10 Common Heart Diseases: ECG Changes with Images

1. ST-Elevation Myocardial Infarction (STEMI)

• Hyperacute T waves - earliest change (tall, broad, peaked)
• ST-segment elevation ≥1 mm in 2 contiguous leads (the key diagnostic finding)
• Reciprocal ST depression in leads facing the opposite wall
• Pathological Q waves - develop within hours to days (necrosis marker)
• T-wave inversion - evolves as injury resolves
• Location identifies the artery: V1-V4 = anterior (LAD), II/III/aVF = inferior (RCA), I/aVL/V5-V6 = lateral (LCx)

Anterior Wall STEMI (LAD occlusion) - ST elevation in V1-V4:

Fig: Anterior wall STEMI. ST elevation is evident in leads V1-V4. Emergency catheterization revealed 90% stenosis of the left anterior descending artery. - Rosen's Emergency Medicine

Anterolateral STEMI - ST elevation extending to V5, V6, I, aVL:

Fig: Anterolateral STEMI with ST elevation in V1-V6 and leads I and aVL. - Rosen's Emergency Medicine

Inferior STEMI (RCA occlusion) - ST elevation in II, III, aVF:

Fig: Inferior MI from RCA occlusion - ST elevation in III greater than II, with ST depression in I and aVL (reciprocal changes). - Tintinalli's Emergency Medicine

Right Ventricular Infarction (complicates inferior STEMI - requires right-sided leads):

Fig: A - Inferior STEMI with ST elevation in V1 suggesting RV involvement. B - Right-sided leads confirming ST elevation in V1R-V6R. - Tintinalli's Emergency Medicine

2. Non-ST Elevation Myocardial Infarction (NSTEMI) / Unstable Angina

• ST depression ≥0.5 mm in 2 contiguous leads (subendocardial ischemia)
• T-wave inversion - especially deep, symmetric inversions ("Wellens' sign" in V2-V3 = critical LAD stenosis)
• Transient ST elevation - may occur during pain, resolves at rest
• No pathological Q waves (no full-thickness necrosis in most cases)
• The ECG may be completely normal in up to 6% of confirmed NSTEMIs

3. Atrial Fibrillation (AF)

• Absence of distinct P waves - replaced by fibrillatory baseline (f waves, irregular undulations at 350-600/min)
• Irregularly irregular RR intervals - the hallmark
• Narrow QRS complexes (unless aberrant conduction or pre-excitation)
• Rate: can be bradycardic (<60), normal (60-100), or with rapid ventricular response (>100)

ECG showing a PAC initiating atrial fibrillation:

Fig: ECG showing sinus P waves, a blocked PAC, then a PAC initiating atrial fibrillation. - Harrison's Principles of Internal Medicine 22E

Atrial fibrillation with fibrillatory p waves (f waves):

Fig: ECG of atrial fibrillation - irregularly irregular rhythm with fibrillatory (f) waves replacing normal P waves. - Symptom to Diagnosis, 4th Ed.

4. Complete Heart Block (Third-Degree AV Block)

• P waves and QRS complexes are completely independent (AV dissociation)
• Regular P-P intervals (atrial rate normal, 60-100/min)
• Regular but slower RR intervals (ventricular escape rate 20-40/min if ventricular, 40-60/min if junctional)
• Wide QRS complexes if ventricular escape; narrow QRS if junctional escape
• PR interval is completely variable (not constant) - this distinguishes it from 2:1 block

Complete Heart Block ECG with His-bundle recording:

Fig: Complete heart block. Surface leads show AV dissociation - atrial (A) and His (H) potentials occur without relationship to ventricular (V) activity. Most beats are conducted through an escape rhythm. - Fuster and Hurst's The Heart, 15th Ed.

5. Ventricular Tachycardia (VT)

• Wide QRS complexes (≥120 ms) - the defining feature of VT
• Rate: 100-250 bpm (usually 140-200)
• Regular rhythm (monomorphic VT) or irregular (polymorphic VT / Torsades)
• AV dissociation - P waves independent of QRS (present in ~50%; confirms VT)
• Fusion beats - partial capture of ventricle by sinus impulse (pathognomonic for VT)
• Capture beats - narrow QRS amid wide complexes (brief AV conduction; diagnostic)
• Morphology criteria: Brugada, Josephson's notching, concordance in chest leads

6. Ventricular Fibrillation (VF)

• No identifiable P waves, QRS complexes, or T waves
• Chaotic, irregular deflections varying in amplitude and morphology
• Can be fine (low amplitude, <3 mm - worse prognosis, harder to defibrillate) or coarse (high amplitude - more recently onset)
• Coarse VF can mimic VT morphologically

Fig: Three examples of VF. A - Fine amplitude. B - Coarse amplitude. C - Coarse amplitude mimicking VT. - Tintinalli's Emergency Medicine

7. Acute Pericarditis

• Stage 1 (acute, hours-days): Diffuse concave-upward ST elevation in most leads (I, II, aVF, V2-V6) PLUS PR segment depression (atrial injury) - most specific finding. Reciprocal ST elevation in aVR with PR elevation in aVR.
• Stage 2 (days-weeks): ST normalizes, T waves flatten
• Stage 3: Diffuse T-wave inversion throughout
• Stage 4: ECG normalization (or permanent T inversion)

Fig: Acute pericarditis ECG - widespread concave (saddle-shaped) ST elevation across multiple leads with PR depression. Note the characteristic changes in V2-V5 and inferior leads. - LITFL ECG Library

8. Left Ventricular Hypertrophy (LVH)

• Voltage criteria (several, pick one):
  • SV1 + RV5 or RV6 >35 mm (Sokolow-Lyon)
  • RaVL >20 mm (women) or >28 mm (men)
  • R wave in lead I + S wave in lead III >25 mm (Cornell)
• Left atrial enlargement - broad, notched P wave (P mitrale) in lead II, or biphasic P in V1
• Left axis deviation (QRS axis -30° to -90°)
• "LVH strain pattern": ST depression + T-wave inversion in I, aVL, V5-V6 (the leads with dominant R waves)
• QRS widening as LVH progresses toward LBBB

9. Wolff-Parkinson-White (WPW) Syndrome

1. Ventricular pre-excitation during sinus rhythm (causing delta waves)
2. Re-entrant tachycardias (AV reciprocating tachycardia at 160-220 bpm)
3. Rapid ventricular response in AF (potentially causing VF)

• Short PR interval (<120 ms) - impulse bypasses AV node delay
• Delta wave - slurred initial upstroke of the QRS (earliest ventricular activation via accessory pathway)
• Wide QRS (>120 ms) - fusion of delta wave + normal His-Purkinje activation
• Discordant ST-T changes - ST/T waves directed opposite to the delta wave and QRS
• Pseudo-Q waves - negative delta waves can mimic infarction

• Orthodromic AVRT: narrow QRS, regular, 160-220 bpm (no delta wave)
• Antidromic AVRT: wide QRS, mimics VT
• AF with accessory pathway: irregular wide bizarre QRS, rate can reach 300 bpm

Fig: A - 12-lead ECG in WPW syndrome showing delta waves. B - Single complex with short PR and delta wave (slurred upstroke). C - Wide QRS fusion complex. D - Diagram of accessory pathway (AP) bypassing the AV node (AVN). - Tintinalli's Emergency Medicine

10. Pulmonary Embolism (PE)

• Sinus tachycardia - most common finding (occurs in ~44% of PE)
• S1Q3T3 pattern - deep S wave in lead I + Q wave in III + T-wave inversion in III (occurs in ~20%)
• Right bundle branch block (RBBB) - new incomplete or complete RBBB (right ventricular strain)
• Right axis deviation
• T-wave inversions in V1-V4 - right ventricular strain pattern (anterior leads)
• P pulmonale - tall peaked P waves in lead II (right atrial enlargement)
• Atrial fibrillation or flutter - may be triggered by right atrial stretch
• Low-voltage QRS in massive PE with cardiac tamponade physiology
• Important: ECG is normal in ~25% of PE cases; a normal ECG does not exclude PE

Quick Reference Summary Table