Explain me 10 common heart diseases with ECG changes and ECG images of those diseases

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10 common heart diseases ECG changes electrocardiogram findings

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ECG images STEMI atrial fibrillation heart block hypertrophic cardiomyopathy pericarditis

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ECG example images heart failure LVH Wolff-Parkinson-White long QT syndrome ventricular tachycardia

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site:litfl.com ECG STEMI atrial fibrillation pericarditis images

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ECG images STEMI inferior anterior pericarditis long QT complete heart block litfl OR ecgwaves

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10 Common Heart Diseases: ECG Changes and Images

1. ST-Elevation Myocardial Infarction (STEMI)

Pathophysiology: Complete occlusion of a coronary artery causes transmural myocardial ischemia and necrosis.

ECG Changes:

Phase	Finding
Hyperacute (minutes)	Tall, broad "hyperacute" T waves before ST elevation
Acute (hours)	ST elevation in the territory of the infarcted artery; reciprocal ST depression in opposite leads
Evolved (hours-days)	Pathological Q waves (>40 ms wide, >25% of R wave) develop; T-wave inversion
Chronic	Persistent Q waves; ST normalizes

Location-based criteria (from Tintinalli's Emergency Medicine):

Anteroseptal: ST elevation V1-V3
Anterior: ST elevation V1-V4
Anterolateral: ST elevation V1-V6, I, aVL
Inferior: ST elevation II, III, aVF (always get right-sided leads to exclude RV infarction)
Right ventricular: ST elevation in RV leads V3R-V6R
Posterior: Tall R wave in V1-V2, R/S ratio ≥1 (mirror image STEMI)

Hyperacute Inferior STEMI - tall T waves in II, III, aVF with reciprocal changes in aVL

Hyperacute Inferior STEMI: ST elevation in leads II, III, aVF with reciprocal ST depression in aVL. Source: LITFL ECG Library

2. Atrial Fibrillation (AF)

Pathophysiology: Chaotic, disorganized atrial electrical activity with multiple re-entrant wavelets replacing organized P-wave-driven atrial contraction.

ECG Changes:

From the Tintinalli's Emergency Medicine (Table 18-8):

Feature	Description
P waves	Absent - replaced by irregular, chaotic fibrillatory baseline
Baseline	Flat or chaotic (fine or coarse AF)
QRS	Narrow unless pre-existing bundle branch block or accessory pathway (WPW)
RR interval	Irregularly irregular - the hallmark of AF
Ventricular rate	Usually 100-160 bpm if uncontrolled

Atrial Fibrillation and Atrial Flutter - ECG examples

Figure A shows irregularly irregular rhythm with no visible P waves - classic AF. Figure B shows regular flutter waves in II/III/aVF (atrial flutter). Source: Tintinalli's Emergency Medicine

3. Acute Pericarditis

Pathophysiology: Inflammation of the pericardial sac (usually viral) causes widespread sub-epicardial injury producing characteristic diffuse ST changes.

ECG Changes (4 Stages):

Stage	Timing	ECG Findings
Stage 1	Days 1-2	Diffuse concave (saddle-shaped) ST elevation in most leads; PR depression in II, V4-V6; PR elevation in aVR; no reciprocal ST depression (except aVR, V1)
Stage 2	Days 1-3	ST normalizes; T waves flatten
Stage 3	Days 1-3	Diffuse T-wave inversions
Stage 4	Weeks-months	ECG normalizes

Key distinguisher from STEMI: Pericarditis has concave (saddle-shaped) ST elevation in virtually all leads simultaneously - STEMI has convex elevation localized to one territory.

Pericarditis ECG showing diffuse concave ST elevation and PR depression

Pericarditis vs Benign Early Repolarisation: Both show concave ST elevation, but pericarditis has PR depression and ST/T wave ratio >0.25. Source: LITFL Pericarditis

4. Complete (Third-Degree) AV Heart Block

Pathophysiology: Complete failure of conduction between atria and ventricles - the atria and ventricles beat independently at their own intrinsic rates.

ECG Changes:

P waves: Regular at normal atrial rate (60-100 bpm), independent of QRS complexes
QRS complexes: Slow escape rhythm: narrow (40-60 bpm) if junctional; wide and bizarre (20-40 bpm) if ventricular
AV dissociation: P waves "march through" QRS complexes with no fixed PR relationship
Cannon A waves may be noted clinically

Complete Heart Block with inferior STEMI - independent P waves and slow escape rhythm

Complete heart block complicating inferior STEMI: Note the independent P-wave activity and a slow, regular escape rhythm. Source: LITFL AV Block

5. Left Ventricular Hypertrophy (LVH)

Pathophysiology: Chronic pressure overload (hypertension, aortic stenosis) causes increased left ventricular mass, producing larger electrical potentials on ECG.

ECG Changes (Harrison's Principles, 22nd Ed.):

Sokolow-Lyon criteria: SV1 + RV5 or RV6 > 35 mm
Cornell criteria: RaVL > 20 mm (women) or > 28 mm (men); or SV3 + RaVL > 28 mm (men), > 20 mm (women)
Repolarization changes: ST depression + T-wave inversion in lateral leads (I, aVL, V5-V6) - formerly called "LV strain pattern"
Left atrial abnormality (broad notched P wave in II, negative terminal deflection in V1) often accompanies LVH
LVH often progresses to left bundle branch block (LBBB)

6. Wolff-Parkinson-White (WPW) Syndrome

Pathophysiology: An accessory pathway (Bundle of Kent) bypasses the AV node, causing ventricular pre-excitation. The ventricles are activated early via the bypass tract AND through the normal AV node.

ECG Changes (Tintinalli's Emergency Medicine, Fig. 130-1):

Short PR interval: < 120 ms (pre-excitation bypasses AV nodal delay)
Delta wave: Slurred, broad upstroke at the start of the QRS (accessory pathway depolarization)
Widened QRS: > 120 ms (due to delta wave + fusion complex)
Secondary ST-T changes in opposite direction to delta wave
During AF with WPW: Irregular, very rapid wide-complex rhythm (>250 bpm) - life-threatening

WPW Syndrome ECG showing short PR interval, delta waves and widened QRS complex

Wolff-Parkinson-White syndrome: Short PR interval with slurred delta waves (best seen in I, II, V4-V6) and widened QRS. Source: Tintinalli's Emergency Medicine, Fig. 130-1

7. Long QT Syndrome (LQTS)

Pathophysiology: Inherited (channelopathy) or acquired (drug-induced, electrolyte disorders) prolongation of ventricular repolarization, predisposing to torsade de pointes (TdP) and sudden cardiac death.

ECG Changes (Tintinalli's Emergency Medicine):

Prolonged QTc: > 440 ms (men), > 460 ms (women); risk of events rises sharply at QTc > 500 ms
Notched T waves in 3 or more leads (particularly LQT2)
Prominent U waves (especially LQT3)
T-wave alternans: Beat-to-beat variation in T-wave morphology (sign of electrical instability)
Torsade de pointes: Polymorphic VT where QRS complexes rotate around the isoelectric baseline ("twisting of the points") - can degenerate to VF

Common causes of acquired LQTS: Macrolide antibiotics, fluoroquinolones, antipsychotics (haloperidol, quetiapine), antiarrhythmics (amiodarone, sotalol), hypokalemia, hypomagnesemia.

8. Hypertrophic Cardiomyopathy (HCM)

Pathophysiology: Genetic mutation (usually sarcomere proteins) causes asymmetric LV hypertrophy, diastolic dysfunction, and dynamic LVOT obstruction.

ECG Changes:

LVH voltage criteria - often very prominent (Sokolow-Lyon > 35 mm)
Deep, narrow ("dagger-like") Q waves in lateral and inferior leads (II, III, aVF, V4-V6) - due to septal hypertrophy (not infarction)
T-wave inversions in lateral and/or anterior leads
Left atrial abnormality
Apical HCM (Yamaguchi variant): Giant, deeply inverted T waves in precordial leads V3-V5 (called "giant negative T waves"), with tall R waves - a distinct pattern
Arrhythmias: AF, SVT, ventricular arrhythmias
Normal ECG is present in ~5-10% of patients with HCM

9. Pulmonary Embolism (PE)

Pathophysiology: Sudden obstruction of pulmonary vasculature causes acute right ventricular pressure overload and dilation.

ECG Changes (Harrison's Principles, 22nd Ed.):

Sinus tachycardia - most common finding (present in >40%)
S1Q3T3 pattern: Prominent S wave in lead I + Q wave in lead III + T-wave inversion in lead III (classic but present in only ~20%)
Right axis deviation (RAD)
Right bundle branch block (RBBB): New or incomplete RBBB
T-wave inversions in V1-V4 (right ventricular strain pattern - the most sensitive sign of large PE)
P pulmonale: Tall peaked P wave in II, III, aVF (right atrial enlargement)
Atrial fibrillation or flutter may occur
Normal ECG does NOT exclude PE

10. Ventricular Tachycardia (VT)

Pathophysiology: Rapid ventricular rhythm originating from the ventricular myocardium or conduction system below the His bundle, usually in the context of ischemic heart disease or cardiomyopathy.

ECG Changes:

Feature	Description
Rate	100-250 bpm
QRS	Wide (>120 ms), bizarre morphology
Regularity	Usually regular
AV dissociation	P waves march independently through QRS (diagnostic when seen)
Fusion beats	P wave conducts partially through normal pathway fusing with VT complex (diagnostic)
Capture beats	Occasional narrow QRS from supraventricular capture (diagnostic)
Concordance	All precordial QRS complexes pointing same direction (positive or negative) - highly specific for VT

Distinction from SVT with aberrancy: Brugada criteria: (1) no RS in precordial leads, (2) RS interval >100 ms in any precordial lead, (3) AV dissociation, (4) morphology criteria - any one positive = VT.

Torsade de pointes (TdP): Polymorphic VT - QRS twists around baseline, seen in LQTS.

Quick Reference Summary Table

Disease	Key ECG Features
STEMI	ST elevation in culprit territory + reciprocal depression + Q waves
Atrial Fibrillation	Absent P waves, irregularly irregular RR, narrow QRS
Pericarditis	Diffuse concave ST elevation, PR depression, all leads affected
Complete Heart Block	AV dissociation, slow escape rhythm, P waves independent of QRS
LVH	High voltage (SV1+RV5 >35mm), lateral strain pattern (ST depression + T inversion)
WPW	Short PR, delta wave, widened QRS
Long QT	QTc >500ms, notched T waves, U waves, risk of TdP
HCM	LVH + deep lateral Q waves + giant T inversions (apical variant)
Pulmonary Embolism	S1Q3T3, sinus tachycardia, RV strain (V1-V4 T inversions), RBBB
Ventricular Tachycardia	Wide QRS tachycardia, AV dissociation, fusion/capture beats

Sources: Tintinalli's Emergency Medicine (9th Ed.) - Tables 18-8, 49-4, 130-1; Harrison's Principles of Internal Medicine (22nd Ed., 2025) - Chapters 247; LITFL ECG Library

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