10 Common Heart Diseases: ECG Changes & Images

1. ST-Elevation Myocardial Infarction (STEMI)

• Hyperacute T waves - tall, peaked T waves are the earliest sign (minutes after onset)
• ST elevation - convex ("tombstone") or flat ST elevation in leads corresponding to the affected territory
• Reciprocal ST depression in mirror-image leads (e.g., inferior STEMI shows ST elevation in II, III, aVF with reciprocal depression in I and aVL)
• Pathological Q waves - develop within hours to days; represent dead myocardium (>40 ms wide, depth >25% of R wave)
• T-wave inversion - follows ST elevation during evolution

• Anterior (LAD): V1-V4
• Inferior (RCA): II, III, aVF
• Lateral (LCx): I, aVL, V5-V6
• Posterior: ST depression V1-V3 (reciprocal) + tall R in V1-V2

Wellens T-wave sign: deep symmetric T-wave inversions in V2-V5 indicating critical LAD stenosis. From Harrison's Principles of Internal Medicine 22E.

A: Subendocardial ischemia - ST vector points inward → overlying leads show ST depression. B: Transmural (epicardial) ischemia - ST vector points outward → overlying leads show ST elevation. From Harrison's Principles of Internal Medicine 22E.

2. Atrial Fibrillation (AF)

• Absent P waves - replaced by fibrillatory baseline (irregular, low-amplitude f-waves at 350-600 bpm)
• Irregularly irregular RR intervals - the hallmark; no two RR intervals are the same
• Narrow QRS complexes (unless aberrant conduction or bundle branch block present)
• Ventricular rate typically 100-160 bpm if uncontrolled
• Coarse vs fine AF - coarser fibrillatory waves suggest more recent onset

ECG with atrial fibrillation: no organised P waves, irregularly irregular ventricular rate. Also shows right axis deviation and ST depressions V1-V3 consistent with right ventricular strain (this patient had pulmonary hypertension). From Tintinalli's Emergency Medicine.

3. Complete (Third-Degree) Heart Block

• Complete AV dissociation - P waves and QRS complexes march independently, with no relationship to each other
• Regular P waves at atrial rate (usually 60-100 bpm)
• Regular but slow QRS at escape rate: junctional escape 40-60 bpm (narrow QRS), ventricular escape 20-40 bpm (wide, bizarre QRS)
• No fixed PR interval - PR interval varies continuously
• Wide, broad QRS complexes if the escape pacemaker is below the bundle of His

Complete heart block: P waves (atrial activity) and broad QRS complexes (ventricular escape) are completely dissociated. The slow ventricular rate with wide QRS indicates a ventricular escape rhythm.

4. Acute Pericarditis

• Stage 1 (hours-days): Diffuse saddle-shaped (concave upward) ST elevation in almost all leads EXCEPT aVR and V1; PR depression (hallmark - pathognomonic of pericarditis)
• Stage 2: ST segments normalize, T waves flatten
• Stage 3: Diffuse T-wave inversions
• Stage 4: ECG normalizes

• ST elevation is DIFFUSE (multiple territories) - not focal
• ST morphology is concave (saddle-shaped), not convex
• No reciprocal changes except in aVR (ST elevation in aVR, PR elevation)
• No Q waves
• PR depression is present

Acute pericarditis ECG: widespread concave ST elevation with PR depression across multiple leads. Note the diffuse distribution without the focal territory pattern of STEMI. From LITFL ECG Library.

5. Left Bundle Branch Block (LBBB)

• QRS duration ≥120 ms (broad QRS)
• Broad, notched R waves in lateral leads (I, aVL, V5, V6) - the "M" shape
• Deep S waves or QS complex in V1-V2 - initial R absent or small
• Secondary ST-T changes - T waves discordant (opposite polarity) to terminal QRS deflection; ST elevation in V1-V2 (can mimic STEMI)
• Left axis deviation common
• LBBB + new chest pain = treat as STEMI equivalent (Sgarbossa criteria used)

6. Wolff-Parkinson-White (WPW) Syndrome

• Short PR interval (<120 ms) - impulse bypasses the slow AV node
• Delta wave - slurred upstroke at the start of the QRS, representing early ventricular preexcitation via the accessory pathway
• Wide QRS complex (>120 ms) - due to fusion of preexcited and normally conducted depolarization
• Secondary ST-T wave changes (discordant T waves)
• Risk of AF with rapid ventricular response - life-threatening (bypass tract can conduct at 200-300 bpm)

WPW syndrome ECG: the slurred delta wave at the start of the QRS complex is clearly visible, along with a short PR interval. The QRS is broadened due to preexcitation via the accessory pathway. From LITFL ECG Library.

7. Hypertrophic Cardiomyopathy (HCM)

• Left ventricular hypertrophy (LVH) voltage criteria - increased QRS amplitude (S in V1 + R in V5/V6 >35 mm - Sokolow-Lyon criteria)
• Deep, symmetric T-wave inversions in lateral leads (I, aVL, V4-V6) - often dramatic
• Septal Q waves in lateral leads (I, aVL, V5, V6) due to exaggerated septal depolarization - can mimic lateral MI
• Left axis deviation
• ST depression - widespread
• Apical variant HCM: giant negative T waves ("giant T-wave inversion") across precordial leads
• Normal ECG occurs in only ~5% of confirmed HCM cases

8. Pulmonary Embolism (PE)

• Sinus tachycardia - the most common finding (>90% of cases)
• S1Q3T3 pattern - deep S wave in lead I, Q wave and inverted T wave in lead III (classic but not sensitive)
• Right axis deviation (new)
• Right bundle branch block (new) - complete or incomplete RBBB
• T-wave inversions in V1-V4 - right ventricular strain pattern (most common finding after tachycardia)
• Atrial fibrillation/flutter - can occur
• ECG may be entirely normal in small PE

9. Long QT Syndrome

• Prolonged QTc interval - the primary finding
  • Normal: <440 ms (men), <460 ms (women)
  • Borderline: 440-470 ms
  • Prolonged: >470-480 ms
  • High risk: >500 ms
• T-wave morphology changes:
  • LQTS type 1: broad-based T waves
  • LQTS type 2: notched or bifid T waves
  • LQTS type 3: flat T wave with late onset and prolonged ST segment
• Torsades de pointes - "twisting of the points" - polymorphic VT with characteristic twisting QRS axis around the isoelectric line
• T-wave alternans (beat-to-beat variation in T-wave amplitude) may precede torsades

10. Left Ventricular Hypertrophy (LVH)

• Increased QRS voltage (hallmark):
  • Sokolow-Lyon: S(V1) + R(V5 or V6) >35 mm
  • Cornell: R(aVL) + S(V3) >28 mm (men) or >20 mm (women)
  • R in aVL >11 mm
• LV strain pattern - downsloping ST depression and asymmetric T-wave inversion in I, aVL, V5-V6 (left-sided leads)
• Left axis deviation (>-30°)
• QRS prolongation - mild widening (but typically <120 ms)
• Left atrial enlargement - broad, notched P waves (P mitrale) in lead II; negative terminal component of P wave in V1

Summary Table

Clinical note: ECG interpretation must always be correlated with clinical context. ECG changes are not 100% sensitive or specific for any single diagnosis, and patterns overlap. Always compare with prior ECGs when available.Here is a complete breakdown of 10 common heart diseases with their ECG changes and representative images. The content was sourced from Harrison's Principles of Internal Medicine 22E, Tintinalli's Emergency Medicine, Fuster and Hurst's The Heart 15E, and the Washington Manual of Medical Therapeutics.

1. STEMI - ST elevation in a coronary territory, Q waves, Wellens sign for LAD stenosis
2. Atrial Fibrillation - absent P waves, irregularly irregular rhythm
3. Complete Heart Block - total AV dissociation, slow escape rhythm
4. Acute Pericarditis - diffuse concave ST elevation + PR depression (no reciprocal changes)
5. Left Bundle Branch Block - wide QRS, M-pattern lateral leads, discordant ST-T
6. WPW Syndrome - short PR + delta wave + wide QRS
7. Hypertrophic Cardiomyopathy - LVH voltage + deep T inversions + septal Q waves
8. Pulmonary Embolism - tachycardia + S1Q3T3 + right heart strain
9. Long QT Syndrome - prolonged QTc >480 ms, torsades de pointes risk
10. LVH - tall voltages (Sokolow-Lyon >35 mm) + strain pattern in lateral leads