10 Common Heart Diseases — ECG Changes & Images

1. ST-Elevation Myocardial Infarction (STEMI)

• ST elevation ≥1 mm in ≥2 contiguous leads (≥2 mm in V1–V3)
• Hyperacute (peaked) T-waves — earliest sign
• Reciprocal ST depression in opposing leads
• Pathological Q waves develop within hours (indicate necrosis)
• T-wave inversion in the subacute phase
• Tombstone morphology in severe anterior STEMI

Convex ST elevation in V1–V6, I, aVL with hyperacute T-waves and reciprocal depression in II, III, aVF. Consistent with proximal LAD occlusion.

ST elevation in II, III, aVF with dominant R-waves and ST depression in V1–V3 indicating posterior wall involvement.

2. Atrial Fibrillation (AF)

• Absent P waves — replaced by low-amplitude fibrillatory (f) waves, best seen in V1 and II
• Irregularly irregular R-R intervals — hallmark finding
• Narrow QRS (unless aberrant conduction/bundle branch block)
• Ventricular rate varies: controlled (<100 bpm), uncontrolled (>100 bpm)

Classic AF: absent P-waves replaced by fine fibrillatory baseline, irregularly irregular narrow QRS complexes, no ST changes.

3. Complete (Third-Degree) Heart Block

• Complete AV dissociation — P waves and QRS complexes are independent, no fixed PR interval
• Atrial rate > ventricular rate (e.g., atrial 80 bpm, ventricular 30–40 bpm)
• Escape rhythm QRS: narrow if junctional (AV nodal block), wide/bizarre if ventricular (infra-Hisian)
• Severe bradycardia
• Prolonged QTc common with ventricular escape

Profound bradycardia (~33 bpm), complete AV dissociation with P-waves (arrows) marching independently of wide escape QRS (174 ms, RBBB morphology). QTc 560 ms.

4. Ventricular Tachycardia (VT)

• Wide complex tachycardia (QRS ≥120 ms) at rate 100–250 bpm
• AV dissociation — P waves independent of QRS (pathognomonic when visible)
• Fusion beats and capture beats (diagnostic when present)
• Concordance — all precordial leads positive or all negative
• North-West axis (aVR positive, negative in I and aVF)
• No preceding P waves

Regular wide-complex tachycardia, positive concordance across V1–V6, superior axis (negative II/III/aVF), no visible P-waves — classic monomorphic VT.

5. Acute Pericarditis

• Stage 1 (acute): Diffuse concave ("saddle-shaped") ST elevation in almost all leads (except aVR, V1 which show reciprocal depression); PR segment depression (best seen in II and V5); Spodick's sign (downsloping TP segment)
• Stage 2: ST returns to baseline, T-waves flatten
• Stage 3: Diffuse T-wave inversions
• Stage 4: ECG normalizes

Diffuse concave ST elevation in I, II, III, aVF, V2–V6. PR depression in II (Spodick's sign present). Reciprocal ST depression and PR elevation in aVR. Sinus tachycardia.

6. Hypertrophic Cardiomyopathy (HCM)

• Left ventricular hypertrophy (LVH) voltage criteria — Sokolow–Lyon: S in V1 + R in V5/V6 ≥35 mm
• Deep symmetric ("giant") T-wave inversions — most prominent in V4–V6 (apical HCM/Yamaguchi variant)
• Pathological Q waves in lateral/inferior leads (septal hypertrophy)
• Left axis deviation
• Non-specific ST depression
• May show AF or pre-excitation

High-voltage QRS (LVH criteria), deep symmetric "giant" T-wave inversions in V2–V6 and lateral limb leads with ST depression — hallmark of apical HCM.

7. Pulmonary Embolism (PE)

• Sinus tachycardia — most common finding (>44% of cases)
• S1Q3T3 pattern (McGinn-White sign): prominent S wave in I, Q wave in III, T-wave inversion in III
• Right heart strain: T-wave inversions in V1–V4
• Incomplete/complete RBBB — due to right ventricular strain
• Right axis deviation
• P pulmonale (peaked P waves in II/III/aVF)
• Atrial arrhythmias (AF, flutter)
• Massive PE may show electrical alternans

Sinus tachycardia (~116 bpm), classic S1Q3T3 pattern, T-wave inversions V1–V3, incomplete RBBB (110 ms) — acute right ventricular strain from PE.

8. Wolff-Parkinson-White (WPW) Syndrome

• Short PR interval (<120 ms) — accessory pathway bypasses AV node delay
• Delta wave — slurred upstroke at the start of QRS (slow ventricular pre-excitation)
• Widened QRS (>120 ms) due to fusion of normal and anomalous conduction
• Secondary ST-T changes (discordant to QRS direction)
• "Pseudo-infarction" Q waves from negative delta waves (especially inferior leads)
• Pathway localization by delta wave polarity in 12 leads

Short PR (<120 ms), prominent delta waves (slurred QRS onset) in II, III, aVF, V2–V6, widened QRS — classic ventricular pre-excitation of WPW.

9. Dilated Cardiomyopathy (DCM)

• Left bundle branch block (LBBB) — broad notched R in I, V5, V6; QS in V1–V3 (most common)
• Non-specific intraventricular conduction delay
• Low QRS voltage in limb leads (<5 mm) — especially in infiltrative causes (amyloid)
• Poor R-wave progression in precordial leads
• Pathological Q waves (pseudo-infarction pattern)
• Atrial fibrillation (common in advanced disease)
• Frequent PVCs or ventricular tachycardia
• Left axis deviation

Sinus bradycardia, first-degree AV block (PR 208 ms), complete LBBB (QRS 159 ms): broad monophasic R in I, aVL, V5/V6; deep QS in V1–V3; discordant ST-T changes laterally.

10. Inferior NSTEMI / Unstable Angina

• ST depression ≥0.5 mm (horizontal or downsloping) in ≥2 contiguous leads — key marker
• T-wave inversions — symmetric, deep ("Wellens' warning" in V2–V3 = critical LAD stenosis)
• No ST elevation, no pathological Q waves
• May be dynamic — changes resolve with pain relief
• Transient ST elevation possible during ischemic episodes
• Normal ECG in ~30% at presentation — serial ECGs mandatory

Side-by-side comparison: (a) Acute anterolateral STEMI with convex ST elevation V2–V5, I, aVL + reciprocal inferior depression. (b) After nitroglycerin/verapamil — ST segments normalize, demonstrating the dynamic, reversible nature of ischemic ST changes seen in ACS.

Summary Table

Clinical note: ECG interpretation must always be integrated with the clinical history, symptoms, biomarkers (troponin, BNP), and imaging. A normal ECG does not exclude serious cardiac pathology — serial tracings and continuous monitoring are often essential.