I now have excellent ECG images for all 10 conditions. Let me compile the comprehensive response.
10 Common Heart Diseases with ECG Changes
1. π« ST-Elevation Myocardial Infarction (STEMI)
Pathophysiology: Complete occlusion of a coronary artery β transmural ischemia β necrosis of full myocardial thickness.
ECG Changes:
- Hyperacute T waves β earliest change; tall, broad, peaked T waves
- ST-segment elevation β₯ 1 mm in β₯ 2 contiguous limb leads or β₯ 2 mm in precordial leads (convex "tombstone" shape)
- Reciprocal ST depression in opposite leads
- Pathological Q waves (>40 ms wide, >25% QRS height) β evolve over hours/days
- T-wave inversion follows in the recovery phase
Territory localization:
| Territory | Leads with ST elevation | Culprit artery |
|---|
| Anterior | V1βV4 | LAD (proximal) |
| Anterolateral | V1βV6, I, aVL | LAD |
| Inferior | II, III, aVF | RCA or LCx |
| Posterior | V1βV3 (depression + tall R) | LCx or RCA |
ECG β Anterolateral STEMI:
2. π« Atrial Fibrillation (AF)
Pathophysiology: Chaotic, disorganized atrial electrical activity from multiple re-entrant wavelets β loss of coordinated atrial contraction β irregular ventricular response.
ECG Changes:
- Absent P waves β replaced by irregular fibrillatory (f) waves, best seen in V1
- Irregularly irregular R-R intervals (hallmark finding)
- Narrow QRS (unless aberrant conduction/BBB)
- Ventricular rate varies (bradycardic if controlled, tachycardic if uncontrolled)
- Baseline shows fine, chaotic oscillations (350β600 impulses/min from atria)
ECG β Atrial Fibrillation with rapid ventricular response:
3. π« Complete (Third-Degree) AV Block
Pathophysiology: Complete failure of conduction through the AV node or His-Purkinje system β total dissociation between atrial and ventricular activity.
ECG Changes:
- Complete AV dissociation β P waves and QRS complexes march independently
- Regular P-P intervals (atrial rate, typically 60β100 bpm)
- Regular R-R intervals (slow escape rhythm, typically 20β45 bpm)
- No constant PR interval β P waves can fall before, within, or after QRS
- Wide QRS if escape is ventricular (>120 ms); narrow QRS if junctional escape
- Requires urgent pacemaker implantation
ECG β Complete Third-Degree AV Block:
4. π« Ventricular Tachycardia (VT)
Pathophysiology: Three or more consecutive ventricular ectopic beats at β₯100 bpm, arising below the His bundle. Most commonly occurs in structural heart disease (post-MI scar, dilated cardiomyopathy).
ECG Changes:
- Wide complex tachycardia (QRS β₯120 ms), rate 100β250 bpm
- Regular or slightly irregular rhythm
- AV dissociation (P waves independent of QRS) β pathognomonic when seen
- Fusion beats and capture beats (Dressler beats) β diagnostic
- Concordance β all precordial leads positive (positive concordance) or negative (negative concordance)
- Extreme axis deviation ("northwest" axis, β90Β° to Β±180Β°)
- Brugada criteria and Vereckei criteria used to differentiate from SVT with aberrancy
ECG β Ventricular Tachycardia (monomorphic wide complex):
5. π« Left Bundle Branch Block (LBBB)
Pathophysiology: Failure of conduction through the left bundle branch β delayed depolarization of left ventricle β abnormal ventricular activation sequence. Can be caused by hypertension, CAD, cardiomyopathy, or acute MI (new LBBB = STEMI equivalent).
ECG Changes (WILLIAM mnemonic β W in V1, M in V6):
- QRS duration β₯120 ms
- Broad, notched (M-shaped) R waves in lateral leads (I, aVL, V5, V6)
- Deep, broad S waves or QS pattern in right precordial leads (V1, V2)
- No septal Q waves in I, V5, V6
- Discordant ST/T changes (ST and T in opposite direction to main QRS deflection β secondary repolarization change)
- Left axis deviation common
ECG β Left Bundle Branch Block:
6. π« Wolff-Parkinson-White (WPW) Syndrome
Pathophysiology: Accessory pathway (Bundle of Kent) bypasses the AV node β pre-excitation of the ventricle before normal AV node conduction arrives β fusion QRS complex. At risk of rapid AF conducting via the accessory pathway β life-threatening.
ECG Changes (classic triad):
- Short PR interval (<120 ms) β bypass of AV nodal delay
- Delta wave β slurred upstroke at start of QRS (pre-excitation of ventricle)
- Wide QRS (>120 ms) β fusion of pre-excited and normally conducted activation
- Secondary ST/T changes discordant to delta wave
- Accessory pathway localization possible by delta wave polarity (negative delta in inferior leads β posteroseptal pathway; positive V1 β left-sided pathway)
ECG β Wolff-Parkinson-White Syndrome:
7. π« Pulmonary Embolism (PE)
Pathophysiology: Acute obstruction of pulmonary vasculature β sudden increase in right ventricular afterload β acute RV strain and dilation β leftward septal shift, impaired LV filling.
ECG Changes:
- Sinus tachycardia β most common finding
- S1Q3T3 pattern (McGinn-White sign) β S wave in lead I + Q wave in lead III + inverted T wave in lead III
- Right axis deviation
- Incomplete or complete RBBB β due to RV strain
- T-wave inversions in V1βV4 β reflects right ventricular strain pattern
- P pulmonale (tall P in II >2.5 mm) β right atrial enlargement
- Atrial fibrillation may occur
- Normal ECG does NOT exclude PE
ECG β Pulmonary Embolism (S1Q3T3 pattern, annotated):
8. π« Acute Pericarditis
Pathophysiology: Inflammation of the pericardium β diffuse superficial myocardial injury β characteristic widespread repolarization and depolarization changes distinct from MI.
ECG Changes (4 classic stages):
| Stage | Timing | ECG Change |
|---|
| I | Hoursβdays | Diffuse concave ("saddle-shaped") ST elevation + PR depression |
| II | Daysβweeks | ST normalizes, PR still depressed |
| III | Weeks | Diffuse T-wave inversions |
| IV | Months | ECG normalizes |
- PR segment depression in most leads (II, V2βV6) β highly specific; aVR shows reciprocal PR elevation
- Diffuse ST elevation β concave upward, not confined to one coronary territory
- No reciprocal ST depression (except aVR and V1)
- Spodick's sign β downsloping TP segment
- No pathological Q waves (differentiates from MI)
ECG β Acute Pericarditis:
9. π« Hyperkalemia
Pathophysiology: Elevated serum KβΊ β reduces resting membrane potential β slows conduction, impairs repolarization β progressive ECG changes correlating with serum KβΊ level, potentially fatal.
ECG Changes (progressive with rising KβΊ):
| Serum KβΊ | ECG Finding |
|---|
| 5.5β6.5 mEq/L | Peaked (tented) T waves β tall, narrow-based, most in V2βV4 |
| 6.5β7.5 mEq/L | PR prolongation, P wave flattening/disappearance |
| 7.0β8.0 mEq/L | QRS widening (intraventricular conduction delay) |
| >8.0β9.0 mEq/L | Sine-wave pattern β QRS merges with T waves |
| >9.0 mEq/L | Ventricular fibrillation / asystole |
ECG β Severe Hyperkalemia:
10. π« Hypertrophic Cardiomyopathy (HCM)
Pathophysiology: Genetic (sarcomeric protein mutations) β asymmetric left ventricular hypertrophy (most commonly the interventricular septum) β increased QRS voltage, abnormal repolarization, myofiber disarray β arrhythmia risk and sudden cardiac death.
ECG Changes:
- LVH voltage criteria β Sokolow-Lyon: SV1 + RV5/V6 β₯35 mm; Cornell criteria >28 mm men / >20 mm women
- Deep, "giant" T-wave inversions in V2βV6 β especially in apical HCM (Yamaguchi syndrome); T waves can be >10 mm deep
- Deep, narrow Q waves in inferior (II, III, aVF) and lateral leads (V4βV6, I, aVL) β from septal hypertrophy
- Abnormal septal Q waves absent in I, V5, V6 (opposite of normal)
- ST-segment depression with lateral strain pattern
- Prolonged QTc in some variants
- Left axis deviation
- Increased risk of VT/VF β sudden cardiac death in young athletes
ECG β Hypertrophic Cardiomyopathy (HCM):
HCM ECG variants compared (concentric, septal, apical):
Quick Reference Summary
| # | Condition | Key ECG Finding |
|---|
| 1 | STEMI | ST elevation (convex) in contiguous leads + reciprocal changes + Q waves |
| 2 | Atrial Fibrillation | No P waves + irregularly irregular rhythm |
| 3 | 3rd-Degree AV Block | Complete AV dissociation + slow escape rhythm |
| 4 | Ventricular Tachycardia | Wide complex tachycardia + AV dissociation + fusion beats |
| 5 | LBBB | QRS β₯120 ms + WiLLiaM pattern + discordant ST/T |
| 6 | WPW Syndrome | Short PR + delta wave + wide QRS |
| 7 | Pulmonary Embolism | Sinus tachycardia + S1Q3T3 + RV strain (TWI V1βV4) |
| 8 | Acute Pericarditis | Diffuse saddle-shaped ST elevation + PR depression (no reciprocals) |
| 9 | Hyperkalemia | Peaked T waves β wide QRS β sine wave β VF |
| 10 | HCM | LVH voltage + giant T inversions V2βV6 + deep narrow Q waves |
Clinical Pearl: Always interpret ECGs in the clinical context. A single ECG can be normal even in serious disease (e.g., early STEMI, PE), and pathological findings (e.g., LBBB, LVH) require clinical correlation to guide management.