Explain me 10 heart diseases common ecg change and ecg images
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10 common heart diseases ECG changes findings 2024
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ECG Wolff-Parkinson-White Brugada syndrome hyperkalemia complete heart block Torsades de pointes patterns
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10 Common Heart Diseases and Their ECG Changes
Sources: Harrison's Principles of Internal Medicine 22E (2025), Rosen's Emergency Medicine, Tintinalli's Emergency Medicine
1. ST-Elevation Myocardial Infarction (STEMI)
Mechanism: Complete occlusion of an epicardial coronary artery causes transmural ischemia. Current of injury flows outward toward epicardial leads, producing ST elevation.
ECG Changes:
- Hyperacute T waves - the earliest sign: broad, tall T waves preceding ST changes
- ST elevation ≥1 mm in ≥2 contiguous leads (convex/tombstone morphology)
- Pathological Q waves - develop within hours to days (>40 ms wide, >25% of R wave height)
- T wave inversions - evolve as ST normalizes
- Reciprocal ST depression in opposite leads (increases specificity)
Localization:
- Anterior STEMI: V1-V4 (LAD)
- Inferior STEMI: II, III, aVF (RCA)
- Lateral STEMI: I, aVL, V5-V6
- Posterior MI: tall R wave + horizontal ST depression in V1-V2 (mirror image)
Fig 1. ST segment morphology comparison: (A) Flat/convex ST in STEMI; (B) Concave ST in benign early repolarization and pericarditis; (C) Concave pattern also seen in some STEMIs - serial ECGs help distinguish. (Rosen's Emergency Medicine)
Fig 2. Inferior STEMI: Marked ST elevation in leads II, III, aVF; classic reciprocal ST depression in I and aVL. (Rosen's Emergency Medicine)
2. Non-ST Elevation Myocardial Infarction (NSTEMI) / Unstable Angina
Mechanism: Subendocardial ischemia. The ST vector shifts toward the subendocardium/ventricular cavity, causing overlying leads to show ST depression.
ECG Changes:
- ST depression (horizontal or downsloping) - most typical; upsloping is less specific
- T wave inversions - narrow, symmetrical; isoelectric or slightly upward-bowed ST preceding them
- Wellens syndrome - deep symmetrical T wave inversions (Type I) or biphasic T waves (Type II) in V1-V4, indicating critical LAD stenosis; may be present even when pain-free
- May have a normal ECG - does NOT exclude NSTEMI
Fig 3. ST segment depression in ACS: (A) flat/horizontal pattern, (B) upsloping (less ischemic), (C) horizontal in posterior MI (right precordials), (D) marked downsloping, (E) biphasic Wellens T waves. (Rosen's Emergency Medicine)
Fig 4. Wellens T wave sign - deep symmetric T wave inversions in precordial leads V1-V6 with severe LAD stenosis. (Harrison's Principles of Internal Medicine 22E)
3. Atrial Fibrillation (AF)
Mechanism: Chaotic, disorganized atrial electrical activity from multiple micro-reentrant circuits. Associated with ischemic heart disease, valvular disease, cardiomyopathy, thyrotoxicosis, and "holiday heart" (alcohol binge).
ECG Changes (from Tintinalli's Table 18-8):
- Absent P waves - replaced by a chaotic, fibrillatory baseline (f waves, 350-600/min)
- Irregularly irregular RR intervals - the hallmark
- Narrow QRS unless pre-existing bundle branch block or pre-excitation (WPW)
- Ventricular rate typically 100-160/min if uncontrolled
Fig 5. (A) Tachycardia with irregular baseline - atrial fibrillation; (B) Regular narrow-complex tachycardia with flutter waves (sawtooth) in leads II, III, aVF - atrial flutter with 2:1 block; (C) Atrial flutter response to carotid sinus massage unmasking flutter waves. (Tintinalli's Emergency Medicine)
4. Complete Heart Block (Third-Degree AV Block)
Mechanism: Complete dissociation between atrial and ventricular conduction. No impulses pass through the AV node. The ventricles are driven by a slow escape rhythm (junctional or ventricular).
ECG Changes:
- P waves present but bear no fixed relationship to QRS complexes (AV dissociation)
- PP intervals regular, RR intervals regular, but PR intervals vary completely
- Bradycardia - escape rate 20-40/min if ventricular, 40-60/min if junctional
- Wide QRS (>120 ms) if ventricular escape; narrow QRS if junctional escape
- Ventricular rate is slower than atrial rate
5. Left/Right Bundle Branch Block (LBBB / RBBB)
Mechanism: Impaired conduction in one bundle system prolongs QRS and shifts its vector toward the side of delayed depolarization.
ECG Changes:
| Feature | RBBB | LBBB |
|---|---|---|
| QRS duration | ≥120 ms | ≥120 ms |
| V1 morphology | rSR' ("rabbit ears") | QS or rS (negative) |
| V6 morphology | qRS with terminal S | Broad monophasic R, no Q |
| T wave | Opposite to last QRS deflection | Opposite to last QRS deflection |
| Axis | Right or normal | Left |
- LBBB is a marker of underlying CAD, hypertensive heart disease, aortic valve disease, or cardiomyopathy - and can mask STEMI
- RBBB can be normal or associated with atrial septal defect, pulmonary hypertension
Fig 6. RBBB vs LBBB comparison. RBBB: rSR' in V1, qRS in V6, T wave inverted (arrow). LBBB: QS in V1, broad R in V6, T inverted (arrow). (Harrison's Principles of Internal Medicine 22E)
6. Left Ventricular Hypertrophy (LVH)
Mechanism: Increased muscle mass from pressure overload (hypertension, aortic stenosis) generates larger electrical potentials directed leftward and posteriorly.
ECG Changes (Sokolow-Lyon criteria and others):
- Increased voltage: SV1 + RV5 or RV6 ≥35 mm; RaVL >20 mm (women) or >28 mm (men)
- Left axis deviation
- ST depression + T wave inversion in leads I, aVL, V5-V6 ("strain pattern") - a secondary repolarization change
- Left atrial abnormality (P mitrale) - broad, notched P waves in lead II; biphasic P in V1
- May progress to LBBB
Note: Voltage criteria have low sensitivity, especially in obese patients and smokers.
7. Acute Pericarditis
Mechanism: Diffuse pericardial inflammation affects the subepicardial myocardium, causing widespread repolarization changes. There is also PR depression from atrial involvement.
ECG Changes (4 evolutionary stages):
- Stage 1 (acute): Diffuse ST elevation (concave/saddle-shaped) in almost all leads EXCEPT aVR and V1; PR segment depression (most specific finding)
- Stage 2: ST returns to baseline; T waves flatten
- Stage 3: T wave inversions develop diffusely
- Stage 4: Normalization
Key distinguishing features from STEMI:
- ST elevation is concave (not convex), diffuse (not regional)
- PR depression present
- No reciprocal ST depression (except aVR)
- No Q waves
- ST:T ratio in V6 >0.25 favors pericarditis
(Differential included in Table 64.3 from Rosen's - see Fig 1 above for ST morphology comparison)
8. Pulmonary Embolism (PE)
Mechanism: Acute right heart pressure overload from massive PE causes right ventricular dilation and strain, shifting the electrical axis rightward.
ECG Changes:
- Sinus tachycardia - the most common finding
- S1Q3T3 pattern - prominent S wave in lead I, Q wave in lead III, T wave inversion in lead III
- Right axis deviation
- New RBBB or incomplete RBBB (right ventricular conduction delay)
- ST-T changes in V1-V4 simulating anterior infarction (right ventricular strain)
- Right precordial T wave inversions (V1-V3)
- Atrial fibrillation or flutter may occur
- A normal ECG does NOT rule out PE
9. Wolff-Parkinson-White Syndrome (WPW)
Mechanism: An accessory bypass tract (Bundle of Kent) pre-excites the ventricles, bypassing the AV node delay. Ventricular activation begins earlier via the accessory pathway and the rest continues via the normal conduction system.
ECG Changes (the "WPW triad"):
- Short PR interval (<120 ms) - early ventricular activation bypassing AV node
- Delta wave - slurred upstroke at the beginning of the QRS (slow accessory pathway conduction through ventricular myocardium)
- Wide QRS (≥120 ms) - due to delta wave + fusion beat
- Secondary ST-T changes - discordant from QRS
- Risk of rapid conduction of AF down the bypass tract causing ventricular fibrillation
From Harrison's: "Prolongation of QRS duration...may be due to pre-excitation of the ventricles via a bypass tract, as in Wolff-Parkinson-White (WPW) patterns"
10. Brugada Syndrome
Mechanism: Autosomal dominant sodium channel mutation (SCN5A) causes abnormal early repolarization of right ventricular outflow tract. Associated with risk of sudden cardiac death from ventricular fibrillation.
ECG Changes:
- Type 1 (diagnostic - "coved" type): ST elevation ≥2 mm with coved (convex dome) morphology in V1-V2 (or V1-V3 in 2nd/3rd intercostal space), followed by a negative T wave - this is the ONLY diagnostic pattern
- Type 2 ("saddle-back"): ST elevation with saddle-back morphology - not diagnostic alone
- Pattern may be intermittent and provoked by fever, sodium channel blockers, or vagal tone
- Normal intervals otherwise; structurally normal heart
- Simulates RBBB morphology in right precordial leads
Harrison's: "A distinctive abnormality simulating right bundle branch block with ST-segment elevations in the right chest leads is seen with the Brugada pattern"
Summary Table
| # | Disease | Key ECG Finding | Leads Affected |
|---|---|---|---|
| 1 | STEMI | Convex ST elevation + Q waves + hyperacute T | Regional (I, V1-V4, II/III/aVF) |
| 2 | NSTEMI/UA | Horizontal/downsloping ST depression; Wellens T | V1-V4, diffuse |
| 3 | Atrial Fibrillation | Absent P waves; irregularly irregular RR | All leads |
| 4 | Complete Heart Block | AV dissociation; bradycardia; varying PR | All leads |
| 5 | LBBB / RBBB | Wide QRS ≥120 ms; rSR' (RBBB) vs QS (LBBB) | V1, V6 |
| 6 | LVH | Tall voltage; strain pattern (ST depression, T inversion) | Left precordial leads |
| 7 | Acute Pericarditis | Diffuse concave ST elevation; PR depression | Widespread (except aVR) |
| 8 | Pulmonary Embolism | S1Q3T3; new RBBB; sinus tachycardia | I, III, V1-V4 |
| 9 | WPW Syndrome | Short PR; delta wave; wide QRS | All leads |
| 10 | Brugada Syndrome | Coved ST elevation V1-V2; RBBB-like morphology | V1-V3 |
Sources:
- Harrison's Principles of Internal Medicine 22E (2025, McGraw Hill) - Chap. 247
- Rosen's Emergency Medicine - Chap. 64
- Tintinalli's Emergency Medicine: A Comprehensive Study - Chap. 18
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