Explain me 10 common heart disease with there characteristic ECG changes and illustrative ECG images

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STEMI ST elevation myocardial infarction ECG 12 lead

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ventricular tachycardia ECG wide complex rhythm strip

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Wolff-Parkinson-White WPW delta wave ECG short PR

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pericarditis diffuse ST elevation saddle shaped ECG

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pulmonary embolism ECG S1Q3T3 right heart strain

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left bundle branch block LBBB ECG QRS morphology

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hypertrophic cardiomyopathy HCM ECG left ventricular hypertrophy deep Q waves

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atrial flutter sawtooth P waves ECG flutter waves

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long QT syndrome QT prolongation ECG torsades de pointes

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ventricular fibrillation ECG chaotic waveforms cardiac arrest

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10 Common Heart Diseases: ECG Changes & Illustrative Images

1. ST-Elevation Myocardial Infarction (STEMI)

ECG Hallmarks

Acute MI produces three sequential electrophysiological defects in infarcted cells (Ganong's Review of Medical Physiology):

Defect	Current Flow	ECG Change
Rapid repolarization	Out of infarct	ST elevation
Decreased resting membrane potential	Into infarct	TQ depression (manifests as ST elevation)
Delayed depolarization	Out of infarct	ST elevation

Hyperacute T waves — earliest change (first minutes); tall, peaked, symmetric
Convex ("tombstone") ST elevation ≥1 mm in ≥2 contiguous leads; reciprocal ST depression in opposite leads
Pathological Q waves — appear hours–days later; indicate irreversible necrosis (>40 ms wide, >25% of R height)
T-wave inversion — evolves as infarct matures
R-wave loss ("failure of R-wave progression") in anterior infarcts

Localisation:

Anterior (LAD): V1–V4 elevation
Inferior (RCA): II, III, aVF elevation
Lateral (Cx): I, aVL, V5–V6 elevation

12-lead ECG showing acute anterior STEMI with prominent convex ST elevation in V2–V5 and reciprocal depression in inferior leads

12-lead ECG: Acute anterior STEMI. Prominent ST elevation in V2–V5 with "tombstoning" morphology and reciprocal ST depression in II, III, aVF — consistent with proximal LAD occlusion.

2. Atrial Fibrillation (AF)

ECG Hallmarks

AF arises from chaotic multi-wavelet re-entry in the atria, producing (Guyton & Hall Textbook of Medical Physiology):

Absence of discrete P waves — replaced by fine, irregular fibrillatory baseline ("f-waves") at 350–600/min
Irregularly irregular ventricular rhythm — variable RR intervals; hallmark of AF
Ventricular rate 100–160 bpm (untreated)
Normal narrow QRS morphology (unless pre-existing aberrancy or WPW)

The variable spacing of QRS complexes on ECG is one of the primary diagnostic findings.

ECG lead II in atrial fibrillation — absent P waves with irregularly irregular QRS complexes

Lead II: Classic AF. No discrete P waves; chaotic baseline; QRS complexes are narrow but irregularly spaced. — Guyton & Hall Textbook of Medical Physiology

3. Atrioventricular (AV) Heart Block

ECG Hallmarks

AV conduction can be delayed, periodically blocked, or completely interrupted (Washington Manual of Medical Therapeutics):

Degree	ECG Findings
1st degree	PR interval >200 ms; every P conducts
2nd degree Mobitz I (Wenckebach)	Progressive PR lengthening → dropped QRS; "group beating"; RR intervals shorten before dropped beat
2nd degree Mobitz II	Fixed PR before sudden non-conducted P wave; often with bundle branch block
3rd degree (Complete)	Complete AV dissociation; atrial rate > ventricular rate; escape rhythm (junctional ~40–60 bpm or ventricular ~20–40 bpm)

Five ECG rhythm strips A–E illustrating first-degree, Mobitz I (Wenckebach), Mobitz II, 2:1 block, and complete heart block

A: First-degree AV block (PR >200 ms). B: 3:2 Mobitz I with group beating. C: Mobitz II with abrupt dropped beats. D: Advanced AV block. E: Complete heart block with AV dissociation. — Washington Manual of Medical Therapeutics

4. Left Bundle Branch Block (LBBB)

ECG Hallmarks

LBBB indicates depolarisation travels via slow cell-to-cell spread rather than the fast conduction system:

Widened QRS ≥120 ms
Broad, monophasic, often notched R waves in lateral leads (I, aVL, V5, V6)
Deep, broad S waves (QS or rS pattern) in V1–V3
Discordant ST-T changes — ST elevation in V1–V3 (opposite to QRS vector); ST depression and T-wave inversion in lateral leads
Left axis deviation
New LBBB can indicate acute MI (Sgarbossa criteria apply)

12-lead ECG showing classic LBBB with broad M-shaped R waves in lateral leads and deep S waves in V1–V3

12-lead ECG: LBBB. Wide QRS (>120 ms), monophasic R waves in leads I, aVL, V5–V6, deep S waves in V1–V3, and discordant ST/T-wave changes.

5. Wolff-Parkinson-White (WPW) Syndrome

ECG Hallmarks

WPW results from an accessory atrioventricular pathway (bundle of Kent) that bypasses the AV node, causing ventricular pre-excitation (Washington Manual):

Short PR interval (<120 ms) — impulse bypasses AV node delay
Delta wave — slurred, slow upstroke at onset of QRS; best seen where positive
Widened QRS (>110 ms) — due to fusion of pre-excited and normal conduction
Secondary ST-T changes — opposite to delta/QRS vector (not ischaemic)
Pseudo-Q waves in inferior leads (mimics inferior MI) when posterior accessory pathway

With AF, the accessory pathway can conduct rapidly → rapid, wide-complex pre-excited AF ("pre-excited AF") that mimics VT and is life-threatening if treated with AV nodal blockers.

12-lead ECG demonstrating WPW with short PR interval, prominent delta waves in multiple leads, and widened QRS

12-lead ECG: WPW syndrome. Short PR interval, delta waves most prominent in leads II, III, aVF, V2–V6. QRS widening from ventricular pre-excitation.

6. Ventricular Tachycardia (VT)

ECG Hallmarks

VT originates below the bundle of His; it is potentially life-threatening and must be distinguished from SVT with aberrancy (Goldman-Cecil Medicine):

Wide QRS tachycardia (QRS >120 ms) at rate typically 100–250 bpm
AV dissociation — P waves march through at their own (slower) rate; pathognomonic of VT
Fusion beats — P wave conducts simultaneously with ventricular beat; QRS is a hybrid
Capture beats — rare sinus impulse conducts fully; produces a narrow QRS amid wide complexes
Concordance — all precordial QRS complexes pointing in same direction (all positive or all negative)
Monomorphic vs polymorphic (varying QRS axis/morphology)

12-lead ECG showing monomorphic ventricular tachycardia — rapid regular wide QRS complexes with no visible P waves

12-lead ECG: Monomorphic VT. Rapid, regular, wide QRS complexes with LBBB morphology and inferior axis — consistent with RVOT origin. Termination with a single narrow-complex beat.

7. Acute Pericarditis

ECG Hallmarks

Pericardial inflammation produces characteristic four-stage ECG evolution:

Stage I (acute): Diffuse concave ("saddle-shaped") ST elevation in almost all leads (I, II, III, aVF, V2–V6); PR segment depression (most specific sign, due to atrial epicarditis); PR elevation in aVR (reciprocal)
Spodick's sign — downsloping TP segment
NO reciprocal ST depression (except in aVR/V1) — this distinguishes from STEMI, which has reciprocal changes in anatomically opposite leads
Stage II: ST normalises; T waves flatten
Stage III: T-wave inversion
Stage IV: ECG normalises

12-lead ECG showing acute pericarditis with diffuse concave saddle-shaped ST elevation, PR segment depression in lead II, and PR elevation in aVR

12-lead ECG: Acute pericarditis. Diffuse saddle-shaped ST elevation across I, II, III, aVF, V2–V6; PR segment depression in lead II; reciprocal PR elevation in aVR. Sinus tachycardia.

8. Pulmonary Embolism (PE)

ECG Hallmarks

Massive PE causes acute right ventricular pressure overload; ECG changes reflect right heart strain (the S1Q3T3 pattern, or McGinn-White sign):

Sinus tachycardia — most common finding
S1Q3T3 pattern — deep S wave in lead I; Q wave in lead III; inverted T wave in lead III
Right axis deviation (QRS axis >90°)
Incomplete or complete RBBB — QRS >120 ms in V1 with rSR' (rabbit-ear) morphology
T-wave inversions in V1–V4 — right ventricular strain pattern
P pulmonale — peaked P wave in lead II >2.5 mm (right atrial enlargement)
Electrical alternans — if large pericardial effusion is also present

ECG changes can be transient and are found in only ~50% of confirmed PE cases.

12-lead ECG demonstrating S1Q3T3 pattern in pulmonary embolism — deep S wave in I, Q wave in III, T-wave inversion in III; annotated with circles

12-lead ECG: Acute PE with S1Q3T3 pattern. Deep S wave in lead I, Q wave in lead III, inverted T wave in lead III (circled). Sinus tachycardia.

9. Hypertrophic Cardiomyopathy (HCM)

ECG Hallmarks

HCM (usually due to sarcomere gene mutations) produces abnormal LV mass with myofibre disarray. The ECG is abnormal in ~90% of cases (Goldman-Cecil Medicine):

Left ventricular hypertrophy (LVH) — high QRS voltage; Sokolow-Lyon criteria: S in V1 + R in V5 >35 mm
Deep, symmetric T-wave inversions in precordial and lateral leads — characteristic "strain pattern"
Pathological Q waves in inferolateral leads (I, aVL, V4–V6) — due to septal hypertrophy (not infarction); can mimic old MI
Apical HCM (Yamaguchi syndrome): "Giant" T-wave inversions (>10 mm) in V3–V5 are diagnostic
Left axis deviation
AF — occurs in up to 25% over time

12-lead ECG in HCM showing LVH voltage, ST depression with deep symmetric T-wave inversions in precordial and lateral leads, strain pattern

12-lead ECG: HCM (septal variant). High-amplitude R waves in V2–V4 meeting LVH criteria; diffuse ST depression and deep symmetric T-wave inversions in precordial and lateral leads; classic strain pattern.

10. Long QT Syndrome (LQTS) & Risk of Torsades de Pointes

ECG Hallmarks

LQTS is characterised by delayed ventricular repolarisation; it may be congenital (channelopathy: KCNQ1, KCNH2, SCN5A) or acquired (drugs, electrolytes) (Harrison's Principles of Internal Medicine):

Prolonged QTc interval:
- Males: >440 ms
- Females: >460 ms
- High risk: >500 ms
QTc calculated by Bazett's formula: QTc = QT / √RR
Broad, notched, or "humped" T waves — in LQT2; biphasic T waves in some subtypes
Prominent U waves — large positive deflection after T wave; especially in LQT1/LQT2
T-wave alternans (beat-to-beat variation in T-wave morphology) — precursor to TdP

Torsades de Pointes (TdP) — the signature dangerous arrhythmia:

Polymorphic VT with QRS complexes that twist around the isoelectric baseline ("twisting of the points")
Often initiated by "short-long-short" RR sequence (PVC on preceding T wave: "R-on-T")
Self-terminating but can degenerate to VF

Panel A: 12-lead ECG with markedly prolonged QT interval (680 ms) and U waves in V1 (arrows). Panel B: Initiation of polymorphic VT (torsades de pointes) from a PVC — long-short-short RR sequence

Panel A: Long QT syndrome — QTc 680 ms; prominent U waves (arrows in V1). Panel B: PVC on long-interval beat triggers initiating beat of polymorphic VT (torsades de pointes). — Harrison's Principles of Internal Medicine

Quick Reference Summary Table

#	Condition	Key ECG Findings
1	STEMI	Convex ST elevation ± reciprocal depression; Q waves; hyperacute T
2	Atrial Fibrillation	Absent P waves; irregularly irregular RR; narrow QRS
3	AV Heart Block	PR prolongation; dropped beats; AV dissociation (complete)
4	LBBB	QRS >120 ms; broad R in I/V5–V6; QS in V1–V3; discordant ST-T
5	WPW	Short PR; delta wave; wide QRS; secondary ST-T changes
6	Ventricular Tachycardia	Wide QRS tachycardia; AV dissociation; fusion/capture beats
7	Acute Pericarditis	Diffuse saddle-shaped ST elevation; PR depression; no reciprocal ST ↓
8	Pulmonary Embolism	Sinus tachycardia; S1Q3T3; RBBB; T inversions V1–V4
9	HCM	LVH voltage; deep T inversions; septal Q waves; strain
10	Long QT Syndrome	QTc >440–500 ms; broad/notched T; U waves → torsades de pointes

Sources: Ganong's Review of Medical Physiology (26th ed.) • Guyton & Hall Textbook of Medical Physiology (14th ed.) • Harrison's Principles of Internal Medicine (22nd ed., 2025) • Washington Manual of Medical Therapeutics • Goldman-Cecil Medicine (International ed.) • Tintinalli's Emergency MedicineThis guide covers the 10 most clinically important heart diseases with their characteristic ECG patterns, backed by authoritative textbooks and illustrated with real ECG tracings from the medical literature. Here are a few key teaching points worth remembering:

Critical differentiators:

STEMI vs Pericarditis: Pericarditis has diffuse saddle-shaped ST elevation with PR depression but no reciprocal ST depression (except aVR/V1). STEMI has focal convex ST elevation with reciprocal depression.
VT vs SVT with aberrancy: Favour VT if QRS >160 ms, northwest axis, AV dissociation, or fusion/capture beats are present. When in doubt, always treat as VT.
WPW + AF: Never give AV nodal blockers (adenosine, verapamil, digoxin) — they can accelerate accessory pathway conduction, leading to VF.
New LBBB: Always consider acute MI (Sgarbossa criteria); new LBBB in the right clinical context should be treated as STEMI equivalent.
QTc >500 ms: Substantially increases risk of torsades de pointes; review and remove offending drugs, correct electrolytes (K⁺, Mg²⁺).

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