By. Devon Fuller EMT-P

12 Lead Interpretation

• Action potential of myocardial tissue and areas of ischemia/ infarction

• Proper 12 lead placement and augmented leads

• Wave formation and pathology

• Recognize and diagnose ectopic and idiopathic segments

• Recognize st-segment elevation and depression

• Differentiate between STEMI and Non-STEMI

• Learn areas of ischemia/ infarction and reciprocal changes

• 6 most common STEMI mimickers

• Learn diagnose ectopic rhythms using axis and axis deviation

• Sgarbossa Criteria

• 15 lead and right side 12 lead placement

• Uncommon 12 lead presentation

• Medications and arrhythmias

Introduction

• Occurs in 4 phases (some interpret 3 or 5)

• Sodium (Na+)- influx creates depolarization

• Calcium (Ca2+)- Controls the STRENGTH of depolarization

• Potassium (K+)- influx repolarizes (resets) the action potential

• Resting state average -90mV, then depolarization lifts to approx. +40mV

• During resting state, the outside of the cell is MORE positive than the inside of the cell meaning by default, the inside of the cell is negative

• During depolarization, the inside of the cell becomes MORE positive than the outside resulting in contraction

Action Potential

• Na+ begins to slowly enter the cell until around -70mV, then it enters the cell rapidly increasing voltage to approx. +40 (phase 0)

• This influx causes K+ to rapidly leave the cell which is where the voltage decreases (phase 1)

• As this occurs, Ca2+ begin to enter the cell resulting in NO difference in voltage (plateau phase, Also Phase 2)

• Once depolarization occurs, the cell begins to switch again, causing Na+ and K+ to leave and Ca2+ to be reabsorbed out of the cell back to resting state (phase 3 and 4)

Action Potential

Action Potential

Einthovens Triangle• “White on right, smoke over fire”• Negative to positive• Flow of conduction towards a positive

lead• Augmented leads AVR, AVL, AVF• Augmentation refers to voltage change• Voltage change through leads allows

additional segments to be captured on 12 lead

Augmented Leads

• Lead voltage changes to reflect positive lead• Augmentation results in variable deflection• When voltage moves TOWARDS a positive lead, always a POSITIVE deflection• When voltage moves AWAY from a positive lead, shows a NEGATIVE deflection• AVR is NOT a useless lead

Lead Placement

• V1: 4th intercostal space right of sternum• V2: 4th intercostal space left of sternum• V3: Midway between v2 and V4• V4: Midclavicular line left side• V5: Anterior Axillary line same level of V4• V6: Midaxllary line same level of V5

• Measured in milliseconds and millimeters/ millivolts

Time and Size

Time and Size

• 0.1 mV = 1 mm (height)• 1 small box= 0.04 seconds

(width)• 1 highlighted box= 0.2 seconds• 5 highlighted boxes =1 second• 0.5 mV = 5 mm• Height and width used to

determine additional ectopy during cardiac rhythm

• Based on location of isoelectric line

Isoelectric line

• Base electrical line on ECG• Used to determine elevation or • Depression• Dependent on upward and • Downward deflection of QRS• Registered in time and mV

Isoelectric Line

• Elevation determined by positive deviation from isoelectric line• Depression determined by negative deviation from isoelectric line• ST-Segment can be above or below but the J-point must be determined to

diagnose elevation or depression

The “Quick 6”

• Half of a 12 lead• Shows a reflection of basic leads and

augmented leads• May show possible areas of infarction/

ischemia• Will not show PRI/ QRS/ QT segment

timing• 12 lead is still the standard for diagnosis

The 12 Lead

•Shows time and elevation in exact sequence

•Considered always reliable

•Do NOT go by the computer interpretation of the rhythm, that’s why you were trained to manually interpret

Normal range

•PRI- 0.12-0.20 seconds

•QRS- 0.04-0.12 seconds

•QT- Females- 340-400 MS

Males- 330-390 MS

• Prolonged QT segment begins over the limit of gender

Numbers?

QT-Segment

Normal vs. Abnormal

•Can be typical or atypical

•Caused by CAD

•Can also be caused by coronary artery spasms

•Angina is brought on by stress, vigorous activity or by nothing at all

•Typical presents with frequency and is predictable

•Atypical presents with no rhyme or reason and is often not relieved by nitro or positioning

•Regardless of the cause, all angina patients need a 12 lead to rule out STEMI

•CAD is the leading cause of STEMI in the WORLD

Angina

12 Lead Reflection

“ I See All Leads”

• Lie Lie Say All

• Alternative to diagnosis of 12 lead

• Not often used but other providers will use this method alone, or in conjunction with ISAL to determine proper diagnosis

• Follows the appropriate pattern of 12 lead without skipping over additional leads for completion

• For remainder of the slides, we will be looking at BOTH methods for determination using ISAL as primary

“LII-LI-SSA-ALL”

Arteries of Viewing

• The "LCX", or left circumflex artery is an artery of the heart. It follows the left part of the coronary sulcus, running first to the left and then to the right, reaching nearly as far as the posterior longitudinal sulcus. Can also include the low lateral leads V5-V6

• The right coronary artery originates above the right cusp of the aortic valve, travels down the right atrioventricular groove, and branches into the posterior descending artery and the right marginal artery.

• The left coronary artery arises from the aorta above the left cusp of the aortic valve and feeds blood to the left side of the heart. It is also known as the left main coronary artery and the left main stem coronary artery. An occlusion to this artery is often called “the widowmaker”.

Artery’s Affected

Inferior Leads

• Leads II, III, and AVF• Reflect the circuit flow of the inferior/

partial posterior of the heart• Main focus on RCA and additional

arterial flow from the same

Septal Leads

• Leads V1 and V2• Views the junction/bifercation

of the LAD and Circumflex artery

• Most proximal portion of the left and right coronary arteries

Anterior Leads

• V3 and V4• Most anterior portion of the

LAD• Often defined as the

“widowmaker”• 27% mortality rate• Supplies the greatest amount

of blood to the largest muscle portion of the heart

Lateral Leads

• V5 and V6• Most distal portion of the

LAD and attached arterial flow

Reciprocal Leads• Any lead or group of leads that oppose primary lead viewed

• Not needed or necessary to presume infarction or diagnose a STEMI

• Strong confirmation of STEMI when present

• Can NOT be used as a “rule out” option

Reciprocal Change

Reciprocal Change

J-Point

• Determined by the Joining of the QRS and ST segment

• Can be elevated or depressed• Sometimes is hard to

determine location• Follow the standard rules of

interpretation to find the J-Point

J-Point

• With all 12 lead interpretation of suspected ischemia or infarction, first find the J-Point on the most Isoelectric lead

• Remember that the J-Point is the connection of the S wave and the T wave.

J-Point

• Once you find the J-Point, simply draw a line through the 12 all leads and connect the J-Points

• Technically defined as any negative deflection that precedes an R wave

• It does not have to be a negative deflection to be present however.

• The Q-wave can be isoelectric

• Q-wave represent normal left to right depolarization of the interventricular septum

• Most commonly seen in lateral leads (I, AVL, V5, V6)

• Not normal variant if seen in anterior septal leads (V1-V4)

• Most common cause of q-wave pathology and presence in anterior septal leads is incorrect limb lead placement

Q-wave pathology

• Presence of pathological q-waves usually indicate current or prior myocardial infarction

• Q-wave is considered pathological if:

> 40ms wide

> 2mm deep

> 25 % of the QRS complex

Seen in the anterior septal leads

• If any of these are seen and there is no ST elevation or depression, a high probability of prior MI is present.

• Can be seen in hypertrophic cardiomyopathy and myocardial rotation as well

Pathological Q-Wave

Pathological Q-Wave > 40ms wide > 2mm deep > 25 % of the QRS complex Seen in the anterior-septal

leads

The pathological Q-Wave will NOT form until 1-2 hours into a STEMI. If it’s presence is there, you now know how much time the muscle has been infarcting.

Ischemia VS Infarction

Ischemia VS. Infarction

• Ischemia is noted by ST-Depression• Infarction is noted by ST-Elevation• The higher the ST-Elevation, the worse

the infarction is• Reciprocal change is known as the area

of ischemia opposite area of infarction• As shown in the figure, infarction has

an evolution from start to finish of the area

• Once the evolution is finished, the cardiac muscle is PERMANENTLY damaged

• Best pre-hospital treatment is MONA• Morphine• Oxygen• Nitro• Aspirin

• ST-elevated myocardial infarction

• Must be at least 1 mm elevation in 2 CONTIGUOUS leads

• Contiguous leads are any set of leads the reflect the same area, or are next to the same area

STEMI

• *V6 and Lead I are contiguous*• V2 and V3• V4 and V5

STEMI VS NSTEMI

ST Elevation Patterns

ST elevation in stemi can be reflected either concave, convex, or obliquely straight

• *Smile for me*- The smile of the st-segment means NO STEMI

• *Frown means down*- The frown is in indication or st-segment elevation

STEMI

• Area of infarction is reflected by the area of ST-Elevation

• Reciprocal changes are NOT needed to diagnose a STEMI in the field

• Be careful of the STEMI mimickers

• As long as you have 1 mm elevation in 2 or more CONTIGUOUS leads, a STEMI can be diagnosed

STEMI-Location

Inferior MI

• ST-Elevation in leads II,III, and AVF• Reciprocal changes in leads I and AVL KEY NOTE!!! Inferior AMI have shown an 88% probability to lead with either anInverted or depressed AVL PRIOR to the infarct presenting.•If AVL is inverted or depressed, an AMI may be on the way

Septal MI

• Elevation in leads V1 and V2• Note elevation in anterior leads as well• Septal most often present in anterior MI as well• Reciprocal changes noted?

Anterior MI

• ST-Elevation noted in leads V3 and V4• Note the elevation in leads V1 and V2• Anterior and Septal mi often correlate with each other• Reciprocal changes?

Lateral MI

• Low Lateral AMI

• High Lateral AMI

• Universal in nature

• Deep, depressive, substernal chest pain/ pressure not relieved or reproducible

• Levine sign

• Pain in left or right arm, shoulders, neck, jaw

• Weakness upon exertion

• Nausea

• Diaphoresis

• Ashen grey skin

• Rule of thumb, if pain above the naval, do a 12 lead

Classic Presentation

Inferior Presentation• In majority of population, 90% SA and AV node blood flow comes from the

RCA

• Conduction deficits/ delays

• Brady-arrhythmias

• Sinus Bradycardia

• Sinus Exit Block

• 1st degree heart block

• Hypotension

• Treat hypotension with fluid but DO NOT OVERTREAT

• May result in pulmonary edema

• Morphine and Nitro combined will drop pressure, both vasodilate

• Treat but keep pressure sustainable for cognition

• Most often the LCA occluded partially or fully

• Dull pressure that turns to crushing chest pain

• Pain radiates into the left arm

• Numbness or tingling sensation in fingers

• Pt may appear ashen grey or diaphoretic

Septal Presentation

• LCA / Circumflex occlusion, may be both

• Crushing, substernal chest pain

• Pain radiating into the left arm, right arm, or both

• Pain may appear in the shoulders and jaw

• Nausea

• Vomiting

• Diaphoresis

• Tingling or complete numbness in the fingers

• Shortness of breath

• Weakness upon exertion of any kind

• Near syncopal or positive syncopal episodes

• “Feeling of impending doom”

Anterior Presentation

• May have a combined presentation of both Anterior and Inferior wall MI

• Weakness upon exertion

• Pain radiating to one or both arms

• Syncope or near syncopal episodes

• Hypotension

• Brady-arrhythmias

• New heart blocks

• Most common presentation of new Bundle Branch Blocks

Lateral Presentation

Combination STEMI• STEMI can occur in more than 1 area

• A “combination STEMI” is a STEMI that has ST-elevation in more than the traditional leads yet are still contiguous

• Anterioseptal STEMI- Anterior and septal lead have ST-Elevation

• Anteriolateral STEMI- Anterior and lateral leads have ST-Elevation

• Inferiolateral STEMI- Inferior and lateral leads have ST-Elevation

• Global AMI- ALL leads have ST-Elevation other than AVR which will be depressed

• Some STEMIs will have more than one area with additional involvement

• Eg- “Anterioseptal with lateral involvement”

• This indicates that the elevation is continuing through more than 1 area or view of the 12 lead

Combination STEMI

• Inferiolateral AMI

Combination STEMI

• Anteriolateral AMI

Combination STEMI

• Anterioseptal AMI

• Continue to monitor ABC

• Initiate IV if available

• Continue with serial 12 leads

• ASA is a NESSICITY

• O2 via cannula (wave form capnography if indicated)

• IV fluid to maintain adequate blood pressure

• Nitro PRN

• Morphine is indicated for pain management

• Rapid transport to PCI facility

Treatment

• Obtain SAMPLE and OPQRST

• Be prepared for the worst

• AMI is the most common cause of acute Congestive Heart Failure

• Treat with CPAP if indicated (bp, hr, waveform capnography)

• Be cautious with Morphine and Nitro especially in Inferior AMI due to rapid decrease in blood pressure

• Be cautious with patient allergic to aspirin

• Notify the receiving hospital early of STEMI activation and expected arrival time

• Note area of infarct and ischemia/ reciprocal changes if available

• Remember you DO NOT have to have reciprocal changes to diagnose a stemi

Considerations

• STEMI MIMICKERS!!

• TOP 6

LVH

LBBB

Hyperkalemia

Early Repolarization

Pericarditis

PACED

Could it be?

• Left Ventricular Hypertrophy

• Left ventricle is larger requiring more electrical conduction to depolarize

• This results in a longer QRS complex than normal

• Seen in the precordial leads

• Determination is selective

• Find largest QRS complex in either lead V1 or V2

• Add to the largest complex in lead V5 or V6

• If the number is greater than 30 mm, LVH is present

• If the largest QRS complex in V1 or V2 is greater than 30, LVH is present

LVH

•Most often referred to as athletic heart syndrome

•Often caused by aerobic exercise and strength training

•Is not a disease

•Is usually a marker for disease

•Any disease that causes an increase in afterload over time that causes the heart to increase contractility strength, therefore increasing the myocardium

•Causes are referred to as hypertrophic cardiomyopathies

Aortic stenosis

Aortic insufficiency

Chronic hypertension

LVH

LVH

• Left Bundle Branch Block

• Left main conduction path is injured or blocked

• This results in a “lightning” effect

• The current must come back and re-route itself down the left ventricle to complete conduction in the myocardium

• QRS must be negative deflection in lead V1 and greater than 0.12 ms (3 small boxes)

• Was considered impossible to diagnose a STEMI in the presence of a LBBB

• Sgarbossa criteria now used to diagnose STEMI when LBBB is present

LBBB

LBBB vs RBBB

LBBB vs RBBB

• LBBB

• Can NOT call STEMI w/o sgarbossa

• Negative deflection in V1

• QRS greater than 0.12

• May or may not present with R prime wave

LBBB vs RBBB• RBBB

• CAN call a STEMI • Positive deflection in V1• QRS greater than 0.12 ms• Typically presents with R prime

wave (RsR)

• Clinical presentation

• Nausea

• Dyspnea

• Fatigue and weakness

• Chest pain

• Muscle paralysis

• Parasthesias

• Palpitations

• Absent DTR

• New LBBB

• Late signs include- bradycardia, lethargy/ unconsciousness, bradypnea, flat t-waves, death

Hyperkalemia

• MURDER

• Muscle cramps

• Urine abnormalities

• Respiratory distress

• Decreased cardiac contractility

• Ecg changes

• Reflexes

Hyperkalemia

• Increased serum potassium levels in the blood

• Often found in renal impaired/ failure patients

• ECG reflects peaked T waves

• Pay close attention to the QRS segment as it will begin to get wider

• Do NOT confuse this with hypernatremia where the QRS remains the same or gets more NARROW as the T waves begin to peak

Hyperkalemia

Hyperkalemia

• Goal is to displace potassium and sodium in the blood

• REMEMBER THE SODIUM POTASSIUM PUMP

• Influx of sodium will offset the higher potassium load to be reabsorbed into the kidneys for excretion

• IV access (bilaterally if available)

• CBIGKD

• Calcium gluconate

• Bicarbonate

• Insulin

• G (glucose) D50

• Kayexalate- Sodium polystyrene sulfonate. If total body potassium is an issue

• Dialysis

Hyperkalemia Treatment

• Typically seen in adolescent males who lead a physically active life

• May present in any male under 50

• Also called “high J-point” or “early take off”

• Etiology is still not completely understood but was once believed to be benign in possibility of cardiac disease. This is no longer the case.

• More recent reports have suggested an association between ER and an increased risk for arrhythmic death and idiopathic ventricular fibrillation

• Some level of increased risk of sudden cardiac death has been reported in persons with ER.

Early Repole (not so benign)

• The relatively high prevalence of the ER pattern in the general population (5 to 13 percent) in comparison to the incidence of idiopathic VF (approximately 10 cases per 100,000 population) means that the ER pattern will nearly always be an incidental ECG finding with no clinical implications.

• A primary arrhythmic disorder such as idiopathic VF due to ER is far more likely when associated with syncope or resuscitated sudden cardiac death in the absence of other etiologies

• If seen in males 50-70, consider acute infarct

• Rarely seen in patients over 70

Early Repole (not so benign)

• Presentation

• PR depression

• St depression in AVR with T wave inversion

• Barbed “fish hook” appearance as a J-point with ST elevation in all leads

Early Repole cont.

Early Repole

•“Barbed fish hook” appearance on the ST segment•Will almost always have ST depression and inverted T wave in AVR

• Clinical presentation

• Chest pain radiating to the back that is typically relieved by sitting forward (to relieve pressure on the myocardium)

• Dry cough

• Fever

• Fatigue

• History of infection

• SHARP chest pain

• Often clinically misdiagnosed as STEMI

• Diffuse ST-elevation

• Often with Pr-depression

• Most commonly presents with t-wave inversion or ST depression in AVR

Pericarditis

Pericarditis

•Very common STEMI mimicker

•Additional voltage used to supercharge the muscles externally for cardiac contraction

•Often results in elevation and depression

Paced Rhythm

• A numerical representation of the MAJOR direction of electrical flow through myocardium

• Ranges from 0 to -180 degrees

• Proper range is from -30 to +90

• Referred to as “normal axis”

• Deviation from the normal axis is referred to as “axis deviation” (go figure right?)

• Deviation can be physiological, pathological or extreme

• Extreme is a significant sign of life threatening cardiac abnormality or rhythm

The Axis

Axis Measurments

• Several methods are in use today, we will focus on these 3

• Quadrant method

Utilizes lead I and AVF

• Lead method

Utilizes Lead I and II

Tri-lead method

• Utilizes leads I, II, and III

Determining Axis

• LEAD I LEAD AVF QUADRANT AXIS

• Positive Positive Left Lower Quadrant Normal

• Positive Negative Left Upper Quadrant Possible LAD

• Negative Positive Right Lower Quadrant RAD

• Negative Negative Right Upper Quadrant ERAD

Quadrant Method

Quadrant Method

• Lead I- Positive• Lead AVF- Positive• Quadrant- Lower Left• Axis- Normal

Quadrant Method

• Lead I- Positive• Lead AVF- Negative• Quadrant- Left Upper• Axis- LAD

Quadrant Method

• Lead I- Negative• Lead AVF- Positive• Quadrant- Right Lower• Axis- RAD

Quadrant Method

• Lead I- Negative• Lead AVF- Negative• Quadrant- Right Upper• Axis- ERAD

• Determined by looking at leads I and II

• If the QRS is positive in lead I, it is roughly in the same direction as lead I

• If the QRS is in the same direction as lead II, it puts the axis in roughly the same direction of lead II

• If leads I and II are BOTH positive, it places the axis in the area of -30 and + 90, meaning normal axis variant

Lead Method

•Also referred to as the “rapid-axis” method

•Utilizes the lead method with addition of lead III for better determination

TRI-Lead Method

• Left or Right

• Can be physiological or pathological

• Caused by a number of factors

Deviation

• May be a normal variant

• Conduction issues

Left anterior block

LVH

LBBB

Prior mechanical shift (surgery, lung disease, etc)

Inferior AMI

WPW

Idioventricular rhythms ie. V-tach or accelerated idioventricular

Atrial septal defects

LAD

• Causes

Left posterior fascicular block

RVH

Lung disease (acute or chronic)

Ventricular ectopy

Hyperkalemia

Sodium-channel blocker toxicity

WPW

May also be a normal variant for children or adults with mechanical shifting of the heart

RAD

Physiological LADLead I- positive, Lead II- BIPHASIC, Lead III- Negative

Pathological LADLead I- Positive, Lead II- Negative or R wave more negative than positive q wave, Lead 3- same criteria as lead II

RAD

•ERAD- Extreme right axis deviation

•Physiological vs pathological LAD

•Physiological left axis deviation- typically between 0 and -30

•Pathological left axis deviation- -30 to -90

•Axis deviation can be skewed due to left or right bundle branch blocks

•Be careful when using axis for complete diagnosis as the number do not lie, however they can confuse

Extreme Axis

•Often seen in wide complex tachycardias (V-tach)

•Is possible to have a wide complex tachycardia that mimics v-tach but brought on by “F” waves (flutter waves)

Extreme Axis

ERAD

•FINALLY!!

•Used to diagnose a STEMI in the presence of a LEFT bundle branch block AND a paced rhythm

•Criteria simple to follow

•We as a prehospital provider in our local area can NOT utilize this tool as of yet (2016)

•The criteria has increased in usage and accuracy for the past few years and is being taught to medical providers globally

•The rules are continuing to be modified every year by new clinical evidence and presentations

•What you learn today may NOT be in effect tomorrow

Sgarbossa Criteria

Sgarbossa Criteria:

• ST Elevation ≥ 1 mm and concordant with QRS complex

• ST segment depression ≥ 1 mm in lead V1, V2, V3 • ST elevation ≥ 5mm and discordant with QRS complex

•IF #1 and #2 are present, 98% probability of STEMI

•NEW rules has been added to update the parameters of Sgarbossa

•If positive concordance in ANY lead with the presence of a LBBB, Sgarbossa criteria has been met

• ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave

Sgarbossa

Sgarbossa

Is it Sgarbossa?

Is it Sgarbossa?

Is it Sgarbossa

• Some common medications and drugs can cause cardiac arrhythmias

• Most over the counter medications are relatively harmless

• Stimulant drugs and medications are the most common type to cause an arrhythmia (usually sinus tach)

• Illicit drug use can either speed up or slow down the heart

• Common household items can also cause an arrhythmia (fertilizer, cleaning materials)

• Most drugs that stimulate the sympathetic nervous system can cause a short lived arrhythmia, but will usually subside due to a relatively short half-life

Medication Problem?

• Caffeine

• Tobacco

• Alcohol

• Cold and cough medications

• Appetite suppressors (stimulants)

• ADHD medications

• Antiarrhythmic medications (paradoxical arrhythmias from medications)

• Tricyclic antidepressants

• Beta Blockers (primarily for blood pressure)

• Cocaine, marijuana, methamphetamines

Common medications and drugs

• Most stimulant drugs are dopaminergic (releasing or involving dopamine as a neurotransmitter)

• These drugs will stimulate the release and inhibit the reuptake of dopamine, leaving it at the synaptic cleft

• This leads to an increase in energy and a feeling of alertness and concentration

• Norepinephrine is released as an additional catecholamine along with dopamine which leads to the increase in heart rate and contractility

• If these drugs are taken too much or abused, the heart rate can increase to a dangerous level

• The overstimulation of the sympathetic nervous system cause a fluctuation and lowers parasympathetic response, this leads to an additional side effect of not wanting to eat

Stimulants

• Caffeine

• Tobacco

• Alcohol

• Appetite suppressors

• Cocaine

• Methamphetamines

• ADHD medications

Stimulant Types

Sinus Tachycardia

• Amitriptyline (Elavil)

• Amoxapine

• Clomipramine (Anafranil)

• Desipramine (Norpramin)

• Doxepin (Sinequan)

• Imipramine (Tofranil)

• Nortriptyline (Pamelor)

• Protriptyline (Vivactil)

Tricyclic Antidepressants

• Increase levels of norepinephrine and serotonin

• Block the action of acetylcholine

• Can cause sedation and block histamines as well

• TCA have sodium-channel blocking properties which increase quickly in high doses

• This causes a prolongation of the Q-T segment on an ECG

• Using the ECG and tracing the Q-T Segment can give you a better time frame on potential cardiac arrhythmias

• Most common late stage arrhythmias are V-Fib and Torsades De Pointes

• Best initial treatment via IV is sodium bicarb, NOT for the sodium channel issue alone but to alkalize the blood stream for protein synthesis and reduced bioavailability of the drug

• This increases elimination of the drug

• Calcium Can be given as well (through a different, or well flushed line) to open calcium channels and promote sodium availability

Tricyclics Cont

• A separate reason they are called “TCA’S”

• Mnemonic

• T-Thrombocytopenia- decrease in platelet count, increase in platelet deficiency

• C-Cardiac- AMI, arrhythmia, stroke

• A-Anticholinergic effects- Exact opposite of SLUDGE, everything hot

• S-Seizures

• All signs and symptoms of TCA overdose

• Pay attention to the ECG changes during a suspected TCA overdose

Tricyclics Cont.

• Toxicity usually is apparent within the first hour after ingestion

• New onset of all complexes widening

• Prolonged PRI, QRS and QT segments

• Prolonged PRI is usually the latest sign and high indication of inevitable V-Fib

• Prolonged QT is usually the first ECG change in an overdose

TCA ECG Changes

• These rules apply inconsideration of Sodium Channel Blocker overdose

• QRS > 100ms (0.10s) in lead II

• Terminal R wave in AVR > 3mm

• R-S ratio > 0.7s AVR

• Patients will often be Tachycardic however, the P waves will be hidden in the prior T wave due to elongation of the PRI

TCA ECG Rules

TCA ECG

•Gives additional views of the heart anterior and posterior

•Leads V7, V8, V9, V4R, V5R, V6R

•V7- between V6 and V8

•V8- Midscapular on the same line as V7 and V6

•V9- Between the spine and V8

•V4R- Midclavicular in opposite intercostal space as V4

•V5R- Between V4R and V6R on same plane

•V6R- Midaxillary right side

15 Lead / Right Sided Lead Placement

Posterior 12 Lead

Posterior AMI

Right Leads

•When doing V4R-V6R, simply write “R” after the appropriate V leads

15 Lead

15 Lead V4R-V6R

•12leads are not just for diagnostic properties of a STEMI

•Additional ectopy can be viewed and assist in a diagnosis for life threatening ailments either acute or chronic

•Brugadas syndrome

•Acute pulmonary embolism

•Hypernatremia

•Right Ventricular Hypertrophy

•Dewinters STEMI

What is That?

•An aberrant conduction abnormality that causes sudden cardiac death

•Leading cause in SUDS (sudden unexplained death syndrome)

•Genetic abnormality of the sodium ion pump channels

•SCN5A- influx flow sodium ion channel that fails which results in prolonged, untreatable V-fib

•Can be viewed on a 12 lead in the V-Leads

Brugadas Syndrome

•3 different types of ECG patterns

•Type 1 has a coved type ST elevation with at least 2 mm (0.2 mV) J-point elevation a gradually descending ST segment followed by a negative T-wave

•Type 2 has a saddle back pattern with a least 2 mm J-point elevation and at least 1 mm ST elevation with a positive or biphasic T-wave. Type 2 pattern can occasionally be seen in healthy subjects

•Type 3 has either a coved (type 1 like) or a saddle back (type 2 like) pattern with less than 2 mm J-point elevation and less than 1 mm ST elevation. Type 3 pattern is not rare in healthy subjects

Brugadas Syndrome

Brugadas Syndrome

Brugadas Syndrome 1

Coved type ST elevation with at least 2 mm (0.2 mV) J-point elevation a gradually descending ST segment followed by a negative T-wave

Brugadas Syndrome 2

Saddle back pattern with a least 2 mm J-point elevation and at least 1 mm ST elevation with a positive or biphasic T-wave. Type 2 pattern can occasionally be seen in healthy subjects

Brugadas Syndrome 3

Either a coved (type 1 like) or a saddle back (type 2 like) pattern with less than 2 mm J-point elevation and less than 1 mm ST elevation. Type 3 pattern is not rare in healthy subjects

•The clot that won’t break

•Usually acute in nature with severe difficulty breathing though lungs are clear

•Often misdiagnosed and treated due to its acute nature and inability of the prehospital provider to administer fibrinolytics or perform surgery to remove the clot

•If suspected, look at the 12 lead

•Deemed “S1, Q3, T3”

•Also known as McGinn-White sign

Acute PE

Acute PE

•Large deflection of the S wave in lead I•Presence of a Q wave in lead III•Inverted T wave in lead III•Signals the presence of right heart strain due to overuse/ occlusion of Pulmonary Artery

•Often seen in the elderly

•Hypokalemia can mimic hypernatremia and vise versa

•Serum potassium levels may be normal in comparison to the sodium levels

•Initially present the same way in a 12 lead but subtle differences can be examined

•Always obtain a SAMPLE from EVERY patient to determine the nature of the 12 lead

•Hypernatremia begins to present with prolonged QT segments due to the delay in repolarization from the potassium influx

•This is the PRIMARY difference between Hypokalemia and Hypernatremia

Hypernatremia

Hypernatremia

Hypernatremia

Hypernatremia

•Right ventricular hypertrophy

•Increase in myocardium of the right ventricle

•Often caused by

Pulmonary hypertension

Tetrology of the fallot

Pulmonary valve stenosis

Pulmonic regurgitation

VSD

High altitude

Cardiac fibrosis

COPD

Athletic heart syndrome

RVH

•Peaked P wave in lead II

•Right axis deviation in the presence of disease that causes RVH

•R wave in AVR > 5mm OR

•R wave in AVR > Q in AVR

•ST segment depression AND T wave inversion in right precordial leads

•Any one of the following in V1

R/S ratio > 1 and negative T wave

qR pattern

R > 6mm, or S < 2mm, or rSR` with R` > 10mm

RVH

RVH

•The de Winter ECG pattern is an anterior STEMI equivalent that presents without obvious ST segment elevation.

•Key diagnostic features include ST depression and peaked T waves in the precordial leads.

•The de Winter pattern is seen in ~2% of acute LAD occlusions and is under-recognised by clinicians.

•Unfamiliarity with this high-risk ECG pattern may lead to under-treatment (e.g. failure of cath lab activation), with attendant negative effects on morbidity and mortality.

DeWinters STEMI

•Tall, prominent, symmetric T waves in the precordial leads

•Upsloping ST segment depression >1mm at the J-point in the precordial leads

•Absence of ST elevation in the precordial leads

•ST segment elevation (0.5mm-1mm) in aVR (told yeah it wasn’t useless)

•“Normal” STEMI morphology may precede or follow the deWinter pattern

DeWinters Criteria

•MAY present atypically with no symptoms of cardiac issues

•Most common complication of Diabetes is CAD

•Many patients with Diabetes present with no angina or “silent” AMI

•This is primarily found in patients with persistent higher than normal levels of serum glucose

•Most often these patients with have “diabetic nerve pain” and will not be able to feel the consistent pressure from angina due to either the medications they take, the exact location of nerve damage, the bodies pH, the particular tissue involved and ability to function homeostatically, or prior injury resulting in dead or weakened nerve supply to the area.

Diabetes

Lets Wrap it UP

•Remember to always do a SAMPLE/ OPQRST on your patients

•Make sure the leads go on the appropriated areas for the best picture possible

•Remember the difference between benign elevation and malignant elevation

•A smile is what we want, frowns are bad

•Each lead reflects a particular section of the heart, if you need other angles the 15 lead can very useful

•Not every STEMI will show up, but it may be calculated with the numbers provided by the machine

•Some STEMIs are NOT STEMIs, at least 6 you know can be false

•Sgarbossa may change criteria, but the single concordant lead will remain

•12 leads can help you determine a course of action for treatment if all else gives no answers

Summary

•lifeinthefastlane.com/ecg-library/de-winters-t-waves/

•AHA.ORG

•12leadblogspot.com

•Ekgtoday.net

•12leads.com

•Wikipedia

•McGraw Hill Paramedic

•Nancy Carolines Life in the Streets- Paramedic edition

•Rautaharju PM, Surawicz B, Gettes LS, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part IV: the ST segment, T and U waves, and the QT interval: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society: endorsed by the International Society for Computerized Electrocardiology. Circulation 2009; 119:e241.

•WASSERBURGER RH, ALT WJ. The normal RS-T segment elevation variant. Am J Cardiol 1961; 8:184.

•Haïssaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med 2008; 358:2016.

References