Explain common 10 heart diseases with ECG changes and ECG images of those diseases
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ECG ST elevation myocardial infarction STEMI
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ECG atrial fibrillation electrocardiogram
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ECG ventricular tachycardia electrocardiogram
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ECG complete heart block atrioventricular block
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ECG Wolff-Parkinson-White delta wave pre-excitation
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ECG left ventricular hypertrophy hypertrophic cardiomyopathy
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ECG pericarditis saddle-shaped ST elevation
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ECG pulmonary embolism S1Q3T3 right heart strain
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ECG Brugada syndrome coved ST elevation V1 V2
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ECG long QT syndrome torsades de pointes
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10 Common Heart Diseases — ECG Changes & Images
1. ST-Elevation Myocardial Infarction (STEMI)
ECG Changes
- Hyperacute T waves (earliest sign) — tall, broad, symmetric peaked T waves
- ST-segment elevation ≥1 mm in ≥2 contiguous limb leads or ≥2 mm in ≥2 precordial leads; convex ("tombstone") morphology in severe cases
- Reciprocal ST depression in mirror-image leads (e.g., inferior STEMI → depression in aVL)
- Pathological Q waves (>40 ms wide, >1/4 of R-wave height) develop within hours and indicate transmural necrosis
- T-wave inversion follows as the infarct evolves
Localisation: Anterior (V1–V4 = LAD), Inferior (II, III, aVF = RCA/LCx), Lateral (I, aVL, V5–V6 = LCx)
Anterior STEMI: Convex ST-segment elevation across V1–V6, most pronounced in V2–V4; reciprocal depression in inferior leads. — Harrison's Principles of Internal Medicine 22E
2. Atrial Fibrillation (AF)
ECG Changes
- Absent P waves — replaced by chaotic fibrillatory (f) waves best seen in V1 and lead II; frequency 350–600 impulses/min
- Irregularly irregular R-R intervals — the hallmark finding
- Narrow QRS complexes (unless aberrant conduction or bundle branch block co-exists)
- Ventricular rate typically 100–180/min if uncontrolled; low-voltage QRS in limb leads may suggest infiltrative disease (e.g., amyloidosis)
Atrial fibrillation with rapid ventricular response: absent P waves, fibrillatory baseline, irregular RR intervals. — Tintinalli's Emergency Medicine
3. Complete (Third-Degree) Atrioventricular Block
ECG Changes
- Complete AV dissociation — P waves and QRS complexes fire independently with no fixed PR interval
- Regular P-P intervals (atrial rate faster, typically 60–100/min)
- Regular R-R intervals at a slower escape rate (ventricular 30–50/min)
- Wide QRS if escape rhythm is infra-Hisian/ventricular; narrow QRS if junctional escape
- Secondary ST-T changes from abnormal ventricular activation
Third-degree AV block: slow bradycardic ventricular escape rhythm (~44 bpm), wide QRS, complete AV dissociation with faster independent P waves. — Harrison's Principles of Internal Medicine 22E
4. Ventricular Tachycardia (VT)
ECG Changes
- Wide QRS complex tachycardia (QRS >120 ms) at rate 100–250/min
- AV dissociation — P waves occur independently of QRS (seen in ~50% of VT cases)
- Fusion beats — partial ventricular capture producing intermediate-morphology QRS
- Capture beats — brief normal narrow QRS when sinus impulse fully captures ventricles (pathognomonic of VT)
- Brugada criteria: concordance in precordial leads, RS interval >100 ms, no RS complex in any precordial lead → VT
- Ventricular fibrillation: chaotic, irregular, disorganized baseline with no discernible QRS
Monomorphic ventricular tachycardia: broad regular QRS complexes, capture beat (red circle) indicating AV dissociation. — Tintinalli's Emergency Medicine
5. Wolff-Parkinson-White (WPW) Syndrome
ECG Changes
- Short PR interval (<120 ms) — early ventricular activation via accessory pathway (Bundle of Kent)
- Delta wave — slurred upstroke at the start of QRS, representing ventricular pre-excitation
- Wide QRS complex (>120 ms) — fusion of pre-excited and normal ventricular activation
- Secondary ST-T changes opposite to QRS vector (discordant)
- Risk of rapid AF conduction → ventricular fibrillation if antidromic pathway allows fast impulses
Pathway localisation by delta polarity: Negative deltas in inferior leads (II, III, aVF) → posteroseptal pathway; positive V1 → left free wall pathway
WPW syndrome: shortened PR interval, delta waves (red arrows in leads II and III), widened QRS with pre-excitation. — Harrison's Principles of Internal Medicine 22E
6. Hypertrophic Cardiomyopathy (HCM)
ECG Changes
- Left ventricular hypertrophy (LVH) voltage criteria: Sokolow-Lyon (SV1 + RV5 or RV6 >35 mm); Cornell (RaVL + SV3 >28 mm in men)
- ST-segment depression and T-wave inversion (strain pattern) in lateral leads I, aVL, V4–V6
- Giant, deep symmetric T-wave inversions in V2–V5 (classic in apical HCM / Yamaguchi syndrome, >10 mm depth)
- Absence of septal Q waves in lateral leads (V5, V6, I, aVL) due to abnormal septal depolarisation
- Left axis deviation; possible LAE (P mitrale)
Hypertrophic cardiomyopathy: high-voltage R waves, ST depression, and deep T-wave inversions V2–V6; absent septal Q waves in lateral leads. — Goldman-Cecil Medicine
7. Acute Pericarditis
ECG Changes (evolves in 4 stages)
| Stage | Timing | ECG Finding |
|---|---|---|
| I | Days 1–2 | Diffuse concave ("saddle-shaped") ST elevation in all leads except aVR and V1; PR depression (most sensitive sign) in II, V4–V6; PR elevation in aVR |
| II | Days 3–7 | ST returns to baseline; T waves flatten |
| III | Weeks 1–3 | T-wave inversion in previously elevated leads |
| IV | Weeks–months | ECG normalises |
Key differentiator from STEMI: ST elevation is diffuse (not territorial), concave not convex; no reciprocal depression except aVR; PR depression present; no Q waves.
Acute pericarditis: diffuse concave ST elevation across I, II, III, aVF, V2–V6; PR depression in lead II; reciprocal changes in aVR. Note sinus tachycardia (inflammatory response).
8. Pulmonary Embolism (PE)
ECG Changes
- Sinus tachycardia — the most common finding (>40% of cases)
- S1Q3T3 pattern (McGinn-White sign): prominent S wave in lead I, Q wave in lead III, T-wave inversion in lead III — reflects acute right heart strain
- Right axis deviation and right bundle branch block (complete or incomplete RBBB — rSR' in V1)
- T-wave inversions V1–V4 (right ventricular strain)
- P pulmonale — peaked P waves >2.5 mm in lead II (right atrial enlargement)
- Low-voltage QRS; non-specific ST changes
- New atrial fibrillation or flutter may appear
Acute pulmonary embolism: S1Q3T3 pattern highlighted with circles/arrows — deep S in lead I, Q wave in III, inverted T in III; sinus tachycardia >100 bpm.
9. Brugada Syndrome
ECG Changes
Three pattern types (Type 1 is the only diagnostic pattern):
| Type | ST Morphology | T Wave | Diagnostic? |
|---|---|---|---|
| Type 1 (Coved) | J-point ≥2 mm, convex/coved downsloping ST | Negative (inverted) | ✅ Yes |
| Type 2 (Saddle-back) | J-point ≥2 mm, saddle-back ST | Positive | ❌ Requires pharmacological challenge |
| Type 3 | <2 mm ST elevation | Positive | ❌ Non-diagnostic |
- Changes confined to V1–V2 (right precordial leads), best seen with electrodes in 2nd–3rd intercostal space
- Associated with RBBB-like pattern (rSR' in V1), first-degree AV block, prolonged PR
- Caused by SCN5A loss-of-function mutations → sodium channel dysfunction → risk of polymorphic VT and sudden cardiac death
Brugada syndrome Type 1: Classic coved ST-segment elevation ≥2 mm in V1–V2, descending into inverted T waves — the only spontaneously diagnostic pattern. — Harrison's Principles of Internal Medicine 22E
10. Long QT Syndrome (LQTS)
ECG Changes
- Prolonged QTc interval: ≥450 ms (males) or ≥460 ms (females) is borderline; ≥500 ms is high-risk
- Corrected using Bazett formula: QTc = QT ÷ √RR
- T-wave morphology subtypes:
- LQT1 (KCNQ1): Broad-based smooth T wave
- LQT2 (KCNH2): Bifid (notched) T wave — most common
- LQT3 (SCN5A): Late-onset peaked T wave with long isoelectric ST segment
- Prominent U waves — best seen in V2–V3; can fuse with T wave masking true QT
- T-wave alternans — beat-to-beat alternation in T-wave morphology/amplitude (sign of instability)
- Torsades de Pointes (TdP): Polymorphic VT with QRS complexes twisting around the isoelectric line — the dreaded complication
Long QT syndrome: Panel A shows baseline QTc 680 ms with prominent U waves (arrows); Panel B shows short-long-short sequence triggering polymorphic VT (torsades de pointes). — Harrison's Principles of Internal Medicine
Quick Reference Summary
| # | Disease | Key ECG Finding | Critical Clue |
|---|---|---|---|
| 1 | STEMI | Convex ST elevation + Q waves | Territorial distribution + reciprocal changes |
| 2 | Atrial Fibrillation | No P waves, irregular R-R | "Irregularly irregular" |
| 3 | Complete Heart Block | P-wave/QRS dissociation, slow escape | No PR relationship |
| 4 | Ventricular Tachycardia | Wide QRS tachycardia, AV dissociation | Fusion/capture beats |
| 5 | WPW Syndrome | Short PR + delta wave + wide QRS | Slurred QRS upstroke |
| 6 | HCM | LVH voltage + giant T inversions | Deep V2–V5 T inversions (apical type) |
| 7 | Pericarditis | Diffuse saddle ST + PR depression | All leads (not territorial) |
| 8 | Pulmonary Embolism | S1Q3T3 + sinus tachycardia + RBBB | Right heart strain pattern |
| 9 | Brugada Syndrome | Coved ST elevation V1–V2 + inverted T | Only Type 1 is diagnostic |
| 10 | Long QT Syndrome | QTc >500 ms + T-wave changes | Torsades de pointes risk |
Sources: Harrison's Principles of Internal Medicine 22E (2025); Braunwald's Heart Disease; Tintinalli's Emergency Medicine; Goldman-Cecil Medicine; Fuster and Hurst's The Heart, 15th Ed; Ganong's Review of Medical Physiology
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