval 012 sbull QRS duration
Interpretation Sinus Bradycardia
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Rhythm 2
130 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 016 sbull QRS duration
Interpretation Sinus Tachycardia
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Sinus block
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Missed cycle
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Sick Sinus Syndrome
Sinoatrial block (note the pauseis twice the P-P interval )
Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat
Severe sinus bradycardia
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Sinus Arrhythmia
inspiration expiration
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Atrial Cell Problems
bull fire occasionally from a focus
bull fire continuously due to a looping re-entrant circuit
Premature Atrial Contractions (PACs)
Atrial Flutter
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Premature Atrial Contractions
bull Deviation from NSRndashThese ectopic beats originate in the atria
(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Rhythm 3
70 bpmbull Ratebull Regularity occasionally irreg
27 different contour
008 s
bull P wavesbull PR interval 014 s (except 27)bull QRS duration
Interpretation NSR with Premature Atrial Contractions
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Atrial Fibrillation
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Atrial Fibrillation (A-fib)
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Rhythm 5
100 bpmbull Ratebull Regularity irregularly irregular
none
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Fibrillation
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Atrial Flutter
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Rhythm 6
70 bpmbull Ratebull Regularity regular
flutter waves
006 s
bull P wavesbull PR interval nonebull QRS duration
Interpretation Atrial Flutter
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
AV Junctional Problems
The AV junction canbull fire continuously
due to a looping re-entrant circuit
bull block impulses coming from the SA Node
Paroxysmal Supraventricular Tachycardia
AV Junctional Blocks
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Rhythm 7
74 148 bpmbull Ratebull Regularity Regular regular
Normal none
008 s
bull P wavesbull PR interval 016 s nonebull QRS duration
Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
AVNR tachycardia
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Junctional Premature Beat
bull single ectopic beat that originates in the AV node or
bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the
QRS
bull ndash Retrograde P waves immediately following the QRS
bull ndash Absent P waves (buried in the QRS)
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Premature Junctional Complexes (PJC)
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Junctional Escape Beat
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Junctional Rhythm
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells canbull fire occasionally
from 1 or more focibull fire continuously
from multiple focibull fire continuously
due to a looping re-entrant circuit
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Ventricular Conduction
NormalSignal moves rapidly through the ventricles
AbnormalSignal moves slowly through the ventricles
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Premature Ventricular Complex (PVC)
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Rhythm 4
60 bpmbull Ratebull Regularity occasionally irreg
none for 7th QRS
008 s (7th wide)
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation Sinus Rhythm with 1 PVC
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
PVCs
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Ventricular Tachycardia (VT)
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
160 bpmbull Ratebull Regularity regular
none
wide (gt 012 sec)
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Tachycardia
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Ventricular Fibrillation (VF)
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Rhythm 9
nonebull Ratebull Regularity irregularly irreg
none
wide if recognizable
bull P wavesbull PR interval nonebull QRS duration
Interpretation Ventricular Fibrillation
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Torsade des points
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
AV Junctional Blocks
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR interval
2nd Degree Mobitz Type I Progressive PR interval prolongation
2nd Degree Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
60 bpmbull Ratebull Regularity regular
normal
008 s
bull P wavesbull PR interval 036 sbull QRS duration
Interpretation 1st Degree AV Block
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Second Degree AV Block
bull Mobitz type I or Winckebach
bull Mobitz type II
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Rhythm 11
50 bpmbull Ratebull Regularity regularly irregular
nl but 4th no QRS
008 s
bull P wavesbull PR interval lengthensbull QRS duration
Interpretation 2nd Degree AV Block Type I
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
nl 2 of 3 no QRS
008 s
bull P wavesbull PR interval 014 sbull QRS duration
Interpretation 2nd Degree AV Block Type II
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Third Degree AV Block(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60 BPM
Two independent pacemakers
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Third Degree AV Block(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
40 bpmbull Ratebull Regularity regular
no relation to QRS
wide (gt 012 s)
bull P wavesbull PR interval nonebull QRS duration
Interpretation 3rd Degree AV Block
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Acute Coronary Syndrome
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
ECG assessment
ST Elevation or new LBBBSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
ST Elevation and non-ST Elevation MIs
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
ECG Changes amp the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is
ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
ECG Changes
Ways the ECG can change include
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted
ST elevation amp depression
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TSTR
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
TST
R
P
Q
T
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Views of the Heart
Some leads get a good view of the
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Anatomic Groups(Septum)
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Anatomic Groups(Anterior Wall)
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Anatomic Groups(Lateral Wall)
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Anatomic Groups(Inferior Wall)
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Anatomic Groups(Summary)
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Which part of the heart is affected
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
bull Leads V1 V2 V3 and V4 =
Anterior Wall MI
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary Artery or LAD
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Anterior Wall MI
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
AWMI (pardeersquos sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
What part of the heart is affected
I aVL V5 and V6 Lateral wall of left
ventricle
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Anterolateral MI
This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Infarct Is the ST elevation or depression
Yes Elevation in V2-V6 I and avL Depression in II III and avF
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
What part of the heart is affected II III aVF =
Inferior Wall
IIIIII
aVRaVLaVF
V1V2V3
V4V5V6
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Inferior Wall MI
This is an inferior MI Note the ST elevation in leads II III and aVF
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
177
177
Acute True Posterior MI
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
inferiorposterior STEMI with RV involvement
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
STEMI equivalent
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Acute pericarditis
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Acute pulmonary embolism
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
45 yo female 1 week post-op with shortness of breath
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Findings
bull Accelerated junctional rhythm
bull Right axis deviationbull ldquoS1Q3T3rdquo pattern
bull Clinical history and EKG most consistent with acute PE
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression amp T-wave inversion
The ECG changes seen with a non-ST elevation infarction are
Before injury Normal ECG
ST depression amp T-wave inversion
ST returns to baseline but T-wave inversion persists
Ischemia
Infarction
Fibrosis
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
ST Depression or Dynamic T wave Inversions
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Non-ST Elevation Infarction
Herersquos an ECG of an evolving non-ST elevation MI
Note the ST depression and T-wave inversion in leads V2-V6
Question What area of the heart is infarcting
Anterolateral
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Hypertrophy
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following
ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Slide 15
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm
Right atrial enlargement
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Left atrial enlargement ndash To diagnose LAE you can use the following criteria
bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
199
199
Ventricular Hypertrophybull Ventricular Muscle
Hypertrophybull QRS voltages in V1 and V6 L
1 and aVLbull We may have to record to frac12
standardizationbull T wave changes opposite to
QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Criteria for LVH
bull Sokolow-Lyonndash S v1+R v5v6gt35mm
ndash R I+S IIIgt25mmndash R avlgt11mm
bull Cornellndash S v3+R avl gt28 (men)
gt20( women)
bull Romhilt-Estesndash LV strain
3ndash LAE 3ndash LAD 2ndash QRS duration 1
ndash R v5v6gt3 3
ndash Sv1v2gt33
ndash Largest R or Sgt2 3
5 or more points suggests LVH
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
203
203Left Ventricular Hypertrophy
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
LV+LA
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
205
205Right Ventricular Hypertrophy
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Bundle Branch Blocks
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN
Right Bundle Branch BlocksWhat QRS morphology is characteristic
For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
209
209Complete RBBB
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DRSHAFEI LASHEEN
Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
211
211Complete LBBB
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Miscellaneous
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
K Ca
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Hyperkalaemia
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
K=94 mmoll
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Hypokalaemia
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
K= 15
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Hypocalcaemia
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Pericardial Effusion (electrical alternans)
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Hypothermia (osborne wave)
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Arrythmogenic RV dysplasia(Epsilon wave)
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Digitalis toxicity
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
SAH(t wave +long QT)
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
WPW syndrome
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
WPW + AF
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Ventricular Pacemaker (Single Chamber)
pacemaker
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Dual Paced Rhythmpacemaker
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
AV pacing
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Cable reversal
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Dextrocardia
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Artifacts in Parkinsonrsquos pt
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Movements Artifacts
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Electric noise
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
DR SHAFEI LASHEEN 2010
Thank You
DR SHAFEI LASHEEN 2015
Recommended