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

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I now have enough textbook content and ECG images to write a comprehensive, detailed answer. Let me compile everything:

10 Common Heart Diseases: ECG Changes and Images

Below is a detailed guide to 10 major cardiac conditions, their hallmark ECG changes, and representative ECG tracings. Each ECG is sourced from the LITFL ECG Library (a peer-reviewed free open-access resource) or authoritative medical textbooks (Ganong's, Harrison's).

1. ST-Elevation Myocardial Infarction (STEMI)

Pathophysiology: Complete occlusion of a coronary artery causes transmural ischemia. Three simultaneous electrical events occur - rapid repolarization, decreased resting membrane potential, and delayed depolarization - all producing ST elevation in overlying leads.
ECG Changes (by phase):
PhaseECG Finding
Hyperacute (minutes)Tall, peaked "hyperacute" T waves
Acute (hours)ST elevation (convex/tombstone shape) in affected leads; reciprocal ST depression opposite
Evolving (hours-days)Q waves appear; T-wave inversion begins
Chronic (weeks+)Persistent deep Q waves; isoelectric ST; symmetric T-wave inversion
Lead localization:
  • Anterior STEMI: V1-V4 (LAD occlusion)
  • Inferior STEMI: II, III, aVF (RCA or LCx occlusion)
  • Lateral STEMI: I, aVL, V5-V6
  • Posterior STEMI: tall R in V1-V2 with ST depression (mirror image)
Serial ECG changes in anterior infarction (Ganong's Review of Medical Physiology - textbook Figure 29-17):
Serial ECG changes in anterior MI - from normal (A) to hyperacute ST elevation (B), Q wave formation (C), established pattern (D), and late resolution (E)
Serial ECG patterns in anterior infarction: (A) Normal baseline; (B) Early ST elevation in I, aVL, V3-5 with reciprocal depression in III/aVF; (C) Q waves and QS complexes appear in V3-4; (D) Persistent Q waves, isoelectric ST, deep T-wave inversion; (E) Late normalization possible.
Inferior STEMI ECG example (LITFL ECG Library):
Inferior STEMI - ST elevation in leads II, III, aVF with reciprocal changes in aVL
Key features: ST elevation in II, III, aVF; reciprocal ST depression in I and aVL (mirror image of lead III).

2. Non-ST-Elevation MI / Unstable Angina (NSTEMI/ACS)

Pathophysiology: Partial coronary occlusion causing subendocardial ischemia without full-thickness infarction. Biomarkers (troponin) are elevated in NSTEMI but not in unstable angina.
ECG Changes:
  • ST depression (horizontal or downsloping) - most common finding
  • T-wave inversion, especially in anterior leads (Wellens' syndrome pattern when in V2-V3 = proximal LAD stenosis warning)
  • No ST elevation, no new Q waves
  • May be a completely normal ECG (does NOT exclude NSTEMI)
  • Dynamic changes (evolving over serial ECGs) are diagnostically important
Key pattern - Wellens' Syndrome: Deep symmetrical T-wave inversions or biphasic T waves in V2-V3 indicate critical proximal LAD stenosis; patient is at high risk of massive anterior MI.

3. Atrial Fibrillation (AF)

Pathophysiology: Chaotic, disorganized atrial electrical activity from multiple re-entrant wavelets. Requires an initiating trigger (often pulmonary vein ectopy) and a substrate (dilated atrium, fibrosis).
ECG Changes:
  • No discernible P waves - replaced by irregular fibrillatory baseline (f waves, 350-600/min)
  • Irregularly irregular ventricular response - hallmark finding
  • Narrow QRS complexes (unless aberrant conduction or pre-excitation)
  • Ventricular rate varies (controlled = 60-100 bpm; rapid response = >100 bpm)
  • Fibrillatory baseline may be coarse (coarse AF) or fine
AF ECG - Rhythm Strip (LITFL ECG Library):
Atrial Fibrillation - irregularly irregular rhythm with absent P waves and fibrillatory baseline
Key features: Absent P waves, irregular fibrillatory baseline, completely irregular R-R intervals (irregularly irregular), narrow QRS complexes.

4. Ventricular Tachycardia (VT)

Pathophysiology: Three or more consecutive ventricular beats at >100 bpm, originating from ventricular myocardium (below the bundle of His). Most commonly due to re-entry around scar tissue from prior MI.
ECG Changes (monomorphic VT):
  • Wide QRS complexes (>120 ms), rate 100-250 bpm
  • Regular rhythm
  • AV dissociation (P waves march through at different rate) - pathognomonic when seen
  • Fusion beats (partial capture) and capture beats (full sinus capture) = diagnostic
  • Concordance: All precordial leads pointing same direction (positive = positive concordance; negative = negative concordance)
  • Brugada criteria, Josephson sign (notching near nadir of S wave), Vergovich sign help differentiate from SVT with aberrancy
Monomorphic VT ECG (LITFL ECG Library):
Monomorphic Ventricular Tachycardia - regular wide-complex tachycardia at ~180 bpm
Key features: Regular wide-complex tachycardia (QRS >120 ms), rate ~180 bpm. All QRS complexes identical (monomorphic). No visible P waves.

5. Complete (Third-Degree) Heart Block

Pathophysiology: Complete failure of atrial impulses to conduct to ventricles. Atria and ventricles beat independently - atria driven by SA node; ventricles by a subsidiary pacemaker (junctional or ventricular escape).
ECG Changes:
  • Complete AV dissociation - P waves and QRS bear no relationship to each other
  • P waves regular at normal/near-normal rate (60-100 bpm)
  • QRS complexes regular but slow (escape rhythm):
    • Junctional escape: narrow QRS at 40-60 bpm
    • Ventricular escape: wide QRS at 20-40 bpm
  • P wave "marching through" QRS complexes without capturing them
  • The PP interval and RR interval are both regular but independent
Pericarditis ECG (12-lead showing diffuse changes):
12-lead ECG showing pericarditis with diffuse ST elevation and PR depression
(See pericarditis section below for full interpretation)

6. Acute Pericarditis

Pathophysiology: Inflammation of the pericardium causes epicardial myocarditis producing widespread repolarization abnormalities. The pattern evolves through four stages.
ECG Changes (4 stages):
StageTimingECG Finding
Stage 1Days 1-2Widespread concave ("saddle-shaped") ST elevation in most leads (I, II, III, aVL, aVF, V2-6); PR depression (pathognomonic); ST elevation in aVR
Stage 2Days 3-7ST and PR normalize
Stage 3Week 1-3Diffuse T-wave inversions
Stage 4Weeks-monthsECG normalizes
Key distinguishing features from STEMI:
  • Concave (not convex) ST elevation
  • PR depression (not seen in STEMI)
  • No reciprocal ST depression (except aVR)
  • Affects multiple territories simultaneously
Pericarditis 12-lead ECG (LITFL ECG Library):
12-lead ECG of acute pericarditis - diffuse saddle-shaped ST elevation with PR depression in multiple leads
Key features: Diffuse concave ST elevation in I, II, aVL, V2-V6; PR segment depression especially in lead II; ST elevation in II > III (distinguishes from inferior STEMI where III > II). No reciprocal depression.

7. Left Ventricular Hypertrophy (LVH)

Pathophysiology: Increased LV muscle mass produces greater electrical forces directed leftward and posteriorly, amplifying voltages. Secondary repolarization abnormalities (the "strain" pattern) occur due to subendocardial ischemia.
ECG Changes (Sokolow-Lyon criteria most commonly used):
  • High voltage: SV1 + RV5 or RV6 >35 mm (Sokolow-Lyon); RaVL >11 mm
  • Left axis deviation (QRS axis -30° or more leftward)
  • Repolarization abnormalities (LVH strain pattern):
    • ST depression + asymmetric T-wave inversion in lateral leads (I, aVL, V5-V6)
    • ST elevation in V1-V3
  • Left atrial enlargement (broad notched P wave in II, biphasic P in V1)
  • Prolonged QRS (may progress to LBBB)
Note from Harrison's: Prominent precordial voltages alone are a common normal variant in young/athletic individuals; repolarization abnormalities increase specificity for true LVH.

8. Left Bundle Branch Block (LBBB)

Pathophysiology: Failure of conduction in the left bundle branch forces abnormal activation of the LV - the right ventricle depolarizes first, then septum is activated from right to left (reversed), then LV depolarizes late via slow cell-to-cell spread.
ECG Changes:
  • QRS duration ≥120 ms (complete LBBB)
  • Broad, notched ("M-shaped") R wave in lateral leads (I, aVL, V5-V6) - the classic "M" pattern
  • Deep, broad S wave or QS pattern in V1 - rS or QS
  • No septal Q waves in lateral leads (I, aVL, V5-V6)
  • Discordant ST/T changes - ST/T waves always opposite to main QRS deflection (secondary repolarization abnormality)
  • Left axis deviation common
Clinical significance: New LBBB in a patient with chest pain = treat as STEMI equivalent until proven otherwise (Sgarbossa criteria help identify MI in LBBB).

9. Wolff-Parkinson-White (WPW) Syndrome

Pathophysiology: An accessory pathway (Bundle of Kent) bypasses the AV node, pre-exciting part of the ventricle. This creates a characteristic resting ECG pattern and predisposes to re-entrant tachycardias.
ECG Changes (classic WPW pattern - sinus rhythm):
  • Short PR interval (<120 ms) - early ventricular activation bypassing AV node delay
  • Delta wave - slurred upstroke at beginning of QRS (slow cell-to-cell conduction from accessory pathway insertion)
  • Widened QRS (>120 ms) due to fusion of normal + pre-excited activation
  • Secondary ST-T changes discordant to QRS
  • Pseudo-infarct patterns - delta waves can mimic Q waves (especially inferior leads)
During tachycardia:
  • Orthodromic AVRT: narrow complex tachycardia (most common, 70%)
  • Antidromic AVRT: wide complex tachycardia resembling VT (5-10%)
  • AF with WPW: irregular wide complex tachycardia, very rapid (>250 bpm), irregular - extremely dangerous (risk of VF)

10. Pulmonary Embolism (PE) - Right Heart Strain

Pathophysiology: Massive PE causes acute right ventricular pressure overload, RV dilation, and right axis deviation. The infarcted/ischemic RV produces characteristic ECG patterns.
ECG Changes:
  • Sinus tachycardia - most common finding (in >40% of cases)
  • S1Q3T3 pattern - prominent S wave in lead I, Q wave + T-wave inversion in lead III (classical but present in only ~20%)
  • New right bundle branch block (RBBB) - complete or incomplete
  • Right axis deviation
  • T-wave inversions in V1-V4 (RV strain pattern) - most sensitive finding
  • Atrial fibrillation or flutter may occur
  • Right atrial enlargement (tall peaked P waves in II, "P pulmonale")
  • Low QRS voltage sometimes
Key point: A normal ECG does NOT exclude PE. The finding of T-wave inversions in V1-V4 in a tachycardic patient with dyspnea should raise strong suspicion.

Quick Reference Summary Table

#ConditionKey ECG Findings
1STEMIST elevation (convex) in territory, reciprocal depression, Q waves evolve
2NSTEMI/ACSST depression, T-wave inversion, dynamic changes, possibly normal
3Atrial FibrillationAbsent P waves, irregularly irregular rhythm, fibrillatory baseline
4Ventricular TachycardiaWide complex tachycardia, AV dissociation, fusion/capture beats
5Complete Heart BlockAV dissociation, slow escape rhythm, P waves march independently
6PericarditisDiffuse concave ST elevation, PR depression, no reciprocal changes
7LVHHigh voltage (SV1+RV5>35mm), strain pattern (ST depression/T inversion laterally)
8LBBBQRS ≥120ms, M-shaped R in lateral leads, no septal Q, discordant ST-T
9WPWShort PR, delta wave, wide QRS, pseudo-infarct pattern
10Pulmonary EmbolismSinus tachycardia, S1Q3T3, RBBB, T inversions V1-V4
Sources:
  • Ganong's Review of Medical Physiology, 26th Edition (electrocardiographic changes in MI and ionic abnormalities)
  • Harrison's Principles of Internal Medicine, 22nd Edition (LVH, bundle branch blocks, ischemia)
  • LITFL ECG Library (Ed Burns, emergency physician) - peer-reviewed free open access ECG cases
  • Tintinalli's Emergency Medicine & Goldman-Cecil Medicine (VT, arrhythmia, ACS)
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