Explain me 10 common heart disease with ecg changes and ecg images of those disease
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10 common heart diseases ECG changes with ECG images explained
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ECG images atrial fibrillation ventricular fibrillation heart block LBBB site:litfl.com OR site:ecgwaves.com
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ECG strips STEMI atrial fibrillation heart block hypertrophy Brugada WPW site:ecgwaves.com OR site:litfl.com
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pericarditis ECG saddle shaped ST elevation complete heart block third degree AV block ECG images
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10 Common Heart Diseases: ECG Changes and Images
Below is a clinical guide to the 10 most common cardiac conditions, each with their characteristic ECG findings and images sourced from authoritative medical textbooks (Harrison's, Ganong's, Guyton & Hall, Braunwald's).
1. ST-Elevation Myocardial Infarction (STEMI)
What it is: Complete occlusion of a coronary artery leading to transmural (full-thickness) myocardial necrosis.
ECG Changes:
- Hyperacute T waves - tall, peaked T waves (first minutes)
- ST-segment elevation - convex (tombstone) shape in leads overlying the infarct zone (≥1 mm in limb leads, ≥2 mm in precordial leads)
- Reciprocal ST depression in leads opposite the infarct
- Pathological Q waves - develop over hours to days (>40 ms wide and/or >25% of R-wave height), indicating necrosis
- T-wave inversion - follows the ST elevation as the infarct evolves
- Loss of R-wave progression ("failure of R wave progression") in anterior STEMI
Localization by leads:
| Territory | Artery | Leads |
|---|---|---|
| Anterior | LAD | V1-V4 |
| Inferior | RCA | II, III, aVF |
| Lateral | LCx | I, aVL, V5-V6 |
| Posterior | RCA/LCx | Tall R in V1-V2 (reciprocal) |
Mechanism: Three ECG defects in infarcted cells: abnormally rapid repolarization (K⁺ channels open) → ST elevation; decreased resting membrane potential from K⁺ loss → TQ depression (manifests as ST elevation); delayed depolarization → ST elevation. As the Harrison's textbook explains, with subendocardial ischemia the ST vector points inward (ST depression in overlying leads); with epicardial/transmural injury the ST vector points outward (ST elevation in overlying leads).
2. NSTEMI / Unstable Angina (Non-ST-Elevation ACS)
What it is: Partial occlusion of a coronary artery causing subendocardial ischemia without transmural necrosis (NSTEMI) or reversible ischemia (unstable angina). Troponin elevation distinguishes NSTEMI from unstable angina.
ECG Changes:
- ST depression (horizontal or downsloping, ≥0.5-1 mm) in leads overlying ischemic zone
- T-wave flattening or inversion - particularly prominent (deep symmetric T inversions in V1-V4 = Wellens sign, suggesting high-grade LAD stenosis)
- No ST elevation (by definition)
- ECG may be entirely normal in up to 30% of NSTEMI cases - serial ECGs and troponins are required
- Transient ST elevation may occur with Prinzmetal (vasospastic) angina, resolving completely
Key distinction from STEMI: No persistent ST elevation and no Q-wave formation. Per Harrison's: "The diagnosis of NSTEMI depends on abnormal elevation of cardiac biomarkers but may include ECG changes not meeting criteria for STEMI."
3. Atrial Fibrillation (AF)
What it is: Chaotic, disorganized atrial electrical activity with multiple simultaneous re-entrant wavelets - the most common sustained cardiac arrhythmia. Common causes include mitral valve disease, hypertension, heart failure, and hyperthyroidism.
ECG Changes:
- Absent P waves - replaced by irregular fibrillatory (f) waves, fine undulations at 350-600/min
- Irregularly irregular RR intervals (the hallmark - no two RR intervals are the same)
- Variable ventricular rate - typically 100-160 bpm if uncontrolled
- Normal QRS morphology (unless aberrant conduction or bundle branch block is present)
- The fibrillatory waves may be coarse (recent onset) or fine (longstanding AF)
Mechanism (Guyton & Hall): Numerous depolarization waves spread in all directions through the atria simultaneously; because they are opposite in polarity at any given time they electrically neutralize each other, producing no discernible P wave. AV node acts as a gatekeeper, passing impulses irregularly at rate ≥0.35 s apart.
Clinical risk: Blood stasis in left atrial appendage → thrombus formation → embolic stroke. Anticoagulation (warfarin or DOACs) is the primary stroke-prevention strategy.
4. Left Bundle Branch Block (LBBB)
What it is: Conduction delay or block in the left bundle branch, forcing ventricular activation to spread from right to left in an abnormal, slow fashion. It is a marker of significant heart disease: coronary artery disease, hypertensive heart disease, aortic valve disease, or cardiomyopathy.
ECG Changes (complete LBBB, QRS ≥120 ms):
- Broad, notched or slurred R wave in lateral leads (I, aVL, V5-V6) - often "M-shaped" or plateau-topped
- Wide, deep QS complex in V1 (no r wave, or very small r)
- Absence of normal septal Q waves in I, V5-V6 (septal depolarization reversed, now R→L)
- Discordant ST-T changes - ST depression and T inversion in leads with dominant R; ST elevation and upright T in V1-V3
- Left axis deviation common
- New LBBB in the setting of chest pain is treated as STEMI equivalent (Sgarbossa criteria apply)
Right Bundle Branch Block (RBBB):
- rSR' (RSR') pattern in V1 ("rabbit ears")
- Wide S wave in I, V5-V6
- T-wave inversion in V1-V2 (secondary repolarization change)
- More commonly a benign finding than LBBB; also seen with atrial septal defect and pulmonary embolism
5. Left Ventricular Hypertrophy (LVH)
What it is: Thickening of the left ventricular wall, typically from chronic pressure overload (hypertension, aortic stenosis) or volume overload (aortic/mitral regurgitation).
ECG Changes:
- High-voltage QRS complexes - the most characteristic finding:
- SV1 + RV5 or RV6 > 35 mm (Sokolow-Lyon criterion)
- R in aVL > 20 mm (women) or > 28 mm (men)
- Left axis deviation (-30° to -90°)
- ST depression and T-wave inversion in lateral leads (I, aVL, V4-V6) - "strain pattern"
- Left atrial enlargement - broad, notched P wave (P mitrale) in II; biphasic P in V1
- LVH may progress to LBBB
Right Ventricular Hypertrophy (RVH):
- Tall R wave in V1 (R > S in V1)
- Right axis deviation (>+90°)
- ST depression and T-wave inversion in right precordial leads (V1-V3)
- Dominant S waves in V5-V6
6. Complete (Third-Degree) AV Block
What it is: No electrical impulses are conducted from the atria to the ventricles. Atria and ventricles beat completely independently. The ventricles are sustained by a slow escape rhythm from below the block.
ECG Changes:
- P waves and QRS complexes are completely dissociated - Ps and QRSs march through independently at different rates (AV dissociation)
- Regular P-P intervals (sinus rate, typically 60-100/min)
- Regular but slow RR intervals from the escape pacemaker (junctional escape: 40-60/min with narrow QRS; ventricular escape: 20-40/min with wide QRS)
- More P waves than QRS complexes
- No fixed relationship between P waves and QRS complexes
Causes: Acute inferior MI (usually transient, from AV nodal ischemia via RCA), Lyme disease, hyperkalemia, digoxin toxicity, congenital heart block, infiltrative disease (sarcoidosis, amyloidosis).
Clinical significance: Often requires temporary or permanent pacemaker implantation.
7. Pericarditis (Acute)
What it is: Inflammation of the pericardium, typically from viral infection (Coxsackievirus, echovirus), autoimmune disease, or post-MI (Dressler syndrome). Causes diffuse myocardial surface irritation.
ECG Changes (diffuse, involving multiple lead groups - unlike focal STEMI):
- Diffuse concave ("saddle-shaped") ST elevation in most leads (I, II, III, aVF, V2-V6) - the ST is scooped upward, not convex
- PR segment depression in leads II, V4-V6 (highly specific, from atrial inflammation)
- PR elevation in aVR (reciprocal to PR depression elsewhere)
- No reciprocal ST depression (except in aVR and V1)
- No pathological Q waves (distinguishes from STEMI)
- T-wave inversion develops after ST elevation normalizes (stage III)
- Four classic stages: Stage I (ST elevation + PR depression) → Stage II (ST normalizes) → Stage III (T inversion) → Stage IV (normalization)
Key distinction from STEMI: Saddle-shaped (concave up) vs. convex ST elevation; diffuse multi-lead distribution; PR depression; no Q waves; no reciprocal changes except in aVR.
8. Hypertrophic Cardiomyopathy (HCM)
What it is: Genetic (autosomal dominant, most commonly myosin heavy chain mutations) disorder causing asymmetric ventricular hypertrophy, particularly of the interventricular septum. A leading cause of sudden cardiac death in young athletes.
ECG Changes:
- LVH voltage criteria - often extreme
- Deeply inverted T waves in lateral leads (V4-V6, I, aVL) - among the deepest T inversions seen in any condition
- Abnormal Q waves in inferior and lateral leads (from septal hypertrophy causing abnormal septal depolarization vectors) - can mimic infarction
- Left axis deviation
- Left atrial enlargement
- Short PR interval may be present
- In apical HCM (Yamaguchi variant): giant T-wave inversions (>10 mm) in V4-V6
9. Wolff-Parkinson-White (WPW) Syndrome
What it is: An accessory conduction pathway (Bundle of Kent) connects the atria and ventricles, bypassing the AV node. This allows ventricular pre-excitation - part of the ventricle depolarizes early via the accessory pathway before normal AV node conduction arrives.
ECG Changes (classic triad):
- Short PR interval (<120 ms) - accessory pathway conducts without AV nodal delay
- Delta wave - initial slurring/notching at the onset of the QRS from early ventricular activation via the accessory pathway
- Wide QRS complex (>120 ms) - from the fusion of pre-excitation and normal conduction
- Secondary ST-T changes - discordant T waves (opposite to delta/QRS direction)
- Pseudo-infarction pattern - delta waves in inferior leads can mimic Q waves
Clinical risk: If AF develops in WPW, impulses can travel to the ventricles at extremely rapid rates via the accessory pathway (bypassing AV nodal protection) → pre-excited AF → ventricular fibrillation → sudden death. AV nodal blocking drugs (verapamil, adenosine, digoxin) are contraindicated in WPW with AF.
10. Brugada Syndrome
What it is: A genetic ion channelopathy (most commonly SCN5A mutation, affecting cardiac Na⁺ channels) causing characteristic ECG changes and risk of ventricular fibrillation and sudden cardiac death, typically in young males, at rest or during sleep.
ECG Changes:
- Type 1 (diagnostic - "coved" pattern): ST elevation ≥2 mm with a coved (downward convex) shape followed by a negative T wave in ≥1 right precordial lead (V1 or V2)
- Type 2 ("saddle-back" pattern): ST elevation ≥2 mm with a saddle-back shape and positive/biphasic T wave - considered suspicious but not diagnostic alone
- Changes are most pronounced in V1-V2 (right precordial leads)
- Pattern may be intermittent or unmasked by fever, drugs (Na⁺ channel blockers, cocaine), vagal stimulation
- No structural heart disease is present (ECG is the only abnormality at rest)
Key distinction from STEMI/pericarditis: Restricted to right precordial leads V1-V2; characteristic coved morphology; no reciprocal changes; history of syncope or family history of sudden death.
Quick-Reference Summary Table
| # | Condition | Key ECG Feature | Leads Affected |
|---|---|---|---|
| 1 | STEMI | Convex ST elevation + Q waves | Territory-specific |
| 2 | NSTEMI/UA | ST depression, T inversion | Ischemic zone leads |
| 3 | Atrial Fibrillation | No P waves, irregularly irregular | All leads |
| 4 | LBBB | QS in V1, broad R in V6 (QRS ≥120 ms) | V1, V5-V6, I, aVL |
| 5 | LVH | High voltage + strain pattern | V1, V5-V6, aVL |
| 6 | Complete AV Block | P-QRS dissociation, slow escape | All leads |
| 7 | Pericarditis | Diffuse concave ST↑ + PR depression | Widespread, all except aVR |
| 8 | HCM | Deep T inversions + septal Q waves | V4-V6, inferior leads |
| 9 | WPW | Short PR + delta wave + wide QRS | All leads (V1-V6) |
| 10 | Brugada Syndrome | Coved ST elevation V1-V2 | V1-V2 only |
Sources:
- Guyton and Hall Textbook of Medical Physiology - Atrial fibrillation, conduction system
- Harrison's Principles of Internal Medicine 22E - Ischemia/infarction ECG, bundle branch blocks, hypertrophy
- Ganong's Review of Medical Physiology 26E - ECG mechanisms in MI, ionic changes
- Braunwald's Heart Disease - Brugada syndrome
- Fuster and Hurst's The Heart, 15th Edition - WPW, Brugada patterns
- GOLDMAN-CECIL Medicine - Intraventricular blocks, complete heart block
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