What is an ECG? A graphical representation of the electrical events taking place in the heart during...

What is an ECG?

A graphical representation of the electrical events taking place in the

heart during each beat.

The human body is a very good volume conductor and if electrodes are placed on body surface they will pick up the action potential current and when they are connected to galvanometer with the help on a conducting wire then these currents are recoded on a moving paper as the pen needle of galvanometer deflects or moves.if the wave of depolarization in the heart moves towards the positive electrode an upward deflection occurs but if wave of depolarization moves away towards negative electrode then a downward deflection is produced.the needle stays at neutral point and paper displays an isoelectric line when the myocardium is polarized (resting), completely depolarized or completely hyperpolarized.Durin these three conditions there is no movements of electrical charges and therefore no movement of needle.

Electrocardiogram ECG (EKG)

• Surface electrodes record electrical activity deep within body - How possible?

• Reflects electrical activity of whole heart not of single cell!

• EC fluid = “salt solution” (NaCl) good conductor of electricity to skin surface

• EKG tracing = of all electrical potentials generated by all cells of heart at any given moment

Recording of ECG

In order to record a standardized ECG ,there are internationally accepted conventions to record accurate and standard ECG •For each 1mv input , there must be 1 cm deflection of pen or stylus•Speed of paper ( 25mm/sec)•Placement of electrodes

The two electrodes connected to a conducting wire constitute a “ LEAD” A lead is said to be bipolar if both electrodes are active and their potential difference will determine the voltage of that particular lead. Alead is known as unipolar if all the current is recorded by one active electrode and the second is kept at zero.This is augmentation so all unipolar limb leads are known as augmented unipolar limb leads and written as aVR,aVL,aVF. “a” stands for augmented.

LEADS

• Bipolar leads , both electrodes are activeV1 – V6

• Unipolar leads , one is active and other is inactive , aVR ,aVL, aVF.

RARA LALA

LLLL

II

IIII IIIIII

– +

+

––

+

Einthoven’s Triangle and the 3 Limb Leads:

Fig 14-19

• The sum of voltages at the corners of an equilateral triangle with the source of current (heart) in the center is zero.so if we know the volatge of two bipolar limb leads the electric potential of the third lead can be calculated by the formula:I+III=II this is einthoven’s law.read it from the chapter 11 of guyton with the given example.RA is -0.2mv, LA is+0.3mv and LF is +1.0mv calculate the voltages of lead I,II and III.

• Mean QRS vector of ventricular depolarization determines the mean electrical axis of the heart which is +59 degrees directed to the cardiac apex.the normal range of cardiac axis is from -30 degree to +110 degree.

Placement of unipolar precordial chest leads on precordium

• V1 is in right fourth intercostal space along sternal border

• V2 is in left 4th intercostal space along sternal border

• V3 is between V2 and V4

• V4 is at the apex

• V5 is in left 5th intercostal space along anterior axillary line

• V6 is in left 5th intercostal space along mid axillary line

• V1 and V2 represent right ventricular activity

• V3 and V4 represent activity of ventricular septum

• V4 and V5 represent left ventricular activity

ECG PAPER

• Along horizontal axis , time or duration is represented in seconds

• Along vertical axis amplitude is represented in mv • Side of one small square vertically is equal to 0.1

mv• Side of one small square horizontally is 0.04 seconds• in one second there will be 25 small square

ECG PAPER

• P WAVE• QRS WAVE• T WAVE

P WAVE

• +VE wave due to atrial depolarization ,which occur just before atrial systole

• 0.1-0.2 mv ( 1-2 small square)• Duration is 0.1 sec( 2.5 square)• Top coincide with time when cardiac

impulse reaches AV node

QRS COMPLEX

• Q wave is -ve• R wave is +ve• S wave is -ve• It is due to ventricular depolarization just

before ventricular systole or contraction • Q wave is due to depolarization of upper part

of ventricular septum• R wave is due to depolarization of lower part of

septum and apex of heart

QRS COMPLEX

• S wave is due to depolarization of wall and base of ventricle

• Voltage of QRS from peak of R to bottom of S is about 1 mv or more than 1 mv

• Duration is 0.08—0.1 sec• peak of R wave coincide with onset of

ventricular systole

• T wave is +ve wave due to ventricular repolarization

• Voltage is 0.2-0.3 mv• Duration is o.25-0.27 sec

Standardized EKG’s

• Time and voltage calibrations are standardized as shown on figure 11-1.

Figure 11-1; Guyton & Hall

Cardiac Cycle- the timing of mechanical waves with ECG

EKG Concepts• The P wave immediately precedes atrial

contraction.• The QRS complex immediately precedes

ventricular contraction.• The ventricles remain contracted until a few

milliseconds after the end of the T repolarization wave.

• The atria remain contracted until the atria are repolarized, but an atrial repolarization wave cannot be seen on the electrocardiogram because it is obscured by the QRS wave.

An Electrocardiogram

ECG SEGMENTS

• Segments are isoelectric

• PQ / PR SEGMENT , from end of P wave to beginning of QRS complex

• ST SEGMENT , from end of S wave to the beginning of T wave

ECG INTERVALS

• PR/ PQ INTERVAL From beginning of P WAVE to the beginning of QRS complex

• Represent atrial depolarization and conduction through AV node

• 0.16 sec average ( 0.12-0.2 ) • QRS INTERVAL , It is duration of QRS complex• Duration is 0.08-0.1 sec

• VAT,( ventricular activation time ) , From beginning of Q WAVE to the peak of R wave

ECG INTERVALS

• QT INTERVAL , From the beginning of Q wave to the end of T wave .

• it represents ventricular depolarization and ventricular repolarization

• Duration is 0.36-0.4 sec

• RR INTERVAL it is the interval between two successive R WAVES ,

• IT is equal to duration of one cardiac cycle . (0.8 sec)

• It is used to find out heart rate • Heart rate = 60/RR• 60/0.8= 75 /MIN• HR= no of small sq in 60 sec/ no of small sq bt

two successive R wave • HR =no of cardiac cycle x 10

Correlation of plasma K+ level and the ECG, assuming that the plasma Ca2+

level is normal.

INTRODUCTION TO HEART BLOCKS

• OCCUR WHEN THERE IS A PARTIAL OR COMPLETE INTERRUPTION IN THE CARDIAC ELECTRICAL CONDUCTION SYSTEM.

• CAN OCCUR ANYWHERE IN THE ATRIA BETWEEN THE SA NODE AND THE AV JUNCTION.

• IN THE VENTRICLES BETWEEN THE AV JUNCTION AND PURKINJE FIBERS.

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Normal heart rates in children.

• Newborn: 110 – 150 bpm• 2 years: 85 – 125 bpm• 4 years: 75 – 115 bpm• 6 years+: 60 – 100 bpm

Arrhythmias resulting from block of heart signals within the intracardiac conduction

pathways.

Sino-atrial blockIncomplete atrioventricular block.

Complete atrioventricular blockBundle branch blocks

Hemiblocks

Anatomical Basis

• The SA node consists of two main groups of cells:• A central core of pacemaking cells (“P cells”) that

produce the sinus impulses.• An outer layer of transitional cells (“T cells”) that

transmit the sinus impulses out into the right atrium.• Sinus node dysfunction can result from either:• Failure of the P cells to produce an impulse. This

leads to sinus pauses and sinus arrest.• Failure of the T cells to transmit the impulse. This

leads to sino-atrial exit block.

Intrinsic causes of sick sinus syndrome.

• Idiopathic Degenerative Fibrosis (commonest).

• Ischaemia.• Cardiomyopathies.• Infiltrative Diseases e.g. sarcoidosis,

haemochromatosis.• Congenital abnormalities.

Sick sinus syndrome.extrinsic causes.

• Drugs e.g. digoxin, beta-blockers, calcium channel blockers.

• Autonomic dysfunction.• Hypothyroidism.• Electrolyte abnormalitites — e.g.

hyperkalaemia.

ECG abnormalities seen in sick sinus syndrome.

• Sinus Bradycardia.• Sinus Arrhythmia – associated with sinus node

dysfunction in the elderly in the absence of respiratory pattern association.

• Sinoatrial Exit Block.• Sinus Arrest — pause > 3 seconds.• Atrial fibrillation with slow ventricular response.• Tachy-brady syndrome.

•

Sino-atrial exit block.

• Sino-atrial exit block is due to failed propagation of pacemaker impulses beyond the SA node.

• The sino-atrial node continues to depolarise normally.

• However, some of the sinus impulses are “blocked” before they can leave the SA node, leading to intermittent failure of atrial depolarisation (dropped P waves).

Causes

• Sick sinus syndrome• Increased vagal tone (athletes)• Vagal stimulation (surgery, pain)• Inferior myocardial infarction• Myocarditis• Drugs: digoxin, beta-blockers, calcium channel

blockers, amiodarone.

SA Exit Block.

• There is shortening of PR interval progressively and suddenly no P wave.

SA EXIT BLOCK.

• Another type of SA block black arrow indicates dropped P wave as a result the 4th QRS is a junctional escape beat fllowed by a non conducted P wave.

Sinoatrial exit block.

First Degree Heart BlockDefinition

• PR interval > 0.2 sec(five small squares)

• ‘Marked’ first degree block if PR interval > 0.3sec

• Examples

Causes.• Increased vagal tone• Athletic training• Inferior MI• Mitral valve surgery• Myocarditis (e.g. Lyme disease)• Hypokalaemia• AV nodal blocking drugs (beta-blockers, calcium

channel blockers, digoxin, amiodarone)• May be a normal variant

FIRST-DEGREE BLOCK IS NOT A TRUE BLOCK BUTSIMPLY A DELAY IN THE ELECTRICAL CONDUCTIONSYSTEM.

PROLONGED PRI GREATER THAN 0.20 SECONDS.THE P WAVE OCCURS BEFORE EVERY QRS BUT THEPRI IS ALWAYS GREATER THAN 0.20 SECONDS.

P TO P AND R TO R INTERVALS ARE USUALLYREGULAR DEPENDING ON THE UNDERLYING RHYTHM.

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AV Block: 2nd degree, Mobitz I (Wenckebach Phenomenon)

DefinitionProgressive prolongation of the PR interval culminating in a non-conducted P waveThe PR interval is longest immediately before the dropped beatThe PR interval is shortest immediately after the dropped beatOther FeaturesThe P-P interval remains relatively constantThe greatest increase in PR interval duration is typically between the first and second beats of the cycle.The RR interval progressively shortens with each beat of the cycle.The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4.

DefinitionProgressive prolongation of the PR interval culminating in a non-conducted P waveThe PR interval is longest immediately before the dropped beatThe PR interval is shortest immediately after the dropped beatOther FeaturesThe P-P interval remains relatively constantThe greatest increase in PR interval duration is typically between the first and second beats of the cycle.The RR interval progressively shortens with each beat of the cycle.The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4.

MechanismMobitz I is usually due to reversible conduction block at the level of the AV node.Malfunctioning AV node cells tend to progressively fatigue until they fail to conduct an impulse. This is different to cells of the His-Purkinje system which tend to fail suddenly and unexpectedly (i.e. producing a Mobitz II block).

MechanismMobitz I is usually due to reversible conduction block at the level of the AV node.Malfunctioning AV node cells tend to progressively fatigue until they fail to conduct an impulse. This is different to cells of the His-Purkinje system which tend to fail suddenly and unexpectedly (i.e. producing a Mobitz II block).

CausesDrugs: beta-blockers, calcium channel blockers, digoxin, amiodaroneIncreased vagal tone (e.g. athletes)Inferior MIMyocarditisFollowing cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)

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AV block: 2nd degree, “fixed ratio” blocks

• Definition• Second degree heart block with a fixed ratio

of P waves: QRS complexes (e.g. 2:1, 3:1, 4:1).• Fixed ratio blocks can be the result of

either Mobitz I or Mobitz II conduction.

MOBITZ II HEART BLOCK• OCCURS DUE TO AN INTERMITTENT

INTERRUPTION NEAR OR BELOW THE AV JUNCTION.

• INTERRUPTION IS NOT PROGRESSIVE, BUT OCCURS SUDDENLY AND WITHOUT WARNING!!

• P WAVES BEFORE EVERY QRS COMPLEX AND ALL ARE THE SAME SIZE AND SHAPE.

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2:1 Mobitz type II example.

• THIS OCCURS UNTIL A QRS COMPLEX IS DROPPED.

• THE QRS MAY BE WIDER IF THE BLOCK OCCURS NEAR THE BUNDLE OF HIS.

3:1 Mobitz type II-example.

Third degree complete heart block.

• Definition• In complete heart block, there is complete

absence of AV conduction – none of the supraventricular impulses are conducted to the ventricles.

Third degree complete heart block.

• Perfusing rhythm is maintained by a junctional or ventricular escape rhythm. Alternatively, the patient may suffer ventricular standstill leading to syncope (if self-terminating) or sudden cardiac death (if prolonged).

• Typically the patient will have severe bradycardia with independent atrial and ventricular rates, i.e. AV dissociation.

Third degree heart block.

• P WAVES AND QRS COMPLEXES APPEAR AS WELL AS PR• INTERVAL THAT ARE CONSTANTLY CHANGING IN LENGTH.

• THE PRI’S DO NOT BECOME PROGRESSIVELY LONGER.

• NO RELATIONSHIP EXISTS BETWEEN THE P WAVES AND• QRS COMPLEXES.

• NO TRUE PR INTERVAL.

Third degree heart block.

• THE QRS COMPLEXES ARE WIDE AND BIZZARE WITH A TIME FRAME OF >0.12 SECONDS.

• DEPOLARIZATION IS AT THE INHERENT RATE BUT THE P TO P AND R TO R INTERVALS ARE NOT EQUAL.

• ATRIAL RATE 60 TO 100 VENTRICULAR RATE 20 TO 40.

• THIS IS A LETHAL DYSRHYTHMIA. CAN LEAD TO ASYSTOLE.

Example of III degree Complete heart block.

• No coordination between atria and ventricles.

Causes of complete heart block• The causes are the same as for Mobitz

I and Mobitz II second degree heart block. The most important aetiologies are:

• Inferior myocardial infarction• AV-nodal blocking drugs (e.g. calcium-channel

blockers, beta-blockers, digoxin)• Idiopathic degeneration of the conducting

system (Lenegre’s or Lev’s disease)

Adams-Stokes (A-S) syndrome

• The association of syncope and convulsions with a slow pulse, termed the MorgagniAdams-Stokes or Adams-Stokes (A-S) syndrome, is usually due to venticular standstill secondary to failure of the idioventricular pacemaker in advanced or complete heart block.1 Occasionally the A-S syndrome is due to extreme sinus bradycardia without heart block, e.g., rates below 20 per minute, with consequent intolerably prolonged cerebral ischemia between ventricular beats.

BUNDLE BRANCH BLOCK (BBB)

• INTERRUPTION IN THE ELECTRICAL CONDUCTION SYSTEM OF EITHER THE RIGHT, LEFT OR BOTH BUNDLE BRANCHES.

• CAUSES A DELAY TO THE VENTRICLES.• THE INTERRUPTION FORCES THE IMPULSE TO

“DETOUR” AND TAKE ANOTHER ROUTE TO THE VENTRICLES.

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THIS EXTRA TIME CAUSES THE IMPULSE TO REACH THEVENTRICLE LATER.

THIS CAUSES TWO SEPARATE DEPOLARIZATIONS.

THE RHYTHM STRIP HAS A NOTCHED QRS REFERRED TOAS “RABBIT EARS”.

THE QRS MEASURES WIDER THAN 0.12 SECONDS.

IF BOTH BRANCHES ARE BLOCKED THE IMPULSE TAKESLONGER TO REACH THE VENTRICLES.For more medical presentations -

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PATIENTS ARE MANAGED ONLY IF THEY AREHEMODYNAMICALLY SYMPTOMATIC.

THESE ARE SHOCK SYMPTOMS DUE TO LACK OFCARDIOVASCULAR PERFUSION

• MOBITZ II (2ND DEGREE, TYPE II) – OXYGEN, IV FLUIDS,• ATROPINE IF OVERALL RATE IS BRADYCARDIC, ARTIFICIAL• PACEMAKER, DOPAMINE OR EPINEPHRINE.

• IF HEART RATE IS GREATER THAN 100 BUT LESS THAN• 150 DILTIAZEM, DIGOXIN, OR BETA BLOCKERS.

• 3RD DEGREE BLOCK – OXYGEN, IV FLUIDS, ATROPINE IF• BRADYCARDIC, DOPAMINE, EPINEPHRINE, OR ARTIFICIAL• PACEMAKER.

• BBB- PATIENT ASSESSMENT