10 Cardiac Heart Diseases with ECG Changes

1. ST-Elevation Myocardial Infarction (STEMI)

Mechanism of ST elevation: Epicardial myocytes depolarize from ischemic injury, creating a current of injury. The resulting voltage difference between injured and normal cells depresses the rest of the tracing relative to the ST segment — making ST appear elevated. — Medical Physiology (Boron & Boulpaep)

Pathological Q waves develop because the infarcted zone becomes electrically silent; the net depolarisation vector points away from the dead tissue, inscribing a deep negative deflection in overlying leads. — Medical Physiology

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

• ST-segment depression (horizontal or downsloping) in ischaemic territory
• T-wave inversion — symmetrical, deep ("Wellens' sign" in V1–V3 warns of critical LAD stenosis)
• No pathological Q waves (non-transmural)
• ECG may be normal in 30–50% at presentation

• Type A: Biphasic T waves in V2–V3
• Type B: Deep symmetric T-wave inversions in V2–V3

"The diagnosis of NSTEMI depends on abnormal elevation of cardiac biomarkers but may include ECG changes not meeting criteria for STEMI." — Tintinalli's Emergency Medicine

3. Atrial Fibrillation (AF)

1. Absent P waves — replaced by fine, irregular fibrillatory (f) waves on the baseline (best seen in V1 and lead II)
2. Irregularly irregular R-R intervals — no two consecutive R-R intervals are equal
3. Narrow QRS complexes — unless pre-existing bundle branch block or accessory pathway (WPW) causes aberrant conduction

ECG features: "Absence of discernible P waves with flat or chaotic isoelectric baseline; QRS complexes narrow unless preexisting bundle branch block or preexcitation syndrome; irregularly irregular ventricular rhythm." — Tintinalli's Emergency Medicine

4. Acute Pericarditis

• ST elevation is diffuse (not localised to one coronary territory)
• ST morphology is concave upward (saddle-shaped), not convex
• PR depression present in pericarditis; absent in STEMI
• No reciprocal ST depression except in aVR and V1
• No Q waves

"Typical ECG evolution follows four stages: (1) PR depression and/or diffuse ST segment elevation, (2) normalization of ST segment, (3) T wave inversion with or without ST segment depression, and (4) normalization." — Braunwald's Heart Disease

5. Complete (Third-Degree) AV Block

• Complete AV dissociation: P waves and QRS complexes occur at independent rates (P rate > QRS rate)
• P waves "march through" QRS complexes and T waves with no fixed PR interval
• Escape rhythm QRS: Narrow (junctional, ~40–60 bpm) if block is at AV node level; Wide (ventricular, ~20–40 bpm, QRS > 120ms) if block is infra-Hisian
• Slow ventricular rate → risk of syncope (Stokes-Adams attack)

• Mobitz I (Wenckebach): PR progressively lengthens → dropped beat; benign, usually at AV node
• Mobitz II: Fixed PR interval, abrupt dropped beats; more serious, infra-Hisian, risks progression to complete block

"First-degree AV block — conduction delay results in PR interval >200ms. Mobitz type II block carries less favourable long-term prognosis and is characterised by abrupt AV conduction block without evidence of progressive conduction delay." — Washington Manual of Medical Therapeutics

6. Hypertrophic Cardiomyopathy (HCM)

• Left ventricular hypertrophy (LVH) voltage criteria: Deep S in V1 + tall R in V5/V6 ≥35 mm (Sokolow-Lyon)
• Narrow ("septal") Q waves in lateral leads (I, aVL, V5, V6) — from exaggerated septal depolarisation
• T-wave abnormalities: Upright T waves in leads with septal Q waves (in obstructive HCM); giant deep T-wave inversions (>10 mm) in apical HCM (Yamaguchi variant)
• ST depression / strain pattern in lateral leads
• Left axis deviation
• Atrial fibrillation or flutter may coexist

"Deep S-wave voltage (28 mm in V3) signifies LVH, and narrow septal Q waves in V5 and V6 are noted. T waves are upright in the leads with the septal Q waves." — Tintinalli's Emergency Medicine, describing the HCM ECG

7. Left Ventricular Hypertrophy (LVH) — Hypertensive Heart Disease

• High QRS voltage (Sokolow-Lyon criteria): S in V1 + R in V5 or V6 ≥35 mm
• Cornell criteria: R in aVL >11 mm; or R aVL + S V3 >20 mm (women) / >28 mm (men)
• "Strain pattern": ST depression + asymmetric T-wave inversion in lateral leads (I, aVL, V4–V6) — a marker of severe LVH/subendocardial ischaemia
• Left axis deviation
• Left atrial enlargement (P mitrale: broad, notched P in lead II; biphasic P in V1)

8. Pulmonary Embolism (PE)

• Sinus tachycardia — the most common ECG finding (seen in ~44% of PE patients)
• S1Q3T3 pattern (McGinn-White sign): Deep S wave in lead I + Q wave in lead III + T-wave inversion in lead III (present in ~20%; sensitive but not specific)
• Right axis deviation
• Right bundle branch block (RBBB) — complete or incomplete
• T-wave inversions in V1–V4 (right ventricular strain pattern)
• ST elevation in aVR
• Sinus tachycardia is often the only finding in smaller emboli

The S1Q3T3 pattern reflects a rightward axis shift and clockwise rotation from acute right heart pressure overload.

9. Wolff-Parkinson-White (WPW) Syndrome

• Positive delta in V1 → left-sided pathway
• Negative delta in inferior leads (II, III, aVF) → posteroseptal pathway
• May produce "pseudoinfarction" Q waves mimicking inferior MI

10. Long QT Syndrome (LQTS)

• Prolonged QTc interval: QTc >450 ms (men), >460 ms (women) — corrected using Bazett formula (QTc = QT ÷ √RR)
• T-wave morphology varies by subtype:
  • LQTS1: Broad, prolonged T wave
  • LQTS2: Low-amplitude, notched/bifid T wave
  • LQTS3: Long flat ST segment → late-onset narrow T wave
• Torsades de Pointes: Polymorphic VT with a classic "twisting" of QRS complexes around the isoelectric baseline; initiated by a long-short R-R sequence ("R-on-T")

Summary Table