Complete EKG Interpretation Course

EKG Interpretation
All in a Nutshell
Kerolus Shehata, MD

EKG Waves, Intervals and Segments

P wave
• Represents atrial depolarization.
• Normally: 2.5 mm x 2.5 mm in lead II. Smooth, rounded contour upward deflection in lead II and
Biphasic in V1 (Initial positive RA portion and a terminal negative LA portion).
• In precordial leads: Normal P wave amplitude is <1.5 mm.
• Best leads to check for P wave abnormalities: Lead II and V1
• LAE  P mitrale (Bifid), RAE  P pulmonale (Peaked).
• P wave inversion: Junctional rhythm (short PR <120 msec) or Low atrial rhythm (PR >120 msec).
• >3 P wave morphology and HR <100 BPM: Wandering atrial pacemaker
• > 3 P wave morphology and HR >100 BPM: MAT

PR Interval & Segment
• Represents the physiological AV nodal conduction delay.
• Begins from the onset of the P wave to the onset of the QRS complex.
• PR segment: Isoelectric. Begins from the end of the P wave till the onset of QRS complex.
• Normally: 120-200 msec. (up to one large square).
• Fixed Prolongation of PR interval: First degree AVB.
• Short PR interval (< 3 small squares)  Junctional (AV nodal) rhythm or pre-excitation (WPW & LGL).
• PR segment in Pericarditis (Relative to TP segment): Depressed in lead II and elevated in aVR and V1.
• STEMI + PR elevation or depression = Concomitant atrial infarction  Increased risk of free wall
rupture, supraventricular tachyarrhythmias and AVB.

Q wave
• Any negative deflection before R wave.
• Normally, Q waves shouldn’t be seen in V1-V3
• Normally, Q waves should be seen in V5-6. Usually absent in LBBBB
• Lead III and aVR: May have deep Q wave >2 mm as a normal variant.
• Causes of pathological Q wave: MI, HOCM, Restrictive CMP, Extreme cardiac axis rotation & lead misplacement.
Pathological Q wave
 Any Q wave in V1-3
 >1 mm wide
 >2 mm depth
 >25% of the following R wave

QRS complex
• Normal width: up to 120 msec (3 small squares).
• Narrow (Normal) complex = Supraventricular origin
• Wide complex: Can be of a ventricular origin or supraventricular with aberrancy (BBB, hyper K,
hypothermia, Rate-related, WPW or Sodium channel blocker toxicity e.g. TCA).
• Low voltage QRS: Amplitude of all QRS complexes is <5 mm in limb leads OR <10 mm in precordial leads.

QT interval
• Extends from the start of the Q wave to the end of the T wave (Time
needed for V-depolarization and repolarization).
• QT is inversely related to the heart rate.
• QTc: Estimates the QT interval at a standard heart rate of 60 BPM.
• Prolonged QTc > 440 msec in men or > 460 msec in women.
• QTc > 500 msec  Increased risk of Torsades de pointes.
• Short QTc: <350 msec.
• Causes of prolonged QTc: Hypo K/Mg/Ca/Temp, medication-induced,
High ICP, post cardiac arrest, MI and congenital long QT syndromes.
• Causes of short QTc: Hyper ca, digoxin effect and congenital short QTc.

J point & J wave
• The junction between the end of the QRS complex and the beginning of the ST segment.
• Healthy young males usually have the J point situated above the baseline.
• Other causes of elevated J point: BER, Myocardial ischemia
• N.B: J (Osborn) wave: A positive deflection (-ve in aVR & V1) that occurs before the J point.
Can be seen in patients with hypothermia, BER, Brugada syndrome, subarachnoid
hemorrhage (High ICP), Le syndrome d’Haïssaguerre (Idiopathic VF) and hypercalcemia.

R wave abnormalities
Dominant R wave in V1
 Normal variant: children and young adults.
 RVH
 HOCM
 Muscular dystrophy e.g. Duchenne
 RBBB
 Posterior MI
 WPW type A
 V1 &V3 lead reversal (Biphasic P in V3)
 Dextrocardia
Dominant R wave in aVR
 Left and Right arm lead reversal.
 Sodium channel blockers (e.g. TCA) overdose.
 VT
 Dextrocardia
Poor R wave progression
o Can be a normal variant
o Prior anteroseptal MI
o LVH
o Lead misplacement e.g. obese females.
o LBBB/LAFB
o WPW
o Mediastinal shift e.g. Tension pneumothorax
o Dextrocardia

T wave abnormalities
• Normal direction: Upright in all leads except aVR and V1.
• Isolated TWI in lead III is a normal variant.
• New TWI is always abnormal.
• Normal amplitude: < 5 mm in limb leads, <15 mm in precordial leads.
• Peaked (Tall and narrow-based) TW: Hyperkalemia.
• Hyperacute (Tall and broad-based) TW: Early MI and Prinzmetal angina.
• TW in V1 > TW in V6 = Loss of precordial TW balance = Acute ischaemia.
• Causes of Biphasic TW: Myocardial ischaemia e.g. Wellens type A (Up then
down) & Hypokalemia (Down then up).
• Camel hump TW: Due to fusion of TW with P wave or prominent U wave.
• Flat TW: Ischaemia or electrolyte abnormality e.g. hypokalemia.
Causes of TWI
o Normal finding in children.
o Persistent juvenile T wave pattern
o Isolated TWI is a normal variant in leads III, aVR and V1.
o Myocardial ischaemia including Wellens syndrome
o RBBB & LBBB
o RVH & LVH (Strain pattern)
o PE
o HOCM
o Increased intracranial pressure
o Digoxin effect
o Peri-myocarditis

U wave
• Normally, small 0.5 mm deflection immediately after and in the same direction as the TW. Best seen in V2-3.
• Normal U wave amplitude: <25% of the following TW (2 mm)
• U wave size is inversely proportional to HR.
• Causes of prominent U wave (Many also causes prolonged QTc): Bradycardia, hypo K/Mg/Temp, high ICP,
LVH, HOCM, medication-induced e.g. digoxin, amiodarone, sotalol & procainamide.
• Inverted U wave: Acute ischaemia, HTN, Hyperthyroidism, CMP and congenital heart diseases.

Epsilon Wave
• Small positive deflection in the end of the QRS complex.
• Most specific finding of arrhythmogenic RV dysplasia (ARVD).
• Other EKG changes in ARVD: TWI, localized QRS widening & prolonged S wave upstroke in V1-3.

Determination of the Cardiac Axis
• Cardiac axis: The major direction of the overall electrical activity of the heart.

Causes of axis deviation
Left Axis Deviation
 LVH
 LAFB
 LBBB
 WPW
 Ventricular pacing
 Inferior MI
 Short person (Horizontal heart)
 Primum ASD
Right Axis Deviation
 RVH
 LPFB
 Chronic lung disease
 Acute RV strain e.g. PE
 Lateral MI
 WPW
 Dextrocardia
 Hyperkalemia
 Na channel blockers e.g. TCA overdose
 Secundum ASD
 Normal variant in pediatrics
 Tall thin person (Vertical heart)
Extreme Axis Deviation
 VT
 Accelerated Idioventricular Rhythm
 Severe RVH
 Hyperkalemia

EKG changes in hypothermia
• Bradyarrythmias: Sinus bradycardia, slow A-fib, AVB of any degree or slow junctional rhythm.
• Osborn (J) wave: its amplitude is proportional to the degree of hypothermia.
• Prolongation of PR, QTc intervals
• Widening of QRS.
• Ventricular ectopy.
• Shivering artifact: Fuzziness of the baseline.

EKG changes in hypokalemia
• P wave: Increased amplitude and width.
• PR &QTc (QU): Prolonged
• ST: Depression
• T wave: Flat or inverted
• U wave: Prominent
• Severe cases: Ectopics  supraventricular or even ventricular arrhythmias (TdP)
• N.B: Check K and Mg in any patient with arrhythmia.

EKG changes in hyperkalemia
• Serum potassium level may not correlate closely with the ECG changes.
• Patients with relatively normal ECGs may still experience sudden hyperkalemic
cardiac arrest.
• Always suspect hyperkalemia in any patient with a new bradyarrhythmia or AV
block, especially patients with renal failure, on hemodialysis or taking any
combination of ACEi, potassium-sparing diuretics and potassium supplements.
• Hypokalemia potentiate the arrhythmogenic effect of digoxin.

EKG changes in hypercalcemia
• Shortening of QTc
• QRS: Widening.
• Severe cases: Osborn (J) wave and ventricular arrhythmias.

EKG changes in hypocalcemia
• Prolonged ST segment  QTc prolongation
• Arrhythmias e.g. A-fib or TdP: Uncommon

EKG changes in hypomagnesemia
• QTc prolongation.
• Atrial and ventricular ectopy.
• Torsades de pointes (TdP).

Cardiac conduction system
• SA node (60-100 bpm)
• Atria (< 60 bpm)
• AV node (40-60 bpm)
• Ventricles (20-40 bpm)
• Under normal conditions, subsidiary pacemakers are suppressed by the more rapid impulses from SA node.
• Escape rhythms arise when the rate of supraventricular impulses arriving at the AV node or ventricle is less than
the intrinsic rate of the ectopic pacemaker.

Normal Sinus rhythm
• Origin: SA node
• Regular rhythm +/- sinus
arrhythmia
• Rate: 60-100 BPM
• Each QRS complex is preceded by
a normal P wave morphology.
• Normal P wave axis: P waves
should be upright in leads I and
II, inverted in aVR.
• Constant PR interval.

Sinus Arrhythmia
• Origin: SA node.
• Variation in the P-P interval of
more than 120 msec (3 small
squares).
• The P-P interval gradually
lengthens and shortens in a
respirophasic pattern.
Inspiration increases the heart
rate by decreasing vagal tone.
• Constant P-R interval (no
evidence of Mobitz I).
• Seen in young, healthy people.
• Non-respiratory sinus
arrhythmia is pathological:
Elderly people e.g. Digoxin
toxicity.

Junctional Escape Rhythm
• Origin: AV node
• Rate: 40-60 BPM.
• P wave: before (inverted), during (hidden) or after QRS.
• Narrow QRS complexes <120 msec unless associated with BBB.
• Accelerated junctional rhythm: junctional rhythm at 60-100 BPM.

Ventricular Escape (Idioventricular) Rhythm
• Rate: 20-40 BPM
• QRS complex: Regular and wide >120 msec
• LBBB morphology (dominant S wave in V1): Arises from RBB.
• RBBB morphology (dominant R wave in V1): Arises from LBB.
• Accelerated idioventricular rhythm: e.g. reperfusion arrhythmia: 50-110 BPM (If>110: VT)

Sinoatrial (SA) Exit block
• SA node has 2 cell types:
Core of P cells: generates the impulse. Its
failure results in sinus arrest.
Outer layer of T cells: transmits the impulse to
RA. Its failure results in SA exit block.
• First degree SA block: Delay between impulse
generation and transmission to RA. Can’t be
detected by EKG

Second degree SA block type I
• Progressive shortening of the P-P interval, followed by an absent P wave-QRS complex.

Second degree SA block type II
• Intermittent dropped P waves with a constant interval between impulse generation and atrial depolarization.
• The blue arrows represent normally transmitted impulses, i.e. resulting in P waves.
• The black arrows represent blocked sinus impulses (dropped P waves).
• The pauses around the dropped P waves are exactly double the preceding P-P interval.

Third degree SA block & Sinus arrest
• None of the sinus impulses are conducted to the right atrium.
• Results in long sinus pauses or sinus arrest (may lead to fatal asystole).
• Indistinguishable from sinus arrest due to pacemaker cell failure.
• Causes: Increased vagal tone, myocarditis, MI, and digitalis toxicity.
• Pause is usually>3 sec in sinus arrest.

Bradycardia – Tachycardia syndrome
• A form of sick sinus syndrome.
• Alternating bradycardia with
paroxysmal supraventricular
tachycardia.
• Episodes of tachycardia may be
followed by delayed sinus recovery
(SA block or sinus pause).
• May result in syncope.
 Most common cause: Idiopathic
degenerative fibrosis.
 Other causes: Ischemia,
infiltration, drug-induced,
hypothyroidism, hyperkalemia,
autonomic dysfunction and
congenital.

Sinus Bradycardia
• Sinus rhythm.
• Resting heart rate: < 60 bpm in adults, or below the normal range for age in children.
• Normal during sleep.
• Common causes: Increased vagal tone (e.g. athletes), hypothermia, hypothyroidism, inferior MI, Hyper K/Mg,
myocarditis, meds (BB, non-DHB CCB, precede, clonidine, opiates, BZP, barbiturates, baclofen, amiodarone),
brain stem herniation (Cushing reflex).

Premature Atrial Complex (PAC)
• Premature: occurs earlier than you would expect if you were to measure the previous P-to-P intervals.
• Ectopic: originates outside of the SA node. So, the P wave morphology would be different than the normal sinus P wave.
• Narrow complex unless accompanied by BBB
• Followed by a compensatory pause: The extra atrial action potential causes the SA node to become refractory to generating
its next scheduled beat. Thus, it must skip a beat (SA nodal reset).
• PACs arriving very early in the cycle may not be conducted to the ventricles at all (Blocked PAC).
• Normal electrophysiological phenomenon and doesn’t usually requiring investigation or treatment.
• May cause palpitations if more frequent.
• Either PAC or PVC may trigger for the onset of a re-entrant tachydysrhythmia e.g. Atrial fibrillation, atrial flutter, AVNRT &
AVRT in patients with underlying heart disease (LA enlargement, ischaemia or WPW).

Atrial Bigeminy/Trigeminy
• Atrial Bigeminy: NSR with PAC occurring every other beat.
• Atrial Trigeminy: NSR with PAC occurring every third beat.

Premature Junctional Complex (PJC)
• Premature: occurs earlier than expected.
• Origin: AV node.
• Narrow QRS complex unless accompanied by BBB.
• May occur without a preceding P wave, with a retrograde P wave
which may appear before, during, or after the QRS complex.
• Followed by a compensatory pause.

Premature Ventricular Complex (PVC)
• Premature: occurs earlier than would be expected for the next sinus impulse.
• Wide QRS complex (≥ 120 msec) with abnormal morphology.
• Followed by a full compensatory pause: The next normal beat arrives after an interval that is equal to double the
preceding R-R interval.
• Retrograde capture of the atria (Retrograde inverted P wave) may or may not occur.
• Frequent PVCs: >5/minute on the routine ECG, or >10-30/hour during ambulatory monitoring. Usually benign except
with prolonged QTc where they predispose to R on T phenomenon that may lead to Torsades de Pointes.
• PVCs arising from RV have LBBB morphology (dominant S wave in V1).
• PVCs arising from LV have RBBB morphology (dominant R wave in V1).
• Unifocal PVCs: Arising from a single ectopic focus; each PVC is identical.
• Multifocal PVCs: Arising from two or more ectopic foci; multiple QRS morphologies.

Ventricular Bigeminy/couplets/triplets/NSVT
 V. Bigeminy: PVC occur
every other beat of NSR.
 V. Couplets (Pairs): 2
consecutive PVCs.
 V. Triplets: 3 consecutive
PVCs.
 NSVT: >3 consecutive
PVCs with rate of >120
BPM for less than 30 sec.

Wandering Atrial Pacemaker
• Multifocal atrial rhythm.
• There are 3 or more ectopic foci within the atrial myocardium that serve as the dominant pacemaker
• At least 3 different P wave morphology
• Variable PR interval
• Irregularly irregular rhythm.
• Rate: <100 BPM
• Seen in the very young, very old, and in athletes, and rarely causes symptoms or requires treatment.

First degree AV block
• Fixed prolongation of PR interval>200 msec.
• NO dropped beats.
• Causes: Normal variant, athletes, increased vagal tone, drug-induced (BB, non-DHB CCB, Digoxin,
amiodarone), myocarditis (Lyme disease, Rheumatic), hyperkalemia, Inferior MI and mitral valve surgery.
• No hemodynamic compromise.
• No specific treatment is required.

Second degree AV block (Mobitz type I)
• Wenckebach Phenomenon.
• Progressive prolongation of the PR interval ending in a non-conducted
P wave, then the cycle repeats itself resulting in grouped beats.
• Due to reversible conduction block at the level of the AV node.
• Causes: Same as first degree AV block.
• Usually a benign rhythm.
• Responds to atropine if symptomatic.

Second degree AV block (Mobitz type II)
• Sudden unexpected non-conducted P waves.
• Constant PR interval.
• Due to failure of conduction at the level of the His-Purkinje system
(Below the level of AV node).
• There may be no pattern to the conduction blockade, or a fixed ratio.
• More likely to progress to complete AV block.
• Carries 35% risk of asystole per year.

Second degree fixed ratio AV block
• Second degree AV block (Dropped beats) with fixed ratio of P waves: QRS complexes (e.g. 2:1, 3:1, 4:1)
• Can happen in Mobitz type I or type II.
• Mobitz I: conduction usually improves with atropine, worsens with Valsalva maneuver.
• Mobitz II: Conduction usually worsens with atropine and may improve with Valsalva maneuver.
• Distinction can be challenging.
• Observe the patient and closely monitor the PR interval for accurate differentiation between both types.
• If in doubt, assume that the block is due to type II AV block and proceed accordingly.

High grade AV block
• Second degree: There is still relationship between P waves & QRS complexes.
• P:QRS ratio: 3:1 or higher.
• Can happen in Mobitz type I or type II.
• Results in extremely low ventricular rate.

Third degree (Complete) AV block
• Complete absence of AV conduction resulting in AV dissociation.
• It is essentially the end point of either Mobitz I or Mobitz II AV block.
• Perfusing rhythm is maintained by a junctional or idioventricular escape rhythm.
• High risk of ventricular standstill and sudden cardiac death.
• Usually requires urgent pacing.

Right Bundle Branch Block (RBBB)
• Delayed RV activation
• QRS: Wide >120 msec in complete RBBB.
• RSR’ pattern in V1-3 (‘M-shaped’ QRS complex), with ST depression and TWI.
• Wide, slurred S wave in the lateral leads (I, aVL, V5-6).
• Incomplete RBBB: RSR’ pattern in V1-3 with QRS duration < 120ms. Common in children. No clinical significance.
• Axis: usually WNL.
• Common causes: RV hypertrophy, PE, ASD, Ischaemia.

Left Bundle Branch Block (LBBB)
• Delayed activation of LV.
• QRS: Wide >120 msec in complete LBBB.
• Dominant S wave in V1.
• Broad, notched (‘M’-shaped) R wave in V6.
• Absence of Q waves in lateral leads (I, V5-V6) due to reversal of the normal
Lt to Rt septal activation.
• Axis: Left Axis deviation
• Appropriate discordance: the ST segments and T waves always go in the
opposite direction to the QRS complex.
• Causes: Anterior MI, HTN, AS, Degenerative fibrosis (Lenegre disease)
• Incomplete LBBB: LBBB morphology is + a QRS duration < 120ms.

Non specific Interventricular Conduction Delay (IVCD)
• Wide QRS >120 msec that doesn’t meet criteria of LBBB or RBBB.
• Always exclude hyperkalemia/TCA OD before making that diagnosis.
• Increases the risk of cardiovascular mortality.

Left Anterior Fascicular Block (LAFB)
• Left Axis deviation.
• QRS: Normal <120 msec.
• Tall R waves (qR complexes) in leads I and aVL.
• Deep S waves (rS complexes) in leads II, III, aVF.
• N.B: In LAFB, QRS voltage in lead aVL may meet voltage criteria
for LVH (R wave > 11 mm), but there will be no LV strain pattern.

Left Posterior Fascicular Block (LPFB)
• Right Axis deviation.
• Deep S waves (rS complexes) in leads I and aVL.
• Tall R waves (qR complexes) in leads II, III and aVF.
• Never to diagnose LPFB unless you rule out more significant
causes of Right axis deviation e.g. acute PE, lateral STEMI and RVH.
• It is extremely rare to see LPFB in isolation. It usually occurs along
with RBBB in the context of a bifascicular block.

Bifascicular Block
• RBBB with either LAFB (more common) or LPFB.
• Carries 1%/year risk of progression to CHB.
• Causes: Same as causes of LBBB.

Trifascicular Block
• Most common form: Bifascicular block + First degree AV block
• Misnomer, since the AV node itself is not a fascicle.
• Other forms: (Bifascicular block + 2nd degree AV block) or (RBBB + alternating LAFB / LPFB)
• Complete Trifascicular Block: Bifascicular block + 3rd degree AV block (AV dissociation)
• If trifascicular block is present simultaneously in all three fascicles, CHB would exist.
• Often associated with an underlying structural heart disease, such as CAD, degenerative
disease of the conduction system (Lenegre’s disease).
• Can progress to high-grade and CHB.

Digoxin-related EKG changes
• Downsloping ST depression: Salvador Dali moustache appearance.
• Increased vagal tone: Mild PR interval prolongation.
• May show prominent U waves.
• Shortening of the atrial and ventricular refractory periods: Short QTc.
• Biphasic T wave with an initial negative deflection and terminal positive deflection.

EKG features in digoxin toxicity
• Increased intracellular calcium: Increased automaticity.
• Increased vagal effect: Decreased AV conduction.
• Classic arrhythmia: SVT with slow ventricular response.
• Most common abnormality: Frequent PVCs (including ventricular bigeminy and trigeminy).
• Other forms: Sinus bradycardia, any degree of AV block, Slow A.Fib, Regularized A-Fib and VT (Bidirectional & polymorphic).

Classification of Tachyarrhythmia

SVT Atrial Rate Conduction RR interval P waves QRS
Sinus Tachycardia 100-160 1:1 Regular Upright Narrow
PSVT 160-225 1:1, 2:1 Regular Variable Narrow
Atrial Flutter 225-320 1:1, 2:1, 4:1 Variable Sawtooth Narrow or Wide
A.Fib >320 Variable Variable Not clear Narrow or Wide
MAT 100-250 1:1 Variable Multiform Narrow
Junctional Tachycardia 100-180 1:1, 2:1 Regular Inverted Narrow
WPW 100-300 1:1, 2:1 Variable Upright Delta waves
General characteristics of SVT

Sinus Tachycardia
• Sinus rhythm with a resting heart rate of > 100 BPM in adults.
• Non-pharmacological causes: pain, anxiety, exercise, fever, hyperthyroidism, PE.
• Pharmacological causes: Beta agonists, sympathomimetics, anticholinergics.
• Camel hump: P wave attached or hidden in the preceding T wave.

Atrial Tachycardia
• Origin: ectopic atrial focus outside the SA node.
• P wave morphology and axis are abnormal.
• Must have at least 3 consecutive identical ectopic P waves (Coming from same focus).
• QRS: Normal unless (pre-existing BBB, Rate-dependent aberrancy)
• May be paroxysmal or sustained.
• If sustained, can lead to tachycardia-induced cardiomyopathy.

Multifocal Atrial Tachycardia (MAT)
• Origin: multiple ectopic foci within the atria.
• P waves: At least 3 distinct morphologies in the same lead.
• Rhythm: Irregularly irregular
• Causes: RA dilatation, hypoxia/hypercarbia, hypo K/Mg, sympathomimetics.
• Mostly seen in patients with advanced COPD or CHF.
• Development of MAT during acute illness carries poor prognosis and is associated with increased mortality.
• Usually a transitional rhythm between frequent PACs and A. Flutter or A. Fib.
• Usually resolves with treatment of the underlying disorder.

Atrial Flutter
• Origin: Usually a re-entry circuit within RA.
• Atrial rate: Usually 300 BPM.
• Flutter waves (saw-tooth pattern) are best seen in leads II, III, aVF (Turn the EKG upside
down!).
• Usually associated with AVB (physiological response to rapid atrial rate). Commonest is
2:1 resulting in ventricular rate of 150 BPM.
• Atrial flutter with 1:1 AV conduction can result in with severe hemodynamic instability
and progression to ventricular fibrillation.
• Variable AV block will result in irregular RR interval and may mimic A-Fib.
• Typical (common, Type I): Arises from re-entry circuit in the cavotricuspid isthmus. 90%
will have anticlockwise Re-entry leading to inverted flutter waves in the inferior leads.
• Atypical (Uncommon, Type II): Doesn’t fulfill criteria for typical A-flutter. Usually
associated with a higher atrial rate. Less amenable for ablation.

• Narrow complex tachycardia at 150 BPMSuspect A-flutterTurn the EKG
upside down and look for the flutter waves in the inferior leads.
• Vagal maneuvers and adenosine: Increases AVB which may unmask the flutter
waves. Usually doesn’t cardioverted (unlike AVNRT/AVRT).
• In A-flutter with variable block, the R-R intervals will be multiples of the P-P
interval (unlike coarse A-fib).
• New-onset A-flutter with high-grade AVB is very suspicious for digoxin toxicity.

Atrial Fibrillation
• The most common sustained arrhythmia.
• Life time risk: 1 in 4 individuals >40 years old.
• Increased automaticity or micro re-entry of an atrial focus (usually around the pulmonary vein).
• LA enlargement increases the chance of formation and propagation of wandering wavelets that run in re-entry circuits.
• Causes: HTN, Ischaemia, Valvular e.g. MS, hyperthyroidism, sympathomimetics, cardiomyopathies, PE, sympathomimetics.
• No P waves. Absent isoelectric baseline.
• Fibrillatory waves can be fine (<0.5 mm in amplitude) or coarse (>0.5 mm in amplitude).
• Irregularly irregular rhythm. RVR if QRS rate is >100 BPM (Usually up to 160 BPM).
• QRS: Normal unless (pre-existing BBB, Rate-dependent aberrancy)
• Slow A-fib: QRS rate is <60 BPM. Usually seen in digoxin toxicity, Hypothermia and sinus node dysfunction.
• Paroxysmal A-fib: Terminates spontaneously or with intervention in < 7 days.

Ashman Phenomenon
• Typically seen with A-fib, but can also occur with other supraventricular arrhythmia.
• Aberrantly conducted complexes with RBBB morphology that follows a long RR / short RR cycle.
• Short-long-short RR interval is even more likely to initiate aberration.
• Mechanism: Premature supraventricular impulse (Has a short RR interval) follows a long RR interval whilst the His-
Purkinje system is still refractory. RBB refractory period is longer than the LBB. So, that premature impulse is aberrantly
conducted in a RBBB morphology.

Atrial Fibrillation in Wolff-Parkinson-White Syndrome
• 1 in 5 patients with WPW will experience A-fib.
• The accessory pathway allows for rapid conduction directly to the ventricles bypassing
the physiological delay in the AV node.
• Ventricular rate is usually >200 BPM.
• QRS complex: wide (pre-excitation) and of different morphologies.
• Avoid ABCD (Adenosine/Amiodarone, BBs, CCBs & Digoxin) which can result in 1:1
conduction and induce Ventricular fibrillation.

Wolff–Parkinson–White syndrome
• Bundle of Kent is an accessory pathway that excites the ventricles and bypass the AV node.
• Most accessory pathways allow conduction in both directions.
• Pre-excitation occurs only if the accessory pathway allows antegrade conduction.
• Concealed pathway: Allows retrograde conduction only. So, no pre-excitation. No features
of WPW in EKG. Can still experience tachyarrhythmia as the pathway can be a part of a re-
entry circuit.
• PR interval: Short (<3 small squares).
• Delta wave: Slurred upstroke to the QRS complex
• QRS: wide > 110-120 msec.
• Can be associated with discordant ST Segment and T wave changes.
• Type A: +ve delta wave in all precordial leads with R/S > 1 in V1 (Mimic posterior infarction)
• Type B: -ve delta wave in leads V1 and V2. (pseudo-Q waves, Pseudo-infarction pattern)

Lown–Ganong–Levine syndrome (LGL) Syndrome
• Short PR-normal QRS syndrome.
• Accessory pathway: James fibers that connects the atria directly to the bundle of His (Debatable).
• PR: Short < 3 small squares. NO Delta waves
• No increased risk of sudden cardiac death.
• Can be associated with paroxysmal supraventricular tachyarrhythmia.
• Short PR interval in the absence of symptomatic tachycardia is simply a benign EKG variant.
• Mahaim Fibre Tachycardia: Re-entry tachycardia with LBBB morphology.

Atrioventricular Re-entry Tachycardias (AVRT)
• A re-entry circuit is formed by the normal conduction system and the accessory pathway
resulting in paroxysmal supraventricular tachycardia.
• Usual trigger: PAC or PVC.
• Orthodromic AVRT: anterograde conduction occurs through the AV node and retrograde
conduction through the accessory pathway. Can occur in patients with concealed pathway.
• Antidromic AVRT: Retrograde conduction occurs through the AV node and Antegrade
conduction through the accessory pathway.

Orthodromic AVRT
• Ventricular rate: 200-300 BPM.
• P waves: Buried in QRS or retrograde
• QRS: Normal unless (pre-existing BBB, Rate-dependent aberrancy).
• Usually associated with rate-related ST depression & TW inversion.
• Can be indistinguishable from AV-nodal re-entry tachycardia (AVNRT).
• If hemodynamically unstable: Synchronized DC cardioversion.
• If hemodynamically stable: Vagal maneuvers, adenosine or CCBs.

Antidromic AVRT
• Constitutes only 5% of AVRT in patients with WPW.
• Ventricular rate: 200-300 BPM.
• QRS: Wide >120 msec.
• Delta waves: Can be seen (Absent in case of concealed pathway).
• Can be mistaken for Ventricular Tachycardia.
• If in doubt, treat as VT.

SVT vs VT
 DDx of regular WCT: VT, PSVT with aberrancy (AVNRT
60% & Orthodromic AVRT 30%), antidromic AVRT.
 VT would not terminate with adenosine.
 Adenosine is generally safe in a patient regular WCT
(whether VT or AVRT) and usually will terminate the
rhythm if it is AVRT.
 AV nodal blockers are only contraindicated when there
is atrial fib with WPW.
 Any fast rhythm which worries you may be treated with
electrical cardioversion. If confused, use electricity. If
the patient is unstable, use electricity.
 In regular tachycardias due to WPW (even wide ones),
AV nodal blockers are safe and effective. They block the
limb of the re-entrant rhythm which goes through the
AV node, thus interrupting the circuit.
 Adenosine responsive fascicular VT: Very rare. Can
convert with adenosine. Occurs usually without
structural heart disease.

Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)
• Constitutes 60% of PSVT. More common in females.
• Ventricular rate: 140-280 BPM (Regular QRS complexes).
• Trigger: Premature beats.
• Typical Slow-Fast (Common: 90%) AVNRT: The anterograde conduction
is via the slow pathway and the retrograde conduction is via the fast
pathway.
• Mechanism: PAC causes block in the fast pathway so the conduction
proceeds down the slow pathway until it reaches the point of lower
common pathway fusion where the two pathways join. At this point, the
conduction proceeds back up the fast pathway in a retrograde fashion
creating re-entry circuit.
• P waves: Often hidden with the QRS complex or appear at its end
producing Pseudo r’ wave in V1 and Pseudo S waves in the inferior leads.

Other forms of AVNRT & Acute Management
• Atypical Fast-Slow (Uncommon: 10%) AVNRT: The anterograde conduction is via the fast pathway and the
retrograde conduction is via the slow pathway. P waves appears after QRS (QRS-P-T complexes). Retrograde
in inferior leads and positive in V1.
• Very Atypical Slow-Slow (<1%) AVNRT: Both the antegrade and retrograde pathways are slow. P waves occur
around the ST/TW. Can be mistaken with sinus tachycardia.

Causes of Wide-Complex Tachycardia (WCT)
Ventricular Tachycardia (VT)
SVT with aberrant conduction due to BBB.
SVT with aberrant conduction due to WPW.
Metabolic derangements e.g. hyperkalemia
Poisoning with sodium-channel blocking agents e.g. TCA
Pacemaker mediated tachycardia.

Monomorphic VT
• The most common form of VT
• Origin: Single focus in the ventricle
• QRS: Wide (>120 msec), Uniform, at a rate >100 BPM.
• Strongly associated with pre-existing poor ventricular function.
• Untreated VT causes decreased CO which result in decreased myocardial perfusion and degeneration of VT to VF.
• Sustained VT: lasts >30 sec OR causes hemodynamic compromise requiring an intervention (Hypotension, chest
pain, pulmonary edema, AMS).
• NSVT: Spontaneously terminated in <30 sec.
• Most common mechanism: Re-entry. Usually occurs in scarred myocardium.
• Triggered activity mechanism: due to after-depolarization. Seen in digoxin toxicity and Torsades de pointes (TDP).
• Automatic mechanism: due to increased automaticity of a ventricular focus.

Features of VT
• Usually have very broad QRS complexes >160 msec.
• Absence of typical RBBB or LBBB morphology.
• Extreme axis deviation (Northwest axis): QRS is positive in aVR and negative in the inferior leads.
• AV dissociation
• Capture beats: A sinus impulse transiently captures the ventricles, in the midst of AV dissociation, to produce a narrow QRS complex.
• Fusion beats: A sinus and ventricular beat coincide to produce a hybrid complex of intermediate morphology.
• Precordial leads concordance: Leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen.
• Brugada’s sign: The distance from the onset of the QRS complex to the nadir of the S wave is > 100 msec.
• Josephson’s sign: Notching near the nadir of the S-wave.
• Tall monophasic R wave in V1 with an rS complex in V6 (small R wave, big S wave). This pattern is very specific for VT.
• RSR’ complexes with a taller “left rabbit ear”: This is the most specific finding in favor of VT (Unlike in RBBB).

Right Ventricular Outflow Tract (RVOT) Tachycardia
• A form of Monomorphic VT.
• Origin: RVOT or from the tricuspid annulus.
• QRS: LBBB morphology
• Axis: Rightward axis (Around 90 degrees).
• Trigger: catecholamine excess, stress, and physical activity
• Idiopathic: In structurally normal heart. May respond to adenosine.
• RVOT tachycardia can also be seen in patients with Arrhythmogenic Right Ventricular Dysplasia.

Arrhythmogenic Right Ventricular Dysplasia (ARVD)
• The second most common cause of sudden cardiac death in young people (after HOCM).
• Fibro-fatty replacement of the RV myocardium.
• More common in men of Italian or Greek descent.
• Associated with paroxysmal ventricular arrhythmias (RVOT) and sudden cardiac death.
• Most specific EKG finding: Epsilon wave (30% of patients)
• V1-3: prolonged S-wave upstroke (95%), TWI (85%) and Localized QRS widening.

Polymorphic VT (PVT)
• Origin: Multiple ventricular foci.
• QRS: Wide, Variable amplitude, axis and duration.
• Most common cause: Ischaemia.
• Torsades de pointes (TdP): a form of PVT that occurs in the context of QTc prolongation in which the QRS complexes “twist”
around the isoelectric line. Usually self-limiting, but can degenerate into VF.
• Prolonged QTc  prolonged repolarization  early after-depolarisations (Tall U Waves) that can reach the threshold to propagate
PVC  R on T phenomenon  TdP.
• V. Bigeminy in a patient with prolonged QTc = Imminent TdP.

Bidirectional VT
• Rare form of VT.
• Beat-to-beat alternation of the frontal QRS axis (180 degrees).
• VT with alternating left and right bundle-branch block.
• Most common causes: Digoxin toxicity, Aconite poisoning, familial catecholaminergic
polymorphic ventricular tachycardia (CPVT).
• CPVT: Presents with episodic syncope during exercise or acute emotion in individuals
without structural cardiac abnormalities. Arrhythmia rapidly recede during recovery.

Fascicular (Belhassen-type, verapamil-sensitive) VT
• Only 10% of cases of VT occur in the absence of structural heart disease (Idiopathic VT).
• 90% of idiopathic VT arise from RV e.g. RVOT tachycardia. 10% arise from LV e.g. Fascicular tachycardia.
• Origin: Single focus in LV with a re-entry mechanism.
• Usually seen in young men without structural heart disease.
• Most episodes occur at rest but may be triggered by exercise, stress and beta agonists.
• QRS: Monomorphic, not very wide (100-140 msec) with RBBB morphology.
• Short RS interval (onset of R to nadir of S wave) of 60-80 msec (Usually >100 msec in other types of VT)
• Often misdiagnosed as SVT with RBBB.
• Verapamil is the first line treatment. Often unresponsive to adenosine or vagal maneuvers.
• Digoxin-induced fascicular VT is responsive to Digoxin Immune Fab.

Ventricular Flutter
• Extreme form of VT
• Continuous Monomorphic organized Sine Waves at rate of 250-300 BPM.
• No identifiable P waves, QRS complexes, or T waves.
• The EKG looks identical when viewed upside down!
• Associated with profound hemodynamic compromise.
• Degenerates rapidly into VF.

Ventricular Fibrillation (VF)
• Chaotic irregular deflections of varying amplitude at a rate of up to 500 BPM.
• No identifiable P waves, QRS complexes, or T waves.
• Invariably fatal rhythm if left untreated.
• Prolonged coarse VF  Fine VF  Asystole (Due to depletion of the myocardial energy stores).
• Multiple wavelet mechanism: Due to re-entry circuits formed by multiple wandering wavelets.
• Mother rotor mechanism: Stable re-entry circuit  propagates unstable daughter wavefronts.
• VF should never be diagnosed from the 12-lead EKG!
• VF is the most important shockable cardiac arrest rhythm.

Pacemaker-Mediated Tachycardia (PMT)
• Mechanism: PVC that gets conducted retrogradely into the atria  the atrial lead sense the activity as
incoming P wave  Start ventricular depolarization  Vicious circle (Re-entry mechanism).
• The pacemaker has a set upper rate limit.
• Note that tachycardia in a setting of a pacemaker can also be due to adaptation to a physiologic need e.g.
hydration, Infection, PE. It can also due to increased atrial activity e.g. PSVT, A-fib/RVR.
• Treatment: AV blocking to disrupt the re-entry circuit (adenosine, BB, CCB)
• If unstable, apply the magnet.
• Most modern pacemakers can recognize that and terminate the loop by prolonging the refractory interval
between atria and the ventricle.

Tips for arrhythmia identification &Management
• Maximum rate of sinus tachycardia in adults is 220-age (EXCEPT in hyperthyroidism)
• It’s best to cardiovert unstable tachyarrhythmias EXCEPT Sinus tachycardia & MAT. Treat their
underlying cause.
• Simplest way to identify the type of AVB is to look at the PR interval (Constant in first degree,
gradually increasing in Mobitz I, Randomly changing in Mobitz II).
• A-flutter is the most commonly missed arrhythmia. Always look for flutter waves in ALL leads
especially V1”upright flutter wave(s)”.
• It’s of utmost importance to differentiate between polymorphic VT and TdP is to measure the QTc.
Both look like twisting around a point. TdP has a prolonged QTc and you should maintain your patient
on magnesium and not amiodarone nor procainamide which further increase QTc.
• SVT with a RBBB is the only type of aberrancy that can be differentiated from VT by EKG if the QRS
morphology is the same in ALL leads as the baseline EKG.
• Short PR: Generally think a junctional rhythm or a pre-excitation syndrome.
• WPW with A-fib (> 200 BPM, different QRS morphologies) can be only treated with procainamide or
(Etomidate + 200 J synchronized cardioversion).

Tips, Cont’d
• Whenever you hear an alarm for V-fib, always check the pulse. If you can feel it, it was a false alarm.
• V-fib is NEVER a 12-lead EKG diagnosis, but rather a rhythm strip diagnosis.
• Hyper K is the syphilis of EKG (Can do anything)!
• The only time you shouldn’t give calcium push for hyper K EKG changes is digoxin toxicity (not just a
patient on digoxin). You should use Digibind in that case.
• Always think outside of the ACLS algorithm if you have a bizarre rhythm, mainly toxic/metabolic.
Always think of calcium and bicarbonate.
• Hyper K bradyarrhythmia is often resistant to atropine, transcutaneous and even transvenous pacing.
Use calcium and lower K.
• Stable VT must be cardioverted either chemically with procainamide, Amiodarone or Lidocaine or
electrically with synchronized cardioversion.
• Don’t call WCT a VT unless its rate >120 BPM
• WCT at a rate <120 especially with ultra-wide complexes: Think of AIVR (Reperfusion rhythm: No
intervention, Toxic/metabolic: Give calcium and Bicarbonate).

Anatomical correlation of the EKG

EKG in NSTEMI – ST depression
• Main patterns: ST depression, TW flattening or inversion.
• Main confounders: LVH, digoxin effect
• Dynamic ST/TW changes: Different from baseline ECG or changing over time. Strongly suggestive of ischaemia.
• Other forms of NSTEMI: Hyperacute TW, pseudonormalisation of previously inverted TW and U wave inversion.
• ST depression in NSTEMI: Horizontal or downsloping ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads.
• ST depression ≥ 1 mm: More specific for ischaemia and indicate worse prognosis.
• ST depression ≥ 2 mm in ≥ 3 leads: More specific for ischaemia and predicts 35% mortality over next month.
• Upsloping ST depression: Non-specific for NSTEMI.
• ST depression due to subendocardial ischaemia is usually widespread.
• Generalized ST depression plus STE in aVR > 1 mm = Left main coronary artery occlusion.
• ST depression doesn’t localize ischaemia.
• ST depression limited to a particular territory of leads is likely to represent reciprocal changes of STEMI.

STE in aVR + Widespread ST depression = STEMI equivalent
• Widespread horizontal ST depression
• STE in aVR ≥ 1mm: Highly specific for LAD occlusion proximal to the first septal branch and predicts the need for CABG.
• STE in aVR ≥ V1: Differentiates LMCA from proximal LAD occlusion
• Not specific to LMCA occlusion as it can be seen in proximal LAD occlusion, 3 vessel disease or diffuse subendocardial
ischaemia e.g. post-resuscitation from cardiac arrest and tachycardia-related ST depression.
• NO STE in aVR = NO significant LMCA occlusion.

Causes of ST Depression
• NSTEMI
• Reciprocal change in STEMI & Posterior MI.
• Digoxin effect.
• Hypo K/Mg.
• Tachycardia-related ST depression.
• RBBB & LBBB
• RVH & LVH (Strain pattern)
• Ventricular paced rhythm.

Reciprocal changes - PAILS
• STE during STEMI is associated with simultaneous ST depression in the electrically opposite leads.
• PAILS (Posterior, Anterior, Inferior, Lateral & Septal): ST elevations in these leads will create reciprocal ST
depression in the corresponding leads of the next letter in the mnemonic.
Regions STE Reciprocal ST depression
o Posterior None V1V3
o Anterior V3, V4 II, III, aVF
o Inferior II, III, aVF I, aVL
o Lateral I, aVL, V5, V6 II, III, aVF
o Septal V1, V2 None

Ischaemic T wave inversion (TWI)
• Isolated TWI is a normal variant in leads III, aVR and V1.
• Only significant if seen in leads with upright QRS complexes.
• At least 1 mm deep and present in ≥ 2 contiguous leads.
• Dynamic: Not present on old ECG or changing over time. Seen in acute ischaemia.
• Fixed: Usually seen following MI, in association with pathological Q waves.
• Ischaemic TWI is usually symmetrical and deep (>3mm)

Wellens’ Syndrome
• Type B (75%): Deep, symmetrical TWI in V2-V3
• Type A (25%): Biphasic (initial positivity and terminal negativity) In V2-V3
• T wave changes may extend from V1  V6
• T wave can evolve over time from Type A to Type B pattern.
• Highly specific for a critical LAD stenosis.
• May also occur in normal coronary arteries following an episode of vasospasm (e.g. cocaine-induced).
• Patients may be asymptomatic with normal or mildly elevated troponin.
• Very high risk for extensive anterior wall MI within the next few days to weeks.
• Requires invasive therapy. Poor response to medical management alone.

De Winter T Wave = Anterior STEMI equivalent
• Upsloping ST depression (>1 mm) + Peaked (Tall & symmetrical) T waves in the precordial leads.
• The ascending limb of the T wave starts below the isoelectric baseline.
• Usually evolves to classic anterior STEMI.
• Can be associated with minimal STE in aVR (0.5-1 mm).
• Signifies proximal LAD occlusion.

Causes of TWI
o Normal finding in children.
o Persistent juvenile T wave pattern
o Isolated TWI is a normal variant in leads III, aVR and V1.
o Myocardial ischaemia including Wellens syndrome
o RBBB & LBBB
o RVH & LVH (Strain pattern)
o PE
o HOCM
o Increased intracranial pressure
o Digoxin effect
o Peri-myocarditis
Causes of giant TWI
 Apical HOCM.
 Subarachnoid hemorrhage/CVA.
 Wellens syndrome type B
 Complete heart block
 Severe RVH, severe LVH
 WPW syndrome
 Post-pacemaker syndrome
 Acute pancreatitis
 Elevated ICP

Non-specific ST segment and T wave changes
• ST depression < 0.5 mm
• T wave flattening or TWI < 1 mm
• Upsloping ST depression.
• Non-specific for myocardial ischaemia.
Causes of non-specific ST/TW changes
Electrolyte abnormalities e.g. hypokalemia.
Metabolic derangement (Acidosis or alkalosis)
Fever
Anemia
CVA
Myopericarditis
PE
Chronic lung disease
Cardiomyopathies
High catecholamine states
Post-cardiac surgery

Inverted U waves
• May be the earliest marker of UA and evolving MI.
• Has been associated with LAD or LMCA occlusion and the presence of LV dysfunction.
• Usually seen in lateral leads (I, aVL, V5, V6).
• Other causes: HTN, Hyperthyroidism, Cardiomyopathy, Valvular and congenital heart diseases.

Poor R Wave Progression (PRWP)
• R wave height ≤ 3 mm in V3.
• Normally, R wave height becomes progressively taller from V1 through V6.
• Causes: Normal variant, Prior anteroseptal MI, LVH, RVH, transposition of V1 and V3, Dilated cardiomyopathy,
WPW, LBBB, LAFB, dextrocardia and mediastinal shift (e.g. with tension pneumothorax).

Causes of ST elevation (STE)
 STEMI
 Coronary vasospasm (Printzmetal’s angina)
 Pericarditis.
 Benign Early Repolarization (BER).
 LBBB
 LVH
 Ventricular Aneurysm
 Brugada syndrome
 Ventricular paced rhythm
 High ICP
 Takotsubo cardiomyopathy.
 Aortic dissection (with RCA dissection)
 Post-cardioversion
 Hyper K/Ca (Localized in V1, V2)
 Hypothermia (J waves).
 PE

Benign Early Repolarization (BER)
• Normal variant and usually seen in young healthy patients <50 years old.
• Widespread concave STE (High take-off) especially in V2-V5.
• V4 Fish hook pattern: Notching of J point.
• T waves: Prominent, slightly asymmetrical & concordant with the QRS complex main vector.
• NO reciprocal ST depression.
• Relative temporal stability of ST changes over time.
• STE/TW amplitude ratio in V6 is <25% (differentiates BER from Acute pericarditis)

Types of Myocardial infarction

Electrocardiographic evolution of STEMI
 New onset ST elevation.
 In 2 or more contiguous leads.
 All limb leads, V4, V5, V6: > 1 mm.
 V2, V3: ≥ 2 mm in men above 40 years old, ≥ 2.5 mm in
men younger than 40 years old or ≥ 1.5 mm in all women.
 Reciprocal ST depression in the electrically opposite leads
increases the specificity for STEMI.
 STE localizes the sites of occlusion.
 N.B: Concave STE doesn’t rule out STEMI, however
decreases its probability

Anterior STEMI
• Usually large infarct and carries the worst prognosis of all STEMIs.
• Occluded vessel: LAD
• Earliest changes: Hyperacute (Peaked, narrow and symmetrical) T waves.
• STE ± Q waves: Precordial leads ± High lateral leads (I, aVL).
• Reciprocal ST depression: Inferior leads (II, III, aVF)
• Tombstoning: proximal lesion = large infarction = Poor LV function ± cardiogenic shock
• Other forms: Wellens syndrome, De Winter T waves and STE in aVR.

Anterior – Inferior STEMI
• Due to occlusion of wraparound LAD
• Type III LAD: Wraps around the cardiac apex to supply both the anterior and inferior walls of the LV.
• STE ± Q waves in the precordial and inferior leads.

Site of LAD occlusion in Anterior STEMI
• Septal perforators supply the interventricular septum and
the bundle branches.
• D1 supplies the high lateral wall of the LV.
• LAD occlusion proximal to S1  Basal septal involvement
(STE in V1 & aVR, complete RBBB, ST depression in V5).
• LAD occlusion proximal to D1  High lateral involvement
(STE in I & aVL, ST depression in II, III, aVF)

Subtle Anterior STEMI – Smith Equation
• Differentiates benign early repolarization from subtle anterior STEMI.
• EKG must show ≥1 mm STE in ≥1 of the precordial leads V2-V4.
• The equation doesn’t apply if there is >5 mm STE, Non-concave STE, associated reciprocal ST depression in inferior
leads, Anterior ST depression, Q waves in any of V2 to V4, QRS distortion in V2 or V3 or TWI from V2 to V6.
• 0.052 x (Bazett-corrected QT interval, msec) - 0.151 x (QRS amplitude in lead V2, mm) - 0.268 x (R wave amplitude in
lead V4, mm) + 1.062 x (STE 60 msec after the J point in lead V3, mm).
• Scores ≥18.2: 83% sensitive and 87% specific for subtle anterior STEMI.
• Scores <18.2: Likely benign early repolarization.

Sgarbossa Criteria
• Used to diagnose MI In patients with LBBB or ventricular paced rhythm (LBBB morphology).
• Score of ≥ 3 is reported to have a specificity of 90% for diagnosing MI.

Triaging patients with suspected MI and LBBB

Lateral STEMI
• Usually occurs as part of a larger territory infarction, e.g. anterolateral STEMI.
• LCx occlusion  Infero-postero-lateral MI
• LAD occlusion  Antero-lateral MI (STE in the precordial leads plus the high lateral leads (I and aVL) is
87% predictive of a proximal LAD lesion.
• Isolated lateral STEMI: May occur due to occlusion of D1 of LAD, OM of LCx or the ramus intermedius.
• STE in the lateral leads (I, aVL, V5-6).
• High lateral STEMI: STE that is localized to leads I & aVL.
• Reciprocal ST depression in the inferior leads (II, III & aVF) only if there is STE in leads I & aVL. May be
obliterated if there is concomitant inferior STE (Inferolateral STEMI).

Inferior STEMI
• Constitutes about 50% of all MIs. Better prognosis than anterior STEMI.
• 40% of inferior STEMI have a concomitant RV infarction.
• 20% of inferior STEMI will develop significant bradycardia/AVB.
• Can be associated with posterior MI.
• STE (± Q waves) in leads II, III & aVF
• Reciprocal ST depression in aVL (± lead I).
• RCA culprit: 80%, STE in lead III > lead II, reciprocal ST depression in lead I ± STE in V1 and V4R.
• LCx culprit: 20%, ST elevation in lead II = lead III, STE in lead I, V5-6, No reciprocal ST depression in lead I.
• Anterior – Inferior STEMI: due to wraparound LAD

Right Ventricular Infarction
• Occurs in 40% of inferior MI.
• Isolated RV infarction: Extremely rare (Can be misinterpreted as antero-septal
STEMI due to STE in V1, V2).
• Clinically: shock with clear lungs, elevated JVP, Kussmaul’s sign
• STE in V1 (The only lead that looks directly at RV)
• Inferior MI + STE in lead III> lead II  Look for RV infarction.
• STE in V1 + ST depression in V2: Highly specific for RV infarct.
• Confirmatory finding: STE in Rt sided leads (V4R, V5R & V6R)
• Hemodynamics: High RA pressure >12, PCWP <15. Normal or low PA pressure.
• Management: Volume expansion (Preload dependent), prompt reperfusion.
• Nitroglycerine is contraindicated.

Posterior MI
• Usually associated with inferior or lateral MI.
• Culprit: PDA (85% from a RCA, 15% from LCx)
• V1-V3 (Reciprocal changes from the injured posterior myocardium):
R/S ratio > 1 in V2, tall broad R waves (Q wave equivalent), upright
TW (TWI equivalent), Horizonatal ST depression (STE equivalent).
• Positive mirror test!
• Confirmatory finding: Subtle STE in V7-V9 (You only need 0.5 mm)

Right Atrial Enlargement (Hypertrophy)
• Peaked P wave (P pulmonale): Amplitude is >2.5 mm in the inferior leads or > 1.5 mm in V1, V2
• Primary etiology: Pulmonary HTN e.g. PAH, chronic lung disease (Cor-pulmonale), TS and PS

Left Atrial Enlargement
• Lead II: broad, bifid P wave (P mitrale). > 1mm between both peaks. Total duration >110 msec
• V1: Biphasic with the terminal negative portion > 1 mm in width and depth.
• Causes: Mitral stenosis and in association with LVH (HTN, AS, MR, HOCM)

Biatrial Enlargement
• Lead II: Bifid P wave (> 2.5 mm in width & > 2.5 mm in amplitude).
• V1: Biphasic P with the initial positive deflection > 1.5 mm in amplitude and the
terminal negative deflection > 1 mm x 1 mm.
• Combination criteria: V1 or V2 showing P wave positive deflection >1.5 mm in
amplitude & V5 or V6 or limb leads showing bifid P wave > 3mm in width.

Right Ventricular Hypertrophy (RVH)
• Right axis deviation.
• V1: R/S ratio > 1 OR > 7mm in amplitude.
• V5 or V6: R/S ratio < 1 OR > 7 mm in depth.
• QRS complex: Narrow unless accompanied by complete RBBB.
• RAE: P pulmonale.
• RV strain pattern: ST depression and TWI in the inferior leads (especially lead III
which the most Rightward facing lead) and Right precordial leads (V1-V4)
• S1/ S2/ S3 pattern: Far Right axis deviation with dominant S in leads I, II & III
• Causes: Pulmonary hypertension, PE, Cor-pulmonale…etc.

Left Ventricular Hypertrophy (LVH)
Voltage criteria – Limb leads
 R wave in aVL > 11 mm (Not in LAFB)
 R wave in lead I + S wave in lead III > 25 mm
 R wave in aVF > 20 mm
 S wave in aVR > 14 mm
Voltage criteria – Precordial leads
 R wave in V5 or V6 + S wave in V1 > 35 mm
 Largest R wave + largest S wave in precordial leads > 45 mm
 R wave in V4, V5 or V6 is > 26 mm
Non-voltage criteria
 R wave peak time in V5 or V6 > 50 msec
 LV strain pattern
• Left axis deviation.
• Signs of LAE.
• LV strain pattern: ST depression and TWI in Lt sided leads.
• May find prominent U waves.
• Voltage criteria alone are NOT diagnostic of LVH.
• Patients with significant LVH seen on echocardiography
may still have a relatively normal EKG.
• Severe LVH may mimic LBBB morphology.
• Causes: HTN, AS, HOCM, MR…etc.

Biventricular Hypertrophy
• EKG has a low sensitivity to diagnose biventricular
hypertrophy as the opposing LV & RV forces tend to cancel
each other out.
• There may be signs of both LVH and RVH on the same EKG.
• Katz-Wachtel sign: Large biphasic QRS in V2-5.

R Wave Peak Time (Intrinsicoid deflection)
• It is the time from the onset of Q or R wave to the peak of the R wave in the lateral leads (aVL, V5-6).
• It is the time taken for excitation to spread from the endocardial to the epicardial surface of LV.
• Prolonged RWPT: > 45msec.
• Causes of prolonged RWPT: LBBB, LAFB, LVH.
• Can be used to differentiate VT from SVT with aberrancy: RWPT ≥ 50 msec in lead II is suggestive of VT.

EKG changes in Pulmonary Embolism
• Most common: Sinus tachycardia.
• Most specific finding: Simultaneous TWI in the inferior (II, III, aVF) and Right precordial leads (V1-4).
• RBBB (Complete or incomplete): Associated with worse prognosis and higher mortality.
• RV strain pattern: ST depression/TWI in inferior leads (especially lead III) and Rt precordial leads (V1-4).
• Right axis deviation: Can be extreme (0:-90°)  pseudo-Left axis.
• RAE: P pulmonale
• S1-Q3-T3: Deep S wave in lead I, (Q wave and TWI in lead III). Neither sensitive nor specific.
• Pulmonary disease pattern: RV dilation  Clockwise rotation of the heart  shift of the transition point towards V6
with persistent S wave in V6.
• Atrial Tachyarrhythmias: Atrial tachycardia, A-flutter & A-fib.
• Non-specific ST/TW changes.
• 18% of patients present with a completely normal EKG.
• All of the above changes can also occur with any disease that causes Rt heart strain (Acute or chronic Cor-pulmonale)

Pulmonary disease EKG pattern
• Clockwise rotation of the heart  shift of the transition point towards V6 with persistent S wave in V6.
• Rightward shift of the P wave axis (Prominent in inferior leads, flat or inverted in high lateral leads).
• SV1-SV2-SV3 pattern: Absent R waves in the Right precordial leads (SV1-SV2-SV3 pattern).
• PR and ST sagging (Below TP segment baseline) due to exaggerated atrial depolarization.
• Hyperinflation leads to low voltage QRS complexes.
• RAE: P pulmonale
• Signs of RVH.
• RBBB.
• MAT.

EKG changes in HCM
• Signs of LVH and Left heart strain.
• Asymmetrical septal hypertrophy  deep, narrow & dagger like Q waves
(<1 mm in width, unlike infarction Q waves) in the lateral and inferior leads.
• Signs of LA enlargement: P mitrale.
• One in three patients with HCM will have WPW pattern.
• Arrhythmias: A-fib, SVT, VT
• Apical (Japanese) HCM: Giant TWI in the precordial leads.
• Some patients with HCM will have EKG changes, but with no Echo findings
of LVH  Need cardiac MR for Dx.

EKG changes in Dilated Cardiomyopathy
• Left or Biatrial enlargement.
• LVH or biventricular enlargement.
• Conduction deficits: LBBB (N.B. the presence of Q waves in V6 rules out LBBB) or non-specific IVCD
• Diffuse myocardial fibrosis  Decreased QRs voltage in limb leads.
• Discrepancy of QRS voltage: Signs of hypertrophy in V4-6 and low voltages in the limb leads.
• Poor R wave progression.
• Goldberger’s triad: (low voltage in limb leads, normal voltage in chest leads, and poor R wave
progression). 90% specific for dilated cardiomyopathy.
• Pseudoinfarction pattern: Abnormal Q waves in V1-4.
• Left axis deviation.
• Arrhythmia: PVCs, V-bigeminy, VT or VF.

EKG changes in Restrictive Cardiomyopathy
• Diffuse myocardial infiltration  Low voltage QRS complexes.
• Infiltration of the conduction system (e.g. sarcoid granuloma) AVB or BBB.
• Pathological Q waves e.g. with healing sarcoid granuloma.
• Non-specific ST segment / T wave changes.
• Arrhythmia: A-fib or ventricular arrhythmias.

Low QRS voltage
• QRS amplitude: < 5mm in all limb leads OR <10 mm in all precordial leads.
• Causes: Pericardial effusion, pleural effusion, obesity, Pneumothorax, emphysema, Restrictive
(infiltrative) CMP or loss of viable myocardium (previous massive MI, end stage dilated CMP).
• Triad of pericardial tamponade: Low QRS voltage + Tachycardia + electrical alternans.
• Electrical alternans: Different QRS amplitudes of consecutive and normally conducted complexes.

EKG changes in severe myxedema
• Due to myxedematous deposition in the myocardium and decreased inotropy/chronotropy.
• Classic triad: Low QRS voltage + Bradycardia + widespread TWI
• Other findings: Prolonged QTc, First degree AVB or non-specific IVCD.

EKG features of TCA overdose
• Sodium channel blocker  IVCD with wide QRS.
• Inhibition of K channels  Prolonged QTc
• Sinus tachycardia.
• aVR: Dominant R’>3 mm or R/S ration of >70%
• QRS >100 msec: Predictive of seizures.
• QRS >160 msec: Predictive of V-arrhythmia.
• Treatment: IV sodium bicarbonate (1-2 mEq/kg); repeat every few minutes until BP improves and QRS complexes narrows.
• Avoid procainamide (Ia) and flecainide (Ic), beta-blockers and amiodarone as they worsen the conduction abnormalities.
• The above conduction abnormalities can occur with other sodium channel blockers e.g. quinidine, procainamide, flecainide,
hydroxychloroquine and carbamazepine.

EKG features of Brugada Syndrome
• In part related to sodium channelopathy.
• Syndrome = EKG features + one of the clinical criteria.
• Clinical criteria: Documented VT or VF, syncope, induced VT, nocturnal agonal breathing,
FHx of SCD at <45 years old or type I Brugada EKG pattern in family members.
• Type I: Coved STE > 2 mm followed by TWI in any of V1-3.
• Brugada pattern in isolation is of a questionable significance.
• Unmasking of Brugada: Fever, Ischaemia, Hypo K/Temp, nitrates, CCBs, BBs, cocaine,
alcohol, sodium channel blockers and post DCCV.

EKG changes in Dextrocardia
• Dominant R wav in aVR.
• Lead I global negativity: P wave inversion, TWI, negative QRS.
• Precordial leads: Reverse R wave progression & Dominant S wave throughout.
• N.B: Reversal of Right and Left arm leads produce the above changes with the exception of these in the precordial leads.

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