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Here is a comprehensive guide to 10 common heart diseases with their characteristic ECG changes and illustrative ECG images.

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Here is the comprehensive guide, drawn directly from Harrison's Principles of Internal Medicine (22nd ed.), Tintinalli's Emergency Medicine, Braunwald's Heart Disease, The Washington Manual, Fuster and Hurst's The Heart, and Goldman-Cecil Medicine.

A Guide to ECG Changes in 10 Common Heart Diseases

1. ST-Elevation Myocardial Infarction (STEMI)

Mechanism

Acute transmural ischemia shifts the ST vector toward the outer (epicardial) layer of the affected zone, creating a "current of injury." This produces ST elevations and, in the earliest phase, tall hyperacute T waves over the ischemic zone.

Characteristic ECG Changes

  • Hyperacute T waves - tall, broad, peaked; earliest finding (minutes after onset)
  • ST elevation - convex ("tombstone") shape in the territory of occlusion
  • Reciprocal ST depression - in leads opposite the infarct territory
  • Pathologic Q waves - develop within hours to days; indicate necrosis of sufficient myocardial tissue
  • T-wave inversions - follow ST elevation as infarct evolves

Localization by Lead

TerritoryCulprit ArteryLeads with ST Elevation
AnteriorLADV1-V4, I, aVL
InferiorRCA or LCxII, III, aVF
LateralLCxI, aVL, V5-V6
PosteriorRCA or LCxReciprocal changes V1-V3 (tall R, ST depression)
Right ventricularProximal RCAV1, V4R

ECG Images

Anterior STEMI (acute and evolving) - leads I, II, III, aVR, aVL, aVF, V2, V4, V6:
Anterior ST-elevation Q-wave infarction sequence showing acute and evolving changes across all leads
Acute (top row) and evolving (bottom row) anterior STEMI. Note ST elevation in I, aVL and precordial leads, with reciprocal ST depressions in II, III, aVF. - Harrison's Principles of Internal Medicine, 22nd ed.
Inferior STEMI (acute and evolving):
Inferior ST-elevation Q-wave infarction sequence showing acute and evolving changes
Acute (top row) and evolving (bottom row) inferior STEMI. ST elevation in II, III, aVF with reciprocal ST depression in I, aVL and anterior precordial leads. - Harrison's Principles of Internal Medicine, 22nd ed.
Subendocardial vs. transmural ischemia diagram:
Diagram showing subendocardial ischemia causing ST depression vs. transmural ischemia causing ST elevation in lead V5
Panel A: subendocardial ischemia - ST vector points inward, overlying leads record ST depression. Panel B: transmural/epicardial ischemia - ST vector points outward, overlying leads record ST elevation. - Harrison's Principles of Internal Medicine, 22nd ed.
Wellens T-wave sign (severe LAD stenosis):
Precordial leads V1-V6 showing deep symmetric T-wave inversions indicating critical LAD stenosis
Deep, symmetric T-wave inversions in V1-V6 (Wellens sign). This pattern indicates high-grade LAD stenosis and carries high risk of impending anterior STEMI. - Harrison's Principles of Internal Medicine, 22nd ed.

2. Atrial Fibrillation (AF)

Mechanism

Multiple small, chaotic atrial re-entry circuits fire at rates >600 bpm. There is no coordinated atrial depolarization. The AV node acts as a filter, passing impulses irregularly to the ventricles.

Characteristic ECG Changes

  • Absent P waves - replaced by chaotic, irregular fibrillatory baseline (best seen in V1)
  • Irregularly irregular ventricular rhythm - the hallmark; no two R-R intervals are equal
  • Variable ventricular rate - typically 120-170 bpm when AV node is unaffected; can exceed 200 bpm with accessory pathway
  • Narrow QRS complexes - unless pre-existing bundle branch block or accessory pathway

ECG Features Table (from Tintinalli's Emergency Medicine)

  • Absence of discernible P waves with flat or chaotic isoelectric baseline
  • QRS complexes narrow unless pre-existing bundle branch block or preexcitation syndrome
  • Irregularly irregular ventricular rhythm

ECG Image

Three rhythm strips labeled A, B, and C showing atrial fibrillation with irregularly irregular ventricular response
Three examples of atrial fibrillation. All show the hallmark irregularly irregular ventricular response with absent P waves. Strip A has rapid ventricular response; B and C show slower rates, possibly from AV nodal disease or medications. - Tintinalli's Emergency Medicine, 9th ed.

3. Atrial Flutter

Mechanism

A single, large macroreentrant circuit in the right atrium circles continuously at ~300 bpm, producing uniform flutter waves. Conduction to the ventricles is filtered by the AV node in fixed or variable ratios.

Characteristic ECG Changes

  • Sawtooth flutter waves - uniform, negatively directed "F waves" at ~300 bpm, best seen in leads II, III, aVF and V1
  • Regular ventricular rhythm - determined by the AV conduction ratio
  • 2:1 AV block - most common; ventricular rate ~150 bpm (a regular narrow-complex tachycardia at 150 bpm should immediately raise suspicion for flutter)
  • 3:1 or 4:1 AV block - ventricular rates of ~100 and ~75 bpm respectively
  • No isoelectric baseline between flutter waves - they merge continuously

Key Point

A regular narrow-complex tachycardia at exactly 150 bpm (±5 bpm) is atrial flutter with 2:1 block until proven otherwise.

4. AV Heart Blocks (1st, 2nd, 3rd Degree)

Mechanism

Delay or interruption of conduction between the atria and ventricles at or below the AV node.

First-Degree AV Block

  • PR interval >200 ms on every beat; all P waves conduct
  • No dropped beats
  • Usually benign; may occur in trained athletes, vagal tone, digoxin, or inferior MI

Second-Degree AV Block

Mobitz Type I (Wenckebach):
  • Progressive PR prolongation with each successive beat until a P wave fails to conduct (dropped QRS)
  • RR intervals shorten progressively before the dropped beat
  • Group beating pattern on the rhythm strip
  • Block usually within the AV node; benign prognosis; rarely progresses to complete block
Mobitz Type II:
  • Abrupt failure to conduct without prior PR lengthening
  • PR interval constant before the dropped beat
  • Often associated with bundle branch block
  • Block below the AV node; unpredictable - may progress suddenly to complete heart block
2:1 AV Block:
  • Every other P wave fails to conduct; difficult to distinguish Mobitz I from II
  • Presence of bundle branch block on conducted beats favors Mobitz II (infranodal)

Third-Degree (Complete) AV Block

  • Complete dissociation between atria and ventricles
  • P waves and QRS complexes march independently ("AV dissociation, A > V rate")
  • QRS complex morphology depends on escape pacemaker location:
    • Junctional escape (narrow QRS, 40-60 bpm) if block at AV node level
    • Ventricular escape (wide QRS, 20-40 bpm) if block at bundle branch level

ECG Image

Five ECG rhythm strips A through E showing first-degree, second-degree Mobitz I, second-degree Mobitz II, advanced, and third-degree AV block
A: First-degree AV block - PR >200 ms, no dropped beats. B: Second-degree Mobitz I (Wenckebach) - progressive PR prolongation then dropped beat, "group beating." C: Second-degree Mobitz II - abrupt dropped beat, constant PR. D: Advanced AV block with multiple consecutive non-conducted P waves. E: Third-degree complete heart block (V1) - complete AV dissociation with independent atrial and ventricular activity. - Washington Manual of Medical Therapeutics.

5. Acute Pericarditis

Mechanism

The pericardium itself is electrically silent. ECG changes reflect subepicardial myocardial inflammation, causing diffuse repolarization abnormalities. PR depression results from atrial epicardial involvement and augmented atrial repolarization.

Characteristic ECG Changes (4 Stages)

StageTimingECG Finding
1Hours of onsetDiffuse ST elevation (concave, saddle-shaped) in all leads except aVR and V1; PR depression in most leads; PR elevation in aVR ("knuckle sign")
2DaysST and PR segments return to baseline
3Days-weeksDiffuse T-wave inversions (without Q waves)
4Weeks-monthsECG normalizes

Distinguishing from STEMI

  • ST elevation in pericarditis is diffuse (nearly all leads), concave/saddle-shaped, with PR depression
  • STEMI shows focal, convex ST elevation in a coronary territory with reciprocal ST depression in opposite leads and may form Q waves
  • Pericarditis does not cause reciprocal ST depression (except in aVR, which shows ST depression)
  • Less than 60% of patients progress through all four stages; a normal ECG does not exclude pericarditis

ECG Image

12-lead ECG showing stage 1 acute pericarditis with diffuse ST elevation and PR depression in a non-territory-specific distribution
Stage 1 acute pericarditis: diffuse, concave ST elevation across non-contiguous leads in a non-coronary distribution. PR-segment depression is visible in leads II, V5, and V6. Lead aVR shows the characteristic PR elevation ("knuckle sign") with ST depression. Note the absence of Q waves or reciprocal changes as would be expected with STEMI. - Fuster and Hurst's The Heart, 15th ed.

6. Ventricular Tachycardia (VT)

Mechanism

A reentrant circuit or abnormal automaticity arises within the ventricular myocardium, below the bundle of His. Activation spreads through abnormal (non-Purkinje) pathways, producing a wide QRS.

Characteristic ECG Changes

  • Wide QRS complex (≥120 ms), typically >140 ms
  • Regular tachycardia at 100-250 bpm
  • AV dissociation - P waves march at a different rate from QRS; pathognomonic when present
  • Fusion beats - hybrid QRS from simultaneous sinus and ventricular activation; confirms VT
  • Capture beats - rare narrow QRS during tachycardia when sinus impulse captures ventricle; confirms VT
  • Concordance - all precordial leads with QRS deflection in same direction (positive or negative concordance); strongly favors VT
  • Extreme axis deviation ("northwest axis," -90° to ±180°)
  • QRS morphology: RBBB-like pattern with monophasic R or QR in V1; LBBB-like pattern with R>S in V1

Distinguishing VT from SVT with Aberrancy (Brugada Criteria)

VT is diagnosed if ANY one of these four criteria is present (checked in sequence):
  1. Absence of RS complexes in all precordial leads
  2. R-to-S nadir interval >100 ms in any precordial lead
  3. AV dissociation present
  4. Morphologic criteria for VT in V1/V6
Clinical rule: Any hemodynamically unstable wide-complex tachycardia should be treated as VT.

7. Ventricular Fibrillation (VF)

Mechanism

Completely disorganized depolarization of multiple small ventricular areas without any coordinated mechanical activity. Results in immediate loss of cardiac output.

Characteristic ECG Changes

  • Completely chaotic, irregular waveform with no identifiable P waves, QRS complexes, or T waves
  • No discernible organized rhythm of any kind
  • Variable amplitude: described as fine (low amplitude), intermediate, or coarse (higher amplitude, sometimes resembling VT)

ECG Image

Three ECG strips labeled A, B, and C showing fine, coarse, and very coarse ventricular fibrillation
Three examples of ventricular fibrillation. A: Fine amplitude VF - low-amplitude chaotic undulations with no organized activity. B: Coarse amplitude VF - higher amplitude, may be mistaken for a rhythm. C: Coarse VF that mimics ventricular tachycardia. Immediate defibrillation is required regardless of amplitude. - Tintinalli's Emergency Medicine, 9th ed.

8. Wolff-Parkinson-White (WPW) Syndrome

Mechanism

An accessory conduction pathway (Bundle of Kent) bypasses the AV node, creating a direct atria-to-ventricle connection. During sinus rhythm, the ventricle is activated simultaneously via both the accessory pathway (earlier, slower cell-to-cell conduction) and the normal AV node/His-Purkinje system. The resulting QRS is a fusion of both.

Characteristic ECG Changes During Sinus Rhythm (Classic Triad)

FeatureFindingMechanism
Short PR interval<120 msAccessory pathway bypasses AV nodal delay
Delta waveSlurred initial QRS upstrokeEarly ventricular activation via accessory pathway
Wide QRSSlightly prolonged (fused complex)Combination of accessory + normal activation
  • Secondary ST-T changes discordant (opposite) to the delta wave and QRS direction
  • Delta waves may mimic Q waves, simulating myocardial infarction

Tachyarrhythmias in WPW

  • Orthodromic AVRT (65%) - narrow QRS, 160-220 bpm, no delta wave during tachycardia; indistinguishable from AVNRT
  • Antidromic AVRT (5-10%) - wide QRS, 160-220 bpm; mimics VT
  • AF with WPW (25%) - irregular, very rapid (>200 bpm), wide QRS with varying morphology and delta waves; life-threatening

Critical Note

AV nodal blocking agents (adenosine, beta-blockers, calcium channel blockers, digoxin, amiodarone) are contraindicated in AF with WPW - they may enhance accessory pathway conduction, precipitating VF.

9. Hypertrophic Cardiomyopathy (HCM)

Mechanism

Massive myocardial hypertrophy (particularly septal) increases total myocardial mass, altering depolarization vectors and repolarization patterns. The ECG is abnormal in the vast majority of patients with HCM.

Characteristic ECG Changes

  • Left ventricular hypertrophy (LVH) voltage criteria - tall R waves in lateral leads (I, aVL, V5-V6) and/or deep S waves in right precordial leads (V1-V3); Sokolow-Lyon criteria: S in V1 + R in V5 or V6 >35 mm
  • Deep, narrow ("dagger-like") Q waves in lateral leads (I, aVL, V5-V6) and/or inferior leads - due to septal hypertrophy and abnormal septal depolarization (not infarction); a classic finding
  • Left axis deviation
  • ST depression and T-wave inversions in lateral leads
  • Left atrial enlargement - broad, bifid P wave (P mitrale) in II; biphasic P wave in V1
  • Giant T-wave inversions in apical HCM (Yamaguchi syndrome) - massive, symmetric T-wave inversions across all precordial leads, sometimes with tall R waves

Key Point

The combination of LVH voltage and deep narrow Q waves in the lateral leads in a young patient without prior MI is highly suggestive of HCM. The ECG is abnormal in >90% of HCM patients.

10. Pulmonary Embolism (PE)

Mechanism

Acute right ventricular pressure overload from obstruction of the pulmonary vasculature causes right heart strain. This shifts the cardiac electrical axis rightward and anteriorly, altering depolarization and repolarization.

Characteristic ECG Changes

Most common (but nonspecific):
  • Sinus tachycardia - most frequent ECG finding in PE
  • Non-specific ST-T wave changes - present in the majority
Classic (but uncommon, ~20% of cases):
  • S1Q3T3 pattern - deep S wave in lead I, Q wave in lead III, inverted T wave in lead III; indicates acute right heart strain
  • New right bundle branch block (RBBB) - complete or incomplete; new onset in clinical context of PE
  • Right axis deviation
Other right heart strain findings:
  • T-wave inversions in V1-V4 (anterior right ventricular ischemia pattern) - more common than S1Q3T3 in massive PE
  • Right atrial enlargement - tall peaked P waves (P pulmonale) in lead II
  • Low voltage or electrical alternans if pericardial effusion is also present
  • Sinus tachycardia remains the most sensitive ECG abnormality

Key Point

A normal ECG does not exclude PE. Sinus tachycardia alone with the right clinical scenario should prompt immediate evaluation. The S1Q3T3 pattern, while classic in textbooks, is present in only ~20% of confirmed PE cases. T-wave inversions in V1-V4 in the context of acute dyspnea and hypoxia are actually a more sensitive marker of right ventricular strain.

Summary Table

ConditionKey ECG Finding(s)Hallmark Feature
STEMIFocal convex ST elevation + reciprocal ST depressionTerritory-specific; evolves to Q waves
Atrial FibrillationNo P waves, irregularly irregular RRChaotic baseline, no two RR intervals equal
Atrial FlutterSawtooth flutter waves ~300 bpmRegular 2:1 rate ~150 bpm
1st-degree AV blockPR >200 ms, all beats conductProlonged PR, no dropped beats
2nd-degree Mobitz IProgressive PR lengthening then dropped beatGroup beating, Wenckebach cycles
2nd-degree Mobitz IIConstant PR then sudden dropped beatAbrupt block, often with BBB
3rd-degree AV blockComplete AV dissociationP and QRS march independently
Acute PericarditisDiffuse concave ST elevation + PR depressionSaddle-shaped, all leads except aVR
Ventricular TachycardiaWide QRS tachycardia + AV dissociationFusion/capture beats pathognomonic
Ventricular FibrillationChaotic, no QRS, immediate cardiac arrestNo organized waveform of any kind
WPWShort PR + delta wave + wide QRSPre-excitation triad in sinus rhythm
HCMLVH + deep narrow lateral Q waves"Dagger" Q waves without prior MI
Pulmonary EmbolismSinus tachycardia; S1Q3T3; T inversions V1-V4Right heart strain pattern
Sources: Harrison's Principles of Internal Medicine 22nd ed. | Tintinalli's Emergency Medicine 9th ed. | Braunwald's Heart Disease | The Washington Manual of Medical Therapeutics | Fuster and Hurst's The Heart, 15th ed. | Goldman-Cecil Medicine

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ECG Quick Reference

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What's in the card:
  • Single A4 landscape page - print-ready, compact enough to fit in a pocket folder or laminate
  • 13 conditions covered: STEMI, NSTEMI/UA, AF, Atrial Flutter, 1°/2°/3° AV Block, Acute Pericarditis, VT, VF, WPW, HCM, and Acute PE
  • 9 columns per condition:
    • Numbered colour-coded strip (unique colour per condition)
    • Condition name & abbreviation
    • Rhythm
    • PR interval findings
    • QRS complex findings
    • ST/T changes
    • Additional features (including critical warnings, e.g. "AVOID adenosine in AF+WPW")
    • Hallmark finding - highlighted in red bold italic for fast scanning
    • Key leads
  • Abbreviations legend and source textbooks at the bottom
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