10 Common Heart Diseases: ECG Changes & Diagrams

1. Acute Myocardial Infarction (STEMI)

• Hyperacute phase (minutes): Tall, peaked "hyperacute" T waves
• Acute phase (hours): ST elevation (>1 mm) in leads overlying the infarct; reciprocal ST depression in opposite leads
• Evolving phase (hours-days): Q waves develop (>40 ms wide, >25% of R wave); T-wave inversions appear
• Chronic phase: Persistent Q waves; ST may normalize
• Localisation: Anterior MI (V1-V4), Inferior MI (II, III, aVF), Lateral MI (I, aVL, V5-V6)

Anterior STEMI - ECG sequence (Acute → Evolving):

FIGURE: Anterior MI - acute (top row) shows ST elevation in I, aVL, V2-V6 with reciprocal depression in II, III, aVF. Evolving (bottom row) shows development of Q waves and T-wave inversions.

Inferior STEMI - ECG sequence:

FIGURE: Inferior MI - ST elevation in II, III, aVF with reciprocal ST depressions in I, aVL, and anterior leads.

Ischemia current of injury diagram:

FIGURE: A = subendocardial ischemia → ST depression; B = transmural/epicardial ischemia → ST elevation.

Source: Harrison's Principles of Internal Medicine 22E and Ganong's Review of Medical Physiology

2. NSTEMI / Unstable Angina (Subendocardial Ischemia)

• ST depression (≥0.5-1 mm) in leads over the affected territory
• T-wave inversions (particularly deep T-wave inversions in V1-V4 = "Wellens' sign" - high-grade LAD stenosis)
• No Q waves (non-Q-wave infarct)
• Normal ECG does not exclude NSTEMI - diagnosis depends on elevated troponin

Wellens' T-wave pattern (anterior ischemia):

FIGURE: Severe anterior wall ischemia - prominent T-wave inversions in V1-V6 (Wellens sign), associated with high-grade LAD stenosis.

Source: Harrison's Principles of Internal Medicine 22E

3. Acute Pericarditis

• Stage 1 (hours): Diffuse concave ("saddle-shaped") ST elevation in ALL leads except aVR and V1; PR depression in most leads; PR elevation in aVR ("knuckle sign") - non-territory-specific (distinguishes from MI)
• Stage 2 (days): ST and PR segments normalize
• Stage 3 (days-weeks): Diffuse T-wave inversions
• Stage 4 (weeks-months): ECG returns to normal

Pericarditis 12-lead ECG (Stage 1):

FIGURE: Stage I pericarditis - diffuse ST elevation (non-territory specific) with PR depression in most leads; aVR shows ST depression with PR elevation.

Source: Fuster and Hurst's The Heart, 15th Edition

4. Bundle Branch Block (RBBB & LBBB)

• QRS ≥ 120 ms
• rSR' pattern ("rabbit ears") in V1 - tall terminal R'
• Wide, slurred S wave in I and V6
• T-wave inversion in V1-V2 (secondary repolarization change)
• Causes: Atrial septal defect, PE, ischemic/valvular disease

• QRS ≥ 120 ms
• Broad, monophasic R wave in V5-V6 (no q wave)
• Deep QS complex in V1
• T-wave inversion in lateral leads (V5-V6, I, aVL) - discordant
• Causes: Coronary artery disease, hypertension, cardiomyopathy, aortic valve disease
• Clinical note: New LBBB with chest pain = treat as STEMI equivalent (Sgarbossa criteria)

RBBB vs LBBB - Pattern comparison:

FIGURE: Normal (top), RBBB (middle) showing rSR' in V1 and qRS in V6, LBBB (bottom) showing broad QS in V1 and monophasic R in V6, with discordant T-waves (arrows).

Source: Harrison's Principles of Internal Medicine 22E

5. Complete (Third-Degree) AV Block

• P waves and QRS complexes are completely independent (AV dissociation)
• P wave rate is faster than QRS rate
• PR interval is totally variable (P waves "march through" QRS)
• Narrow QRS if junctional escape; broad/wide QRS if ventricular escape
• Bradycardia (ventricular rate 20-60 bpm)

Second-degree AV block - Type I (Wenckebach) and Type II:

FIGURE: Panel A = Type I (Wenckebach) - progressive PR prolongation until P wave is dropped; Panel B = Type II - constant PR interval with sudden non-conducted P wave.

FIGURE: Type II AV block (top): sudden block with constant PR - block is within the His-Purkinje system. Wenckebach in His-Purkinje system (bottom): increasing H-V interval from 70 to 280 ms.

Source: Braunwald's Heart Disease, 2 Vol Set

6. Atrial Fibrillation (AF)

• Absent P waves - replaced by fibrillatory (f) baseline (fine or coarse irregular undulations at 350-600/min)
• Irregularly irregular RR intervals (hallmark finding)
• Narrow QRS (unless aberrant conduction or BBB)
• Heart rate typically 100-160 bpm if uncontrolled
• No organized atrial activity visible

• AF vs Atrial Flutter: Flutter has organized "sawtooth" flutter waves at ~300/min, usually with regular 2:1 or 4:1 block
• AF vs Multifocal Atrial Tachycardia (MAT): MAT has 3+ distinct P wave morphologies

Source: Braunwald's Heart Disease; Rosen's Emergency Medicine

7. Hypertrophic Cardiomyopathy (HCM)

• Increased QRS voltage (LVH criteria: S in V1 + R in V5/V6 ≥35 mm; or R in aVL ≥11 mm)
• Narrow septal Q waves in lateral leads (V5, V6, I, aVL) - due to exaggerated septal depolarization
• T-wave inversions in lateral leads (V4-V6)
• Left axis deviation
• Atrial fibrillation or atrial flutter (common complication)
• Apical HCM variant: Giant (>10 mm) T-wave inversions in precordial leads (V3-V5) - "Yamaguchi pattern"

HCM ECG - LVH voltage and septal Q waves:

FIGURE: HCM ECG - deep S-wave voltage (28 mm S in V3, large arrow) = LVH; narrow septal Q waves in V5-V6 (arrowheads) are characteristic. Concurrent atrial flutter with 2:1 block (additional P waves in ST segments, small arrows).

Source: Tintinalli's Emergency Medicine; Goldman-Cecil Medicine

8. Pulmonary Embolism (PE)

• S1Q3T3 pattern (classic but only seen in ~20% of cases): Deep S wave in lead I, Q wave in lead III, T-wave inversion in lead III
• Sinus tachycardia (most common finding)
• Right bundle branch block (new RBBB suggests severe RV strain and adverse outcome)
• Right axis deviation
• T-wave inversions in right precordial leads (V1-V4) - RV strain
• P pulmonale (tall peaked P waves in II) - right atrial enlargement
• S1S2S3 pattern (S waves in I, II, III)
• Atrial fibrillation/flutter
• Note: Normal ECG in PE does not exclude the diagnosis; ECG changes reflect RV strain severity

Source: Goldman-Cecil Medicine; Fuster and Hurst's The Heart

9. Ventricular Tachycardia (VT) and Ventricular Fibrillation (VF)

• Monomorphic VT: Regular wide-complex tachycardia (QRS ≥120 ms), rate 100-250 bpm; constant QRS morphology beat to beat; AV dissociation (P waves unrelated to QRS); fusion beats and capture beats (pathognomonic)
• Polymorphic VT / Torsades de Pointes: Beat-to-beat changes in QRS morphology and axis; twisting of QRS around isoelectric line (torsades); associated with prolonged QT interval (congenital or drug-induced)
• Ventricular Fibrillation: Low-amplitude, chaotic continuous electrical activity with no recognizable QRS complexes; rate >300/min; no cardiac output

VF with PVC trigger ECG:

FIGURE: ECG showing recurrent closely coupled PVCs in idiopathic VF, with PVC initiating VF (progressive deterioration into chaotic electrical activity visible on right).

Source: Goldman-Cecil Medicine International Edition

10. Wolff-Parkinson-White Syndrome (WPW) / Pre-excitation Syndrome

• Short PR interval (<120 ms) - bypass tract bypasses AV node delay
• Delta wave - slurred initial upstroke of the QRS (slow conduction through accessory pathway)
• Wide QRS (>120 ms) - due to fusion of pre-excitation and normal conduction
• Pseudo ST-T changes - secondary to abnormal depolarization

• Orthodromic AVRT (most common, ~80%): Narrow-complex tachycardia at 150-250 bpm (down AV node, up accessory tract) - delta wave disappears during tachycardia
• Antidromic AVRT: Broad-complex tachycardia (down accessory tract, up AV node) - maximally pre-excited, widened QRS
• AF with WPW (dangerous): Irregular very rapid broad-complex rhythm (>250-300 bpm) - can degenerate to VF; never give AV-nodal blocking drugs (adenosine, verapamil, digoxin)

Source: Harrison's Principles of Internal Medicine 22E; Braunwald's Heart Disease

Summary Table

• Harrison's Principles of Internal Medicine 22E (McGraw Hill, 2025)
• Braunwald's Heart Disease, 2 Vol Set - A Textbook of Cardiovascular Medicine
• Fuster and Hurst's The Heart, 15th Edition
• Goldman-Cecil Medicine International Edition
• Ganong's Review of Medical Physiology, 26th Edition
• Tintinalli's Emergency Medicine - A Comprehensive Study