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

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ECG electrocardiogram myocardial infarction ST elevation

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ECG atrial fibrillation irregular rhythm no P waves

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ECG heart block first degree second degree third degree AV block

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ECG left ventricular hypertrophy voltage criteria

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

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ECG pericarditis saddle-shaped ST elevation diffuse

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ECG pulmonary embolism S1Q3T3 right heart strain

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ECG ventricular tachycardia wide complex tachycardia

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ECG hypertrophic cardiomyopathy deep Q waves ST changes

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ECG long QT syndrome prolonged QTc torsades de pointes

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I now have comprehensive ECG images and textbook data for all 10 conditions. Let me compile the full answer.Here is a comprehensive guide to 10 common heart diseases with their ECG changes and ECG images.

10 Common Heart Diseases with ECG Changes

1. ST-Elevation Myocardial Infarction (STEMI)

Overview: Acute complete occlusion of a coronary artery causing full-thickness myocardial ischemia and necrosis.

ECG Changes:

Hyperacute T-waves (earliest sign) — tall, peaked, broad T-waves
ST-segment elevation ≥ 1 mm in ≥2 contiguous leads (convex/tombstone morphology)
Reciprocal ST depression in opposing leads
Pathological Q waves — wide (>40 ms) and deep (>25% of R wave) develop over hours
T-wave inversion in the infarcted territory (late sign)

Localisation:

Territory	ST Elevation Leads	Artery
Anterior	V1–V4	LAD
Inferior	II, III, aVF	RCA
Lateral	I, aVL, V5–V6	LCx
Posterior	Tall R in V1, ST depression V1–V3	RCA/LCx

Anterior STEMI – ST elevation V1–V6 with hyperacute T-waves

Anterolateral STEMI showing prominent ST elevation in V1–V6 and leads I, aVL, with reciprocal depression in II, III, aVF

Inferolateral STEMI with annotated reciprocal changes

Inferolateral STEMI: ST elevations in II, III, aVF and V4–V6 (green circles) with reciprocal depressions in I, aVL, V2–V3 (yellow arrows)

2. Atrial Fibrillation (AF)

Overview: Disorganised electrical activity in the atria producing chaotic firing at 350–600 impulses/min, causing an irregularly irregular ventricular response.

ECG Changes:

Absent P waves — replaced by irregular fibrillatory (f) waves, best seen in V1 and II
Irregularly irregular R-R intervals (pathognomonic)
Narrow QRS complexes (unless aberrant conduction or BBB coexists)
Rate can be rapid (uncontrolled AF >100 bpm) or controlled (<100 bpm)

Atrial fibrillation – absence of P waves, irregular R-R intervals

Classic AF: No organised P waves, fine fibrillatory baseline, irregularly irregular narrow QRS complexes

3. AV Heart Block (1st, 2nd, 3rd Degree)

Overview: Impaired conduction through the AV node, ranging from simple delay to complete dissociation.

ECG Changes:

Degree	Key ECG Feature
1st degree	PR interval > 200 ms, every P followed by QRS
2nd degree Mobitz I (Wenckebach)	Progressive PR lengthening until a QRS is dropped
2nd degree Mobitz II	Constant PR interval, then sudden dropped QRS
3rd degree (Complete)	Complete AV dissociation — P waves and QRS complexes at independent rates

AV block comparison chart – 1st, 2nd, 3rd degree

Educational comparison of all three degrees of AV block showing P-QRS relationships

Progression of AV block in myocarditis – all four types

Clinical series showing (a) complete heart block, (b) Mobitz II, (c) Wenckebach, and (d) 1st-degree block in the same patient during treatment

4. Wolff-Parkinson-White (WPW) Syndrome

Overview: An accessory pathway (Bundle of Kent) bypasses the AV node, causing ventricular pre-excitation and predisposing to re-entrant tachyarrhythmias.

ECG Changes (classic triad):

Short PR interval < 120 ms (bypass of AV node delay)
Delta wave — slurred upstroke at the beginning of the QRS complex
Widened QRS complex (> 120 ms) due to fusion of pre-excited and normal depolarisation
Secondary ST/T changes (discordant to QRS)
Risk of pseudo-infarction pattern (negative delta waves mimicking Q waves)

WPW syndrome – short PR, delta waves, widened QRS

Classic WPW: Short PR interval, prominent delta waves visible in II, III, aVF and V2–V6, with secondary QRS widening

5. Acute Pericarditis

Overview: Inflammation of the pericardium (most often viral), producing characteristic diffuse ECG changes that evolve through 4 stages.

ECG Changes (4 Stages):

Stage	Change
I (Acute)	Diffuse concave ("saddle-shaped") ST elevation in all leads except aVR/V1; PR segment depression (hallmark)
II (Days 1–2)	ST returns to baseline; PR depression persists
III (Days 2–3)	Widespread T-wave inversion
IV (Weeks later)	Normalisation

Key differentiators from STEMI:

Diffuse ST elevation (not territory-specific)
PR depression (absent in STEMI)
Concave (not convex) ST morphology
No reciprocal changes (except aVR)
Spodick's sign (downsloping TP segment)

Acute pericarditis – diffuse saddle-shaped ST elevation and PR depression

Pericarditis: Concave ST elevation in I, II, III, aVF, V2–V6; PR depression in II; reciprocal PR elevation and ST depression in aVR

6. Pulmonary Embolism (PE)

Overview: Thrombotic obstruction of the pulmonary vasculature causes acute right heart strain, reflected on ECG.

ECG Changes:

Sinus tachycardia (most common, ~40% of cases)
S1Q3T3 pattern (classic but present in only ~20%): Deep S in lead I + Q wave + T inversion in lead III
Right bundle branch block (complete or incomplete)
T-wave inversions V1–V4 (right ventricular strain pattern)
Rightward axis deviation
Atrial fibrillation may develop

Pulmonary embolism S1Q3T3 – annotated with arrows

Classic S1Q3T3 (black circles/arrows): Deep S in I, Q wave in III, inverted T in III — hallmark of acute right heart strain from PE

PE with T-wave inversions V1–V6 and S1Q3T3

Massive PE: S1Q3T3 plus deep, symmetric T-wave inversions V1–V6 (McGinn-White sign)

7. Left Ventricular Hypertrophy (LVH)

Overview: Increased LV muscle mass from chronic pressure overload (e.g., hypertension, aortic stenosis), causing characteristic voltage and repolarisation changes.

ECG Changes:

Increased QRS voltage (key diagnostic criteria):
- Sokolow-Lyon: S in V1 + R in V5 or V6 ≥ 35 mm
- Cornell: R in aVL + S in V3 > 28 mm (men) / >20 mm (women)
Left axis deviation
LV strain pattern: ST depression and asymmetric T-wave inversion in lateral leads (I, aVL, V5–V6)
Prolonged QRS duration
Left atrial enlargement (broad, notched P wave in II — "P mitrale")

LVH with Cornell voltage criteria and lateral strain pattern

LVH: High-amplitude R in aVL and deep S in V3 meeting Cornell criteria; prominent T-wave inversions in V4–V6 (strain pattern)

8. Hypertrophic Cardiomyopathy (HCM)

Overview: Genetic disorder (sarcomere mutations) causing asymmetric septal hypertrophy, often with dynamic outflow obstruction. Leading cause of sudden cardiac death in young athletes.

ECG Changes:

LVH voltage criteria (prominent R or S waves)
Deep, narrow ("dagger-like") Q waves in lateral leads (I, aVL, V5–V6) and inferior leads — due to septal hypertrophy
Giant T-wave inversions (particularly in apical HCM — Yamaguchi variant) in V3–V6, depth often >10 mm
ST segment depression in lateral leads
Atrial fibrillation (common in advanced disease)
Absent septal Q waves in some variants

HCM with deep T-wave inversions and LVH voltage

HCM (septal variant): High R-wave voltages V2–V4, deep symmetric T-wave inversions V2–V6 (strain pattern), positive T in aVR (arrhythmia risk marker)

Apical HCM – giant T-wave inversions V3–V6

Yamaguchi (apical) HCM: Giant symmetric T-wave inversions deepest in V4–V5 — classic "spade" pattern

9. Ventricular Tachycardia (VT)

Overview: Three or more consecutive ventricular beats at >100 bpm originating below the Bundle of His. A life-threatening arrhythmia requiring urgent treatment.

ECG Changes:

Wide complex tachycardia — QRS ≥ 120 ms (often >160 ms)
Rapid regular rhythm — typically 100–250 bpm
AV dissociation — P waves march through at a slower rate, independent of QRS (pathognomonic of VT)
Fusion beats and capture beats (Dressler beats) — confirm VT
Positive or negative concordance across precordial leads
Brugada criteria used to differentiate VT from SVT with aberrancy

Monomorphic ventricular tachycardia – wide complex regular tachycardia

Monomorphic VT: Wide, bizarre QRS complexes with rapid regular rate, positive concordance in precordial leads, no visible P waves

10. Long QT Syndrome (LQTS)

Overview: A channelopathy (inherited or acquired) impairing ventricular repolarisation, predisposing to the deadly arrhythmia Torsades de Pointes (TdP) and sudden cardiac death.

ECG Changes:

Prolonged QTc interval:
- Normal QTc: ≤ 440 ms (men), ≤ 460 ms (women)
- Borderline risk: 440–500 ms
- High risk / LQTS: > 500 ms
Abnormal T-wave morphology: broad, notched, or biphasic T-waves
T-wave alternans (beat-to-beat variation in T-wave amplitude — harbinger of TdP)
Torsades de Pointes: polymorphic VT with "twisting" of QRS complexes around the isoelectric line

Common causes of acquired LQTS: Hypokalaemia, hypomagnesaemia, drugs (antiarrhythmics, antipsychotics, antibiotics such as azithromycin).

Long QT syndrome with torsades de pointes

LQTS: Panel (a) sinus rhythm with QTc 478 ms; Panel (b) onset of Torsades de Pointes — twisting polymorphic VT

Severe QTc prolongation with T-wave alternans

Extreme QTc 610 ms with macro T-wave alternans (red arrows) — electrical instability immediately preceding TdP

Quick Reference Summary

#	Disease	Key ECG Finding
1	STEMI	ST elevation ≥1mm in ≥2 contiguous leads + Q waves
2	Atrial Fibrillation	Absent P waves + irregularly irregular rhythm
3	AV Heart Block	PR prolonged / dropped beats / AV dissociation
4	WPW Syndrome	Short PR + delta wave + widened QRS
5	Acute Pericarditis	Diffuse saddle ST elevation + PR depression
6	Pulmonary Embolism	Sinus tachycardia + S1Q3T3 + RV strain
7	LVH	High QRS voltage + lateral strain pattern
8	HCM	Deep Q waves + giant T inversions (apical type)
9	Ventricular Tachycardia	Wide complex tachycardia + AV dissociation
10	Long QT Syndrome	QTc >500 ms + T-wave alternans → Torsades

*Sources: Braunwald's Heart Disease, Harrison's Principles of Internal Medicine 22E, Tintinalli's Emergency Medicine, Ganong's Review of Medical Physiology, Goldman-Cecil Medicine.*You've run out of free credits. Sign up for a free account to continue using Orris.

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