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ECG changes diseases STEMI pericarditis hyperkalemia pulmonary embolism

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10 Common Diseases with ECG Changes


1. πŸ«€ ST-Elevation Myocardial Infarction (STEMI)

ECG Changes:
  • ST-segment elevation β‰₯1 mm in β‰₯2 contiguous leads (β‰₯2 mm in precordial leads)
  • Reciprocal ST depression in opposite leads
  • Pathological Q waves (>0.04 s, >25% of R-wave height) β€” indicate completed infarction
  • New LBBB = STEMI equivalent
TerritoryLeads with ST Elevation
AnteriorV1–V4
InferiorII, III, aVF
LateralI, aVL, V5–V6
PosteriorTall R in V1–V2; ST elevation on right-sided leads
Right VentricleII, III, aVF + ST elevation in V3R–V6R
Tintinalli's Emergency Medicine β€” The 12-lead ECG is the single best test to identify AMI on presentation; obtain and interpret within 10 minutes of symptom onset.

2. πŸ’₯ NSTEMI / Unstable Angina

ECG Changes:
  • ST-segment depression (horizontal or downsloping) β€” most significant
  • T-wave inversion (symmetric, deep)
  • May have a normal ECG (1–6% of NSTEMI patients)
  • Dynamic changes (ST/T changes that evolve over serial ECGs) β€” 84% likelihood of CAD with classic symptoms

3. πŸ”΅ Acute Pericarditis

ECG Changes (classically progress through 4 stages):
  • Stage I β€” Diffuse concave ("saddle-shaped") ST elevation in nearly all leads EXCEPT aVR & V1; PR-segment depression (most specific sign); PR elevation in aVR
  • Stage II β€” ST normalizes; T-wave flattening
  • Stage III β€” Diffuse T-wave inversion
  • Stage IV β€” ECG normalizes
Key distinguishing features from STEMI:
  • ST elevation is diffuse (not restricted to one coronary territory)
  • ST elevation is concave (not convex)
  • PR depression is present
  • No reciprocal ST depression (except aVR)
  • Spodick's sign: downsloping TP segment
Pericarditis vs PE ECG β€” concave ST elevation with PR depression vs S1Q3T3 pattern
Classic pericarditis ECG with saddle-shaped ST elevation and PR depression in multiple leads

4. 🌬️ Acute Pulmonary Embolism (PE)

ECG Changes (reflect acute right heart strain):
  • S1Q3T3 β€” deep S wave in lead I, Q wave in lead III, inverted T wave in lead III (classic but present in only ~20%)
  • Sinus tachycardia β€” most common finding
  • New RBBB (complete or incomplete)
  • Right axis deviation
  • T-wave inversion in V1–V4 (right ventricular strain pattern)
  • P pulmonale (tall peaked P wave in II)
  • Atrial fibrillation/flutter

5. ⚑ Hyperkalemia

ECG Changes (progress with rising K⁺ level):
Serum K⁺ECG Finding
5.5–6.5 mEq/LTall, symmetric, peaked T waves (narrow base, "tent-shaped")
6.5–7.5 mEq/LLoss of P waves, prolonged PR interval
7.0–8.0 mEq/LWidened QRS complex, shortened QT
>8.0 mEq/LSine-wave pattern β†’ ventricular fibrillation β†’ asystole
Hyperkalemia ECG progression: normal (left) β†’ peaked T waves with widened QRS (middle) β†’ sine-wave pattern (right)
Morgan & Mikhail's Clinical Anesthesiology β€” Changes progress from symmetrically peaked T waves β†’ QRS widening β†’ loss of P wave β†’ sine wave β†’ ventricular fibrillation or asystole.
Harrison's Principles of Internal Medicine 22E β€” Classically: peaked T waves (5.5–6.5 mM), loss of P waves (6.5–7.5 mM), widened QRS (7.0–8.0 mM).

6. πŸ’§ Hypokalemia

ECG Changes:
  • U waves (prominent β€” the hallmark; follows T wave, best seen in V2–V3)
  • Flattened or inverted T waves
  • ST-segment depression
  • Prolonged QU interval (often mistaken for prolonged QT)
  • Severe: widened QRS, ventricular arrhythmias (VT, VF, torsades de pointes)

7. 🩺 Digoxin Toxicity / Effect

ECG Changes:
  • "Reverse tick" or "Salvador DalΓ­ moustache" ST depression β€” downsloping ST depression with upward concavity (digoxin effect, not toxicity)
  • Shortened QT interval
  • Flattened or inverted T waves
  • PR prolongation (first-degree AV block)
  • Toxicity: bradyarrhythmias, AV blocks (2nd/3rd degree), bidirectional VT (classic for digoxin toxicity), atrial tachycardia with AV block

8. ❀️‍πŸ”₯ Hypertrophic Cardiomyopathy (HCM)

ECG Changes:
  • LVH criteria (Sokolow-Lyon: S in V1 + R in V5/V6 β‰₯35 mm)
  • Deep, narrow Q waves in lateral leads (I, aVL, V5–V6) β€” "septal Q waves" due to abnormal septal depolarization
  • T-wave inversions in lateral leads
  • Left axis deviation
  • Giant inverted T waves in apical variant (Yamaguchi syndrome): deep, symmetric T inversions in V4–V6

9. 🫁 Chronic Obstructive Pulmonary Disease (COPD) / Cor Pulmonale

ECG Changes:
  • P pulmonale β€” tall, peaked P waves (>2.5 mm) in II, III, aVF (right atrial enlargement)
  • Right axis deviation (>+90Β°)
  • RVH β€” tall R in V1, deep S in V5–V6 (R/S ratio >1 in V1)
  • Low voltage throughout (due to hyperinflated lungs)
  • Clockwise rotation β€” persistent S waves across precordial leads (S1S2S3 pattern)
  • Multifocal atrial tachycardia (MAT) β€” three or more distinct P-wave morphologies; highly associated with COPD

10. 🧊 Hypothermia

ECG Changes:
  • Osborn (J) wave β€” pathognomonic: a positive deflection at the J point (junction of QRS and ST segment), best seen in V4–V6 and inferior leads; size correlates with severity of hypothermia
  • Sinus bradycardia β†’ junctional rhythm β†’ atrial fibrillation β†’ ventricular fibrillation (at <28Β°C)
  • Prolongation of all intervals β€” PR, QRS, QT
  • Muscle tremor artifact (shivering)
  • Susceptibility to ventricular fibrillation with stimulation

Summary Table

DiseaseHallmark ECG Finding
STEMIST elevation + Q waves (territory-specific)
NSTEMI/UAST depression + T-wave inversion
PericarditisDiffuse concave ST elevation + PR depression
Pulmonary EmbolismS1Q3T3 + sinus tachycardia + RBBB
HyperkalemiaPeaked T waves β†’ wide QRS β†’ sine wave
HypokalemiaProminent U waves + T flattening
DigoxinReverse-tick ST depression + short QT
HCMLVH + deep septal Q waves + lateral T inversions
COPD/Cor PulmonaleP pulmonale + RAD + RVH + MAT
HypothermiaOsborn (J) waves + bradycardia
Sources: Tintinalli's Emergency Medicine, Morgan & Mikhail's Clinical Anesthesiology 7e, Harrison's Principles of Internal Medicine 22E, Braunwald's Heart Disease, Miller's Anesthesia 10e
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