I now have enough information from Harrison's textbook and the ECG images to provide a comprehensive answer. Let me compile the full detailed response.
10 Common Heart Diseases: ECG Changes & Images
Below is a comprehensive guide to 10 common heart diseases, their characteristic ECG findings, and visual examples. All ECG content is grounded in Harrison's Principles of Internal Medicine 22E (2025) and Goldman-Cecil Medicine.
1. ST-Elevation Myocardial Infarction (STEMI)
ECG Changes:
- Hyperacute T waves (earliest change, within minutes) - tall, broad, peaked T waves
- ST-segment elevation (>1mm in 2+ contiguous limb leads; >2mm in men, >1.5mm in women in V2-V3) - convex/tombstone morphology
- Reciprocal ST depression in opposite leads
- Pathological Q waves develop over hours to days (width >40ms, depth >25% of R wave)
- T-wave inversions follow as infarct evolves
Lead Localization:
| Territory | Artery | ECG Leads |
|---|
| Anterior | LAD | V1-V4 |
| Inferior | RCA | II, III, aVF |
| Lateral | LCx | I, aVL, V5-V6 |
| Posterior | RCA/LCx | Reciprocal ST-depression V1-V3 |
From Harrison's: "Profound ST elevation or depression in multiple leads usually indicates very severe ischemia."
ECG Image (Anterior STEMI - Wellens T-wave pattern showing precordial T-wave inversions):
Figure: Severe anterior wall ischemia - deep T-wave inversions in V2-V6 (Wellens sign), indicating high-grade LAD stenosis.
2. Non-ST Elevation Myocardial Infarction (NSTEMI) / Unstable Angina
ECG Changes:
- ST depression (horizontal or downsloping, ≥0.5mm) - most common finding
- T-wave inversions (symmetric, often in multiple leads)
- Transient ST elevation in variant (Prinzmetal's) angina
- ECG may be completely normal in up to 30% of cases
- No pathological Q waves (subendocardial, not transmural)
Key Distinguishing Features:
- ST depression = subendocardial ischemia; ST vector directed toward ventricular cavity
- Lead aVR may show ST elevation (reciprocal to widespread subendocardial ischemia)
- Serial ECG monitoring is essential - the ECG can change dynamically over time
From Harrison's: "With ischemia confined primarily to the subendocardium, the ST vector typically shifts toward the subendocardium and ventricular cavity, so that overlying leads show ST-segment depression."
3. Atrial Fibrillation (AF)
ECG Changes:
- Absent P waves - replaced by chaotic fibrillatory baseline (f waves, 350-600/min)
- Irregularly irregular RR intervals - the hallmark
- Narrow QRS complexes (unless aberrant conduction)
- Ventricular rate typically 100-170 bpm (uncontrolled)
- Coarse vs. fine AF: coarse (f waves >1mm), fine (barely visible baseline)
ECG Image:
Figure: Classic atrial fibrillation with absent distinct P waves, irregular fibrillatory baseline (coarse f-waves), and irregularly irregular ventricular response. Note the varying RR intervals throughout.
4. Complete Heart Block (3rd Degree AV Block)
ECG Changes:
- Complete AV dissociation - P waves and QRS complexes bear no relationship to each other
- Regular P waves at the sinus rate (60-100 bpm)
- Regular QRS complexes at a slower escape rate (20-60 bpm)
- Wide QRS (>120ms) if escape rhythm is ventricular (below His bundle); narrow if junctional
- P rate > QRS rate always in complete heart block
ECG Image:
Figure: Third-degree (complete) heart block - note the regular P waves (atrial rhythm ~75 bpm) marching through with no relationship to the slow, wide escape QRS complexes (~35 bpm). Complete AV dissociation is evident.
5. Ventricular Tachycardia (VT)
ECG Changes:
- Wide QRS complex tachycardia (QRS >120ms, rate 100-250 bpm)
- Regular rhythm (monomorphic VT) - though may be irregular in polymorphic VT
- AV dissociation - P waves independent of QRS (seen in ~50%)
- Fusion beats and capture beats - pathognomonic of VT
- Concordance in precordial leads (all QRS same direction)
- Brugada criteria / Josephson's sign help differentiate from SVT with aberrancy
From Goldman-Cecil: "For wide-QRS complex tachycardias, the 12-lead ECG is useful in distinguishing a supraventricular tachycardia (with aberrancy) from a ventricular tachycardia. The presence of fusion beats strongly favors VT."
6. Left Ventricular Hypertrophy (LVH)
ECG Changes:
- Increased QRS voltage (tall R in left leads, deep S in right leads):
- SV1 + RV5 or RV6 > 35mm (Sokolow-Lyon criterion)
- R in aVL >20mm (women) or >28mm (men)
- Left axis deviation
- ST depression + T-wave inversion in leads with prominent R waves ("strain pattern") - V5, V6, I, aVL
- Left atrial enlargement - broad, bifid P wave in lead II (P mitrale), terminal negative P in V1
From Harrison's: "Multiple voltage criteria for left ventricular hypertrophy have been proposed based on the presence of tall left precordial R waves and deep right precordial S waves (e.g., SV1 + RV5 or RV6 >35mm). Repolarization abnormalities (ST depression with T-wave inversions, formerly called the LV 'strain' pattern) may appear in leads with prominent R waves."
7. Right Bundle Branch Block (RBBB)
ECG Changes:
- QRS ≥120ms (complete RBBB)
- rSR' ("M-shaped") pattern in V1 - terminal R' wave
- Wide, slurred S wave in I, V5, V6 (terminal S wave)
- Secondary T-wave inversions in V1-V3 (right precordial)
- ST changes discordant from QRS deflection in V1-V3
- In incomplete RBBB, QRS is 110-120ms
From Harrison's: "With right bundle branch block, the terminal QRS vector is oriented to the right and anteriorly (rSR' in V1 and qRS in V6, typically)."
8. Wolff-Parkinson-White Syndrome (WPW)
ECG Changes:
- Short PR interval (<120ms) - due to bypass of AV node delay
- Delta wave - slurred upstroke of QRS (pre-excitation)
- Wide QRS (>120ms) - fusion of delta wave + normal conduction
- Secondary ST-T changes discordant from QRS
- Risk of very rapid conduction in AF (potentially causing VF)
Pathophysiology: Accessory pathway (Bundle of Kent) bypasses the AV node, pre-excites the ventricles. The QRS is a fusion beat of pre-excitation + normal AV conduction.
From Harrison's: "Prolongation of QRS duration does not necessarily indicate a conduction delay but may be due to preexcitation of the ventricles via a bypass tract, as in Wolff-Parkinson-White (WPW) patterns."
9. Acute Pericarditis
ECG Changes (4 classic stages):
| Stage | Timing | ECG Changes |
|---|
| Stage 1 | Hours-days | Diffuse concave ST elevation in all leads except aVR and V1; PR depression (most diagnostic) |
| Stage 2 | 1st week | ST and PR return to baseline; T-wave flattening |
| Stage 3 | Days-weeks | Diffuse T-wave inversions |
| Stage 4 | Weeks-months | ECG normalization (or persistent T-wave inversions) |
Key Features Distinguishing from STEMI:
- Concave (saddle-shaped) vs. convex ST elevation
- Diffuse ST elevation (not territory-limited)
- PR depression (virtually pathognomonic)
- No reciprocal ST changes (except aVR/V1)
- No Q waves
From ESC: "ST elevation in pericarditis is usually greater in lead II than in lead III, whereas the opposite strongly indicates STEMI."
10. Pulmonary Embolism (PE)
ECG Changes:
- Sinus tachycardia (most common finding, ~40%)
- S1Q3T3 pattern - deep S in lead I, Q wave and T-wave inversion in lead III (classic but only ~20% sensitive)
- Right axis deviation and new right bundle branch block (partial or complete)
- T-wave inversions in V1-V4 (right heart strain pattern - most specific finding)
- Atrial arrhythmias (AF, flutter)
- P pulmonale (tall peaked P wave in II >2.5mm)
From Harrison's: "The QRS axis may shift to the right, sometimes in concert with the so-called S1Q3T3 pattern (prominence of the S wave in lead I and the Q wave in lead III, with T-wave inversion in lead III). Acute right ventricular dilation may be associated with slow R-wave progression and ST-T abnormalities in V1 to V4 simulating acute anterior infarction."
Quick Reference Summary Table
| Disease | Key ECG Finding | Pattern |
|---|
| STEMI | ST elevation + Q waves | Territorial, convex ST elevation |
| NSTEMI/UA | ST depression, T-wave inversions | Horizontal/downsloping ST-dep |
| Atrial Fibrillation | No P waves, irregular RR | Irregularly irregular narrow QRS |
| Complete Heart Block | AV dissociation | P rate > QRS rate, independent |
| Ventricular Tachycardia | Wide QRS tachycardia | ≥120ms QRS, ~150-200 bpm |
| LVH | Tall voltage + strain | SV1+RV5 >35mm, ST-dep lateral leads |
| RBBB | rSR' V1, wide S in V6 | Terminal R' in V1, slurred S laterally |
| WPW | Short PR + delta wave | Wide QRS, delta wave slur |
| Pericarditis | Diffuse concave ST-elev + PR-dep | All leads (except aVR/V1), saddle-shaped |
| Pulmonary Embolism | S1Q3T3 + right strain | Sinus tachy, RV strain pattern V1-V4 |
Sources:
- Harrison's Principles of Internal Medicine 22E (2025), Chapter 247: ECG
- Goldman-Cecil Medicine, Chapter 49-52: Electrocardiography & Arrhythmias
- Life in the Fast Lane (LITFL) ECG Library
- European Society of Cardiology pericarditis guidelines
Clinical note: ECG interpretation must always be combined with clinical history, physical examination, and biomarkers. A single normal ECG does not exclude acute MI. Serial ECGs are essential when ischemia is suspected.