Here is a thorough explanation of ECG abnormalities, drawn primarily from Harrison's Principles of Internal Medicine (22nd ed., 2025).
ECG Abnormalities - A Systematic Overview
The ECG records the heart's electrical activity across time. Abnormalities are classified into six major categories.
1. Cardiac Enlargement and Hypertrophy
Atrial Abnormalities
- Right atrial overload: Tall, peaked P waves (≥2.5 mm), historically called "P-pulmonale"
- Left atrial overload: Biphasic P wave in V1 with a broad negative component, OR a broad (≥120 ms), often notched P wave in limb leads ("P-mitrale"). This can also occur with interatrial conduction delays even without true enlargement.
Ventricular Hypertrophy
- Left ventricular hypertrophy (LVH): Increased QRS amplitude directed leftward and posteriorly; ST-segment depression and T-wave inversions in leads with prominent R waves (strain pattern). Common voltage criteria: S in V1 + R in V5/V6 >35 mm.
- Right ventricular hypertrophy (RVH): Rightward QRS axis; tall R in V1 (R, RS, or qR complex); T-wave inversions in right precordial leads. Associated with pulmonary hypertension, pulmonic stenosis.
2. Bundle Branch Blocks and Intraventricular Conduction Defects
Complete bundle branch blocks have QRS duration ≥120 ms; incomplete blocks are 110-120 ms.
| Feature | RBBB | LBBB |
|---|
| V1 pattern | rSR' ("rabbit ears") | Wide QS (broad negative) |
| V6 pattern | qRS (deep S wave) | Entirely positive R (no Q, no S) |
| T wave | Inverted in V1-V3 (secondary change) | Inverted in V5-V6 (secondary change) |
| Clinical associations | ASD, pulmonary embolism, normal variant | Coronary artery disease, hypertension, aortic valve disease, cardiomyopathy |
Fascicular blocks (hemiblocks) do not widen the QRS but shift the axis:
- Left anterior fascicular block: axis more negative than -45° (marked left axis deviation) - most common cause of marked left axis deviation in adults
- Left posterior fascicular block: axis more rightward than +110-120° (rare as isolated finding)
Bifascicular block (RBBB + left anterior or posterior fascicular block) carries ~6% annual risk of progression to complete heart block.
Wolff-Parkinson-White (WPW): Wide QRS due to pre-excitation via an accessory bypass tract, NOT a conduction delay. Shows a delta wave (slurred QRS upstroke) and short PR interval.
3. Myocardial Ischemia and Infarction
Ischemia creates "currents of injury" that manifest as ST-segment deviation:
ST-Segment Elevation MI (STEMI)
- Transmural ischemia shifts the ST vector toward the epicardium → ST elevation in overlying leads
- Earliest sign: tall, peaked "hyperacute" T waves
- Evolution over hours to days: ST elevation → T-wave inversions → Q waves
Localization by leads:
| Territory | Leads with changes | Artery |
|---|
| Anterior/Apical | V1-V6, I, aVL | LAD |
| Inferior | II, III, aVF | RCA or LCX |
| Posterior | Reciprocal ST depression V1-V3 | LCX or RCA |
| Right ventricular | Right-sided leads (V3R, V4R) | RCA |
Non-ST Elevation / Subendocardial Ischemia
- Subendocardial ischemia shifts the ST vector toward the ventricular cavity → ST depression in precordial leads + ST elevation in aVR
- T-wave inversions without ST elevation
Pathological Q Waves
- Width ≥40 ms or depth ≥25% of R-wave height indicates prior transmural infarction
- Exception: septal Q waves in V5-V6 are normal (small, narrow)
4. Arrhythmias and Conduction (Rate/Rhythm Abnormalities)
By Heart Rate
- Tachycardia (>100 bpm): Sinus tachycardia, SVT, atrial flutter/fibrillation, ventricular tachycardia, ventricular fibrillation
- Bradycardia (<60 bpm): Sinus bradycardia, sick sinus syndrome, junctional rhythm
AV Conduction Blocks
| Degree | PR Interval | QRS | Notes |
|---|
| 1st degree | >200 ms (prolonged) | Normal | Benign |
| 2nd degree - Mobitz I (Wenckebach) | Progressive lengthening → dropped beat | Normal | Usually at AV node; relatively benign |
| 2nd degree - Mobitz II | Fixed PR, sudden dropped QRS | Normal or wide | Below the AV node; higher risk |
| 3rd degree (complete) | No relationship between P and QRS | Escape rhythm (wide or narrow) | Full AV dissociation |
Atrial Fibrillation
- Absent P waves, irregularly irregular rhythm, fibrillatory baseline
- Narrow QRS unless aberrant conduction
Ventricular Tachycardia
- Wide QRS (>120 ms), rate >100 bpm, AV dissociation
- Fusion beats and capture beats are diagnostic
5. Metabolic and Drug-Induced Changes
| Cause | ECG Change |
|---|
| Hyperkalemia | Peaked (tented) T waves → widening QRS → loss of P waves → sine-wave → asystole |
| Hypokalemia | Flattened T waves, prominent U waves, prolonged QU interval |
| Hypercalcemia | Shortened QT interval |
| Hypocalcemia | Prolonged QT interval (ST portion lengthened) |
| Hypothermia | Osborn (J) waves, bradycardia, prolonged QT |
| Digoxin | "Scooped" ST-T depression, shortened QT, AV block at toxic levels |
| Class IA/III antiarrhythmics | Prolonged QT → risk of torsades de pointes |
| Intracranial hemorrhage | Deep, wide T-wave inversions ("CVA T waves"), especially with SAH |
6. Other Notable Abnormalities
Brugada Pattern
- Right bundle branch block morphology + ST elevation in V1-V3 (coved or saddleback type)
- Associated with sudden cardiac death risk; inherited channelopathy
QT Prolongation
- QTc >440 ms in men, >460 ms in women (Bazett formula)
- Risk of torsades de pointes and sudden death
- Causes: congenital LQTS, drugs, electrolyte disturbances, hypothermia
Pericarditis
- Diffuse ST elevation (concave/"saddle-shaped") in multiple leads + PR depression
- No reciprocal changes (unlike MI), no Q waves
Low QRS Voltage
- Peak-to-trough QRS ≤5 mm in all limb leads and/or ≤10 mm in chest leads
- Causes: pericardial effusion, pleural effusion, COPD, cardiac amyloid, anasarca
Electrical Alternans
- Beat-to-beat alternation in QRS amplitude (and sometimes T waves)
- Classic finding in large pericardial effusion with cardiac tamponade
Pulmonary Embolism (Acute Cor Pulmonale)
- Sinus tachycardia (most common)
- S1Q3T3 pattern (deep S in I, Q and inverted T in III)
- Right axis deviation, new RBBB, atrial fibrillation
Summary Table of Key ECG Abnormalities
| Category | Pattern | Key Leads | Clinical Significance |
|---|
| LVH | Increased voltage + strain | V5-V6, I, aVL | Hypertension, aortic stenosis |
| RVH | Tall R in V1, right axis | V1, III, aVF | Pulmonary HTN, RV pressure overload |
| RBBB | rSR' | V1, V6 | Can be normal; also PE, ASD |
| LBBB | Wide QS, broad R | V1, V6 | Usually significant heart disease |
| STEMI | ST elevation | Localizes by territory | Emergency reperfusion needed |
| NSTEMI | ST depression, T inv | Diffuse | Subendocardial ischemia |
| Hyperkalemia | Peaked T → sine wave | All | Life-threatening |
| Long QT | QTc >440/460 ms | All | Risk of torsades de pointes |
| AF | No P waves, irregular | All | Stroke risk, rate control needed |
| Brugada | RBBB + V1-V3 ST elev | V1-V3 | Sudden cardiac death |
Sources: Harrison's Principles of Internal Medicine, 22nd ed. (2025), Chapter 247 (Electrocardiography); Fuster and Hurst's The Heart, 15th ed.