Here is a comprehensive guide to ECG changes in the 10 most common and clinically important conditions, sourced from Harrison's Principles of Internal Medicine, Guyton & Hall, Braunwald's Heart Disease, Morgan & Mikhail's Clinical Anesthesiology, and Goldman-Cecil Medicine.
ECG Changes in 10 Common Clinical Conditions
1. Normal Sinus Rhythm (Reference Baseline)
Before covering pathology, here is the baseline for comparison. A normal ECG shows:
- Regular P wave before every QRS
- PR interval: 120-200 ms
- QRS duration: <120 ms
- QT interval varies with heart rate (QTc <440 ms in men, <460 ms in women)
- Upright T waves in lateral leads, inverted in aVR
2. STEMI - ST-Elevation Myocardial Infarction
Mechanism: Total occlusion of a coronary artery causes transmural (full-thickness) ischemia. Injured epicardial cells generate a "current of injury" that shifts the ST vector outward toward the affected zone.
ECG changes (evolving over hours to days):
- Hyperacute T waves - earliest sign; tall, peaked, broad T waves
- ST elevation - convex ("tombstone") upsloping ST elevation ≥1 mm in ≥2 contiguous limb leads or ≥2 mm in ≥2 precordial leads
- Reciprocal ST depression - in leads facing the opposite wall
- Pathological Q waves - develop over hours to days; width ≥40 ms, depth ≥¼ R wave = necrosis marker
- T-wave inversion - follows ST elevation as infarct evolves
Lead localization:
| Territory | Culprit artery | ST elevation in |
|---|
| Anterior | LAD | V1-V6, I, aVL |
| Inferior | RCA | II, III, aVF |
| Lateral | LCx | I, aVL, V5-V6 |
| Posterior | RCA/LCx | Reciprocal V1-V3 depression |
| RV | RCA proximal | V1, V4R |
Anterior STEMI - ECG sequence (acute top row, evolving bottom row):
Inferior STEMI - ECG sequence:
Subendocardial vs. transmural ischemia - current of injury diagram:
Left: subendocardial ischemia → ST vector directed inward → overlying leads show ST depression. Right: transmural/epicardial ischemia → ST vector directed outward → overlying leads show ST elevation. - Harrison's Principles of Internal Medicine 22E, Fig. 247-11
3. NSTEMI / Unstable Angina (Subendocardial Ischemia)
ECG changes:
- ST depression ≥0.5 mm (horizontal or downsloping) in ≥2 contiguous leads
- T-wave inversions - symmetric, deep; in precordial leads V1-V4 with high-grade LAD stenosis = Wellens sign
- No Q waves, no ST elevation
- A normal ECG does not exclude NSTEMI
Wellens T-wave sign - deep symmetric T inversions in V1-V6 (shown in 6-lead strip below):
"Patients who present with deep T-wave inversions in multiple precordial leads (V1-V4) typically have severe obstruction in the left anterior descending coronary artery." - Harrison's Principles of Internal Medicine 22E, p. 1916
4. Atrial Fibrillation (AF)
Mechanism: Multiple chaotic re-entrant circuits in the atria produce disorganized electrical activity at 350-600 impulses/min. The AV node filters these, producing an irregularly irregular ventricular response.
ECG changes:
- No P waves - replaced by low-amplitude fibrillatory (f) waves, best seen in V1
- Irregularly irregular RR intervals - the hallmark; no two consecutive RR intervals are equal
- QRS complexes are narrow (unless aberrant conduction or bundle branch block)
- Ventricular rate typically 100-160 bpm if untreated
"In the ECG, one can see either no P waves or only a fine, high-frequency, very low voltage wave. The QRS-T complexes are normal unless there is some pathology of the ventricles, but their timing is irregular." - Guyton & Hall Textbook of Medical Physiology, Fig. 13.20
5. Atrial Flutter
Mechanism: A single organized macro-reentrant circuit in the right atrium at ~300 beats/min. The AV node typically conducts every 2nd impulse (2:1 block), giving a ventricular rate of ~150 bpm.
ECG changes:
- Sawtooth flutter (F) waves at 250-350/min, best seen in leads II, III, aVF and V1
- Regular atrial rate; ventricular rate typically 150 bpm (2:1) or 100 bpm (3:1)
- No discrete P waves
- Classic pearl: any regular tachycardia at exactly 150 bpm - suspect atrial flutter with 2:1 block
6. Ventricular Tachycardia (VT)
Mechanism: Rapid impulse formation or re-entry within the ventricular myocardium, bypassing the normal His-Purkinje system, causing wide, bizarre QRS complexes.
ECG changes:
- Wide QRS complexes ≥120 ms (usually ≥140 ms)
- Rate 100-250 bpm, typically 140-200 bpm
- AV dissociation - P waves march through at their own rate, independent of QRS
- Capture beats - occasional narrow QRS when a sinus impulse successfully captures the ventricle
- Fusion beats - hybrid QRS between sinus beat and VT beat
- Concordance - all precordial leads with same QRS polarity; negative concordance (all negative) strongly suggests VT
- Left axis deviation common
Key distinction from SVT with aberrancy: Brugada criteria, AV dissociation, fusion/capture beats all favor VT.
"For wide-QRS complex tachycardias, the 12-lead ECG is useful in distinguishing SVT (with aberrancy) from ventricular tachycardia. The presence of fusion beats, capture beats, and AV dissociation all favor VT." - Goldman-Cecil Medicine, Electrocardiography section
7. Complete Heart Block (3rd-Degree AV Block)
Mechanism: No conduction passes from atria to ventricles. Atria and ventricles beat independently. A junctional or ventricular escape rhythm maintains cardiac output.
ECG changes:
- P waves and QRS complexes are completely independent (AV dissociation)
- P-P intervals are regular; RR intervals are regular - but at different rates
- Atrial rate: 60-100/min; ventricular escape rate: 40-60/min (junctional, narrow QRS) or 20-40/min (ventricular, wide QRS)
- The PR interval varies constantly - no fixed relationship between P and QRS
- Classic pearl: more P waves than QRS complexes on the strip
8. Left Ventricular Hypertrophy (LVH)
Mechanism: Increased myocardial mass generates larger electrical forces directed leftward and posteriorly.
ECG changes (voltage criteria + repolarization):
- Tall R waves in lateral leads (V5, V6, I, aVL)
- Deep S waves in right precordial leads (V1, V2)
- Sokolow-Lyon criteria: S in V1 + R in V5 or V6 >35 mm (adults)
- Cornell criteria: R in aVL + S in V3 >28 mm (men), >20 mm (women)
- LV strain pattern: ST depression + T-wave inversion in leads I, aVL, V4-V6 (asymmetric, downsloping)
- Left axis deviation, prolonged QRS
LVH vs. RVH vs. Normal in V1 and V6:
"LVH increases the amplitude of electrical forces directed to the left and posteriorly. Repolarization abnormalities may cause ST-segment depression and T-wave inversion in leads with a prominent R wave." - Harrison's Principles of Internal Medicine 22E, Fig. 247-9
9. Right Atrial / Left Atrial Enlargement (P-wave Changes)
Right Atrial Enlargement (P pulmonale):
- Tall, peaked P waves ≥2.5 mm in leads II, III, aVF
- P wave axis rightward
Left Atrial Enlargement (P mitrale):
- Broad, notched P waves ≥120 ms in limb leads (bifid "m-shaped" P wave)
- Biphasic P wave in V1 with prominent negative component (representing delayed LA depolarization)
- P-wave axis leftward
"Right atrial overload may cause tall, peaked P waves in the limb or precordial leads. Left atrial abnormality may cause broad, often notched P waves in the limb leads and a biphasic P wave in lead V1 with a prominent negative component." - Harrison's Principles of Internal Medicine 22E, Fig. 247-8
10. Hyperkalemia
Mechanism: Elevated extracellular K+ raises the resting membrane potential closer to threshold, slowing conduction through all cardiac tissues. Changes are progressive with rising serum K+ levels.
ECG changes (sequential with rising K+):
| Serum K+ | ECG finding |
|---|
| 5.5-6.5 mEq/L | Tall, symmetrically peaked T waves; shortened QT interval |
| 6.5-7.5 mEq/L | PR interval prolongation; flattened or absent P waves; ST depression |
| 7.5-8.0 mEq/L | Widening QRS complex (>120 ms); loss of R-wave amplitude |
| >8.0 mEq/L | Sine wave pattern (QRS and T merge); precedes VF or asystole |
"ECG changes characteristically progress from symmetrically peaked T waves, often with a shortened QT interval, to widening of the QRS complex, prolongation of the PR interval, loss of the P wave... to an ECG that resembles a sine wave before final progression into ventricular fibrillation or asystole." - Morgan & Mikhail's Clinical Anesthesiology 7e, Fig. 49-7
Bonus: Pulmonary Embolism (PE)
ECG changes (nonspecific but suggestive):
- Sinus tachycardia - most common finding
- S1Q3T3 pattern: deep S wave in lead I, Q wave + T-wave inversion in lead III
- Right axis deviation
- New right bundle branch block (complete or incomplete)
- T-wave inversions in V1-V4 (right heart strain pattern)
- Atrial fibrillation or flutter may occur
"Acute cor pulmonale due to pulmonary thromboembolism may be associated with sinus tachycardia, right axis deviation, the S₁Q₃T₃ pattern, slow R-wave progression, and ST-T abnormalities in V1 to V4 simulating acute anterior infarction." - Harrison's Principles of Internal Medicine 22E, p. 1915
Quick Reference Summary Table
| Condition | Rate | Rhythm | P wave | PR | QRS | ST/T |
|---|
| Sinus rhythm | 60-100 | Regular | Normal | 120-200ms | <120ms | Normal |
| STEMI (acute) | Variable | Regular | Normal | Normal | Normal | ST ↑, hyperacute T |
| NSTEMI | Variable | Regular | Normal | Normal | Normal | ST ↓, T inv |
| Atrial fibrillation | 100-160 | Irregular | Absent (f waves) | None | Normal | Variable |
| Atrial flutter | 75-150 | Regular | Sawtooth F | None | Normal | Variable |
| VT | 140-200 | Regular | Dissociated | Variable | Wide ≥120ms | Concordant |
| 3rd-degree block | 20-60 | Regular (escape) | Present | Variable (dissociated) | Narrow or wide | Variable |
| LVH | Normal | Regular | Normal | Normal | Tall voltage | Strain (ST↓, T inv lat) |
| LA enlargement | Normal | Regular | Broad/bifid/biphasic | Normal | Normal | Normal |
| Hyperkalemia | Bradycardia | Irregular | Absent (severe) | ↑ | Wide, sine wave | Peaked T → flat |
| PE | Tachycardia | Regular | Normal | Normal | Normal or RBBB | S1Q3T3, RV strain |
Sources: Harrison's Principles of Internal Medicine 22E (2025); Guyton & Hall Textbook of Medical Physiology; Braunwald's Heart Disease; Morgan & Mikhail's Clinical Anesthesiology 7e; Goldman-Cecil Medicine.