Explain 10 common heart dieseases with ecg images in detail

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ECG electrocardiogram myocardial infarction STEMI

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atrial fibrillation ECG irregular rhythm absent P waves

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heart block complete AV block ECG bradycardia P wave dissociation

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ventricular tachycardia ECG wide QRS tachycardia

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left ventricular hypertrophy ECG high voltage Sokolow-Lyon criteria

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pericarditis ECG saddle-shaped ST elevation diffuse PR depression

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Wolff-Parkinson-White WPW syndrome ECG delta wave short PR interval

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heart failure dilated cardiomyopathy ECG bundle branch block low voltage

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hypertrophic cardiomyopathy ECG deep Q waves lateral leads

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long QT syndrome ECG prolonged QT interval torsades de pointes

Here is a comprehensive guide to 10 common heart diseases with their ECG findings and representative images.

10 Common Heart Diseases — ECG Guide

1. 🫀 Acute Myocardial Infarction (STEMI)

Overview

A ST-Elevation Myocardial Infarction occurs when a coronary artery is completely occluded, causing transmural (full-thickness) myocardial necrosis. It is a life-threatening emergency requiring immediate reperfusion.

Pathophysiology

Plaque rupture → thrombosis → complete coronary occlusion → ischemia → injury → necrosis. The affected myocardium progresses through hyperacute (minutes), acute (hours), and evolved (days–weeks) phases.

ECG Changes

Phase	Finding
Hyperacute	Tall, peaked "hyperacute" T-waves
Acute (hours)	ST-segment elevation (convex/tombstone shape)
Evolving (days)	Pathological Q-waves (>40 ms, >25% QRS height), T-wave inversion
Reciprocal changes	ST depression in leads facing the opposite wall

Localisation:

Anterior STEMI (LAD): ST elevation in V1–V4, reciprocal depression in II, III, aVF
Inferior STEMI (RCA): ST elevation in II, III, aVF, reciprocal depression in I, aVL
Lateral STEMI (LCx): ST elevation in I, aVL, V5–V6

ECG Image — Anterior STEMI (V2–V5 "tombstoning")

Anterior STEMI ECG — ST elevation V2–V5 with tombstoning morphology

Anterior STEMI: Convex "tombstoning" ST elevation in V2–V5, QS waves indicating necrosis, reciprocal inferior depression.

ECG Image — Inferior STEMI (II, III, aVF)

Inferior STEMI ECG — ST elevation in inferior leads with reciprocal changes in aVL

Inferior STEMI: ≥2 mm convex ST elevation in II, III, aVF; pathologic Q-waves; reciprocal ST depression in I and aVL.

2. 🫀 Atrial Fibrillation (AF)

Overview

AF is the most common sustained cardiac arrhythmia, affecting over 37 million people worldwide. Disorganized atrial electrical activity produces an irregular, often fast ventricular response with no effective atrial contraction, increasing stroke risk 5-fold.

Pathophysiology

Multiple re-entrant circuits in the atria (often triggered by pulmonary vein foci) cause rapid, chaotic depolarisation. The AV node filters impulses irregularly → "irregularly irregular" ventricular rhythm.

ECG Changes

Feature	Finding
P waves	Absent — replaced by fine fibrillatory baseline (best seen in V1)
Rhythm	Irregularly irregular R-R intervals
Rate	Ventricular rate 100–180 bpm (uncontrolled); <100 bpm (controlled)
QRS	Usually narrow (unless aberrant conduction or pre-excitation)

ECG Image — Atrial Fibrillation with Rapid Ventricular Response

Atrial Fibrillation ECG — Absent P waves, irregular R-R intervals, fibrillatory baseline

AF with RVR: No P waves, chaotic fibrillatory baseline visible in V1, classic irregularly irregular rhythm, narrow QRS.

3. 🫀 Complete Heart Block (3rd Degree AV Block)

Overview

Complete AV block is a failure of all atrial impulses to conduct to the ventricles. The atria and ventricles beat independently. It requires urgent pacemaker implantation and can cause syncope or sudden death.

Pathophysiology

Complete interruption of the conduction system (at the AV node, Bundle of His, or below) causes total AV dissociation. An escape rhythm (junctional or ventricular) takes over at a slow rate.

ECG Changes

Feature	Finding
P waves	Regular, at faster rate (60–100 bpm)
QRS	Independent, slower rate (20–50 bpm)
PR interval	No fixed relationship — P waves and QRS completely dissociated
QRS morphology	Narrow if junctional escape; Wide (>120 ms) if ventricular escape

ECG Image — Complete Heart Block

Complete Heart Block ECG — P waves and QRS complexes fully dissociated

Third-degree AV block: Regular P waves at ~80 bpm, completely independent junctional escape rhythm at ~40 bpm, profound bradycardia, no fixed PR interval.

4. 🫀 Ventricular Tachycardia (VT)

Overview

VT is a potentially life-threatening arrhythmia arising from the ventricles, defined as ≥3 consecutive ventricular beats at rate >100 bpm. Sustained VT (>30 sec) causes hemodynamic compromise and can degenerate to ventricular fibrillation.

Pathophysiology

Re-entry circuits, triggered activity, or automaticity within diseased ventricular myocardium (scar, ischemia, cardiomyopathy) cause rapid, abnormal ventricular depolarisation bypassing the normal conduction system.

ECG Changes

Feature	Finding
Rate	100–250 bpm
QRS	Wide (>120 ms), bizarre morphology
P waves	Absent or dissociated from QRS (AV dissociation)
Axis	Often extreme axis deviation
Fusion/capture beats	Pathognomonic when present

Brugada criteria and Vereckei algorithm help differentiate VT from SVT with aberrancy.

ECG Image — Monomorphic Ventricular Tachycardia

Ventricular Tachycardia ECG — Wide complex regular tachycardia, no P waves, positive precordial concordance

Monomorphic VT: High-amplitude wide QRS at ~170 bpm, positive concordance V1–V6, superior axis, no visible P waves, consistent with structural heart disease origin.

5. 🫀 Acute Pericarditis

Overview

Pericarditis is inflammation of the pericardial sac, most commonly viral (Coxsackievirus, Echovirus) but also autoimmune, bacterial, or post-MI (Dressler's syndrome). Presents with sharp pleuritic chest pain relieved by leaning forward.

Pathophysiology

Pericardial inflammation causes superficial myocardial irritation, producing diffuse repolarisation changes. Unlike STEMI, changes affect all leads simultaneously (not a single coronary territory).

ECG Changes (4 Classic Stages)

Stage	Finding
Stage I (acute)	Diffuse concave ("saddle-shaped") ST elevation in all leads except aVR and V1; PR depression (most specific sign)
Stage II (days)	ST returns to baseline; T-waves flatten
Stage III (weeks)	T-wave inversion
Stage IV	ECG normalises

Key distinguishing features from STEMI:

ST elevation is concave (not convex)
Diffuse (not localised to one territory)
PR depression in inferior and lateral leads
No reciprocal ST depression (except aVR)
Spodick's sign: downsloping TP segment

ECG Image — Acute Pericarditis

Acute Pericarditis ECG — Saddle-shaped ST elevation, PR depression in multiple leads, Spodick's sign

Acute pericarditis: Diffuse saddle-shaped ST elevation in I, II, III, aVF, V2–V6; PR depression in II; PR elevation in aVR; Spodick's sign visible. Classic features distinguishing pericarditis from STEMI.

6. 🫀 Left Ventricular Hypertrophy (LVH)

Overview

LVH is thickening of the left ventricular walls, most commonly from chronic hypertension, aortic stenosis, or hypertrophic cardiomyopathy. LVH is an independent risk factor for heart failure, arrhythmias, and sudden death.

Pathophysiology

Chronic pressure overload → myocyte hypertrophy → increased muscle mass → greater electrical voltage recorded on ECG. Impaired subendocardial perfusion causes the characteristic "strain" pattern.

ECG Changes

Feature	Finding
Sokolow-Lyon criterion	S in V1 + R in V5 or V6 ≥35 mm
Cornell criterion	R in aVL + S in V3 ≥28 mm (men), ≥20 mm (women)
Strain pattern	ST depression and T-wave inversion in lateral leads (I, aVL, V5, V6)
Left axis deviation	Common
P wave	Broad, notched P (P mitrale) suggesting left atrial enlargement

ECG Image — LVH with Strain Pattern

Left Ventricular Hypertrophy ECG — High voltage, ST depression and T-wave inversion lateral leads (strain pattern)

LVH: Tall R-waves in V5–V6, deep S-waves in V1–V2 (meeting Sokolow-Lyon criteria); ST depression and T-inversion in II, III, aVF, V5, V6 — the classic "strain pattern" of pressure overload.

7. 🫀 Wolff-Parkinson-White (WPW) Syndrome

Overview

WPW is a pre-excitation syndrome caused by an accessory pathway (Bundle of Kent) bypassing the AV node, connecting atria directly to ventricles. It can cause paroxysmal supraventricular tachycardia and, rarely, sudden cardiac death via rapid conduction of AF to the ventricles.

Pathophysiology

The accessory pathway conducts faster than the AV node, activating part of the ventricle early ("pre-excitation"). This produces the delta wave and widened QRS. During tachycardia, re-entry circuits use the AV node and accessory pathway.

ECG Changes (Classic Triad)

Feature	Finding
PR interval	Short (<120 ms)
Delta wave	Slurred upstroke at start of QRS
QRS	Widened (>120 ms) due to delta wave
ST-T changes	Discordant — secondary to abnormal depolarisation
Pseudo-infarction	Negative delta waves can mimic Q-waves

Localisation: Delta wave polarity in V1 and inferior leads identifies accessory pathway location.

ECG Image — WPW Syndrome

WPW Syndrome ECG — Short PR interval, delta waves, widened QRS in multiple leads

WPW: Short PR (<120 ms), prominent delta waves (slurred QRS upstroke) in II, III, aVF, V2–V6, secondary ST-T discordance — classic triad of ventricular pre-excitation.

8. 🫀 Hypertrophic Cardiomyopathy (HCM)

Overview

HCM is a genetic disorder (autosomal dominant, most commonly MYH7 or MYBPC3 mutations) causing asymmetric left ventricular hypertrophy, usually of the interventricular septum. It is the leading cause of sudden cardiac death in young athletes.

Pathophysiology

Myofiber disarray and fibrosis disrupt normal electrical conduction, producing abnormal repolarisation. Dynamic LV outflow tract obstruction contributes to symptoms (exertional dyspnea, syncope, chest pain).

ECG Changes

Feature	Finding
Voltage	High QRS voltage (LVH criteria met in ~90%)
Q-waves	Deep narrow Q-waves in lateral/inferior leads (due to septal hypertrophy — septal depolarisation vector is abnormally prominent)
T-wave inversions	Deep symmetric T-inversion in lateral leads; "giant" T-inversion in apical HCM (Yamaguchi syndrome, >10 mm)
Left axis deviation	Common
Arrhythmias	AF, VT — common in advanced disease

ECG Image — Apical HCM (Yamaguchi Syndrome)

Hypertrophic Cardiomyopathy ECG — Giant T-wave inversions in precordial leads V2–V6

Apical HCM: Sinus rhythm, high-voltage precordial QRS, giant symmetric T-wave inversions most prominent in V4–V6 with ST depression — the hallmark of apical (Yamaguchi) HCM.

9. 🫀 Dilated Cardiomyopathy (DCM) / Heart Failure with Reduced EF

Overview

DCM is characterised by ventricular dilatation and systolic dysfunction (reduced EF <40%). Causes include idiopathic, viral myocarditis, alcohol, chemotherapy, and genetic. It leads to progressive heart failure and carries a high risk of sudden cardiac death.

Pathophysiology

Myocyte loss and fibrosis impair both contraction and electrical conduction. Ventricular dilation distorts the His-Purkinje system, commonly producing bundle branch blocks. Fibrosis creates re-entry substrates for VT.

ECG Changes

Feature	Finding
LBBB	QRS >120 ms, broad slurred R in I, aVL, V5–V6; rS in V1 — most common finding
RBBB	RSR' in V1, broad S in I, V5–V6
Low voltage	QRS amplitude <5 mm in limb leads (if extensive fibrosis)
PR prolongation	1st degree AV block common
AF	Frequent — marker of poor prognosis
Nonspecific ST-T changes	Diffuse T-inversion

ECG Image — DCM with LBBB

Dilated Cardiomyopathy ECG — Left Bundle Branch Block with prolonged QRS, 1st degree AV block

DCM with NYHA Class IV: 1st degree AV block (PR = 280 ms) and wide LBBB (QRS = 145 ms), indicating ventricular dyssynchrony — a key indication for Cardiac Resynchronization Therapy (CRT).

10. 🫀 Long QT Syndrome (LQTS)

Overview

LQTS is a disorder of ventricular repolarisation causing a prolonged QT interval. It can be congenital (mutations in cardiac ion channel genes: KCNQ1, KCNH2, SCN5A — LQT1, LQT2, LQT3) or acquired (drugs, hypokalemia, hypomagnesemia). The major risk is Torsades de Pointes (TdP) — a polymorphic VT that can degenerate to ventricular fibrillation and sudden death.

Pathophysiology

Reduced outward K⁺ current or increased inward Na⁺/Ca²⁺ current prolongs phase 3 of the action potential → prolonged repolarisation → early afterdepolarisations → triggered activity → TdP.

ECG Changes

Feature	Finding
QTc	≥450 ms (men), ≥460 ms (women) — abnormal; ≥500 ms — high risk
QTc formula	QT ÷ √RR (Bazett formula)
T-wave morphology	LQT1: broad-based T; LQT2: bifid/notched T; LQT3: long flat ST segment, peaked T
T-wave alternans	Beat-to-beat variation in T amplitude — precursor to TdP
Torsades de Pointes	Polymorphic VT with QRS complexes "twisting" around the isoelectric line; initiated by "short-long-short" sequence

ECG Image — Long QT with Torsades de Pointes

Long QT Syndrome and Torsades de Pointes ECG — Prolonged QTc, T-wave alternans, onset of polymorphic VT

LQTS: Panel (a) shows markedly prolonged QTc (478 ms) in sinus rhythm; Panel (b) shows the classic "twisting" polymorphic QRS complexes of Torsades de Pointes triggered by the prolonged repolarisation.

Quick Reference Summary

#	Disease	Key ECG Feature
1	Anterior STEMI	Convex/tombstone ST elevation V1–V4; Q-waves
2	Atrial Fibrillation	Absent P waves; irregularly irregular RR; fibrillatory baseline
3	Complete Heart Block	P waves and QRS totally dissociated; slow escape rhythm
4	Ventricular Tachycardia	Wide QRS >120 ms; rate >100; AV dissociation
5	Pericarditis	Diffuse saddle-shaped ST elevation; PR depression; Spodick's sign
6	LVH	High voltage (Sokolow ≥35 mm); lateral strain pattern
7	WPW Syndrome	Short PR <120 ms; delta wave; widened QRS
8	HCM	Deep narrow Q-waves lateral leads; giant T-inversions (apical)
9	DCM/Heart Failure	LBBB; 1st degree AV block; low voltage; AF
10	Long QT Syndrome	QTc ≥500 ms; T alternans; Torsades de Pointes

Clinical note: ECG interpretation must always be correlated with clinical history, examination, and additional investigations (troponin, echocardiography, cardiac MRI). No single ECG finding is pathognomonic in isolation.

Sources: Braunwald's Heart Disease (10th ed.), Rosen's Emergency Medicine; ECG images from PMC Clinical VQA dataset.

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