10 Common Heart Diseases: ECG Changes & Images

1. ST-Elevation Myocardial Infarction (STEMI)

• Hyperacute T waves - the earliest change (tall, broad, symmetric T waves)
• ST elevation - convex ("tombstone") or straight upsloping, at least 1 mm in two contiguous limb leads or 2 mm in precordial leads
• Reciprocal ST depression - in leads opposite to the infarct
• Pathological Q waves - develop within hours to days (>40 ms wide, >25% of QRS amplitude), indicating necrosis
• T wave inversion - evolves as infarction progresses
• Lead localization:
  • Anterior STEMI: V1-V4 (LAD occlusion)
  • Inferior STEMI: II, III, aVF (RCA occlusion)
  • Lateral STEMI: I, aVL, V5-V6 (LCx occlusion)
  • Posterior STEMI: ST depression + tall R in V1-V2 (mirror image)

"Severe, acute ischemia lowers the resting membrane potential and shortens the duration of the action potential... current flows between normal and ischemic zones... producing ST elevations and sometimes, in the earliest stages of ischemia, tall, positive so-called hyperacute T waves." - Harrison's Principles of Internal Medicine 22E

2. Non-ST Elevation Myocardial Infarction (NSTEMI) / Unstable Angina

• ST depression - horizontal or downsloping (most specific for subendocardial ischemia); at least 0.5 mm in 2 contiguous leads
• T wave inversion - deep symmetric inversions, especially in anterior leads
• No pathological Q waves (by definition - no transmural necrosis)
• May be normal - up to 30% of NSTEMI patients have no ECG changes
• De Winter's sign - upsloping ST depression with tall T waves in V1-V6 (LAD occlusion equivalent)
• Wellens' syndrome - deep symmetric T inversions or biphasic T waves in V2-V3 indicating critical LAD stenosis

3. Atrial Fibrillation (AF)

• No distinct P waves - replaced by irregular fibrillatory baseline (f waves at 350-600 bpm)
• Irregularly irregular RR intervals - the hallmark finding
• Narrow QRS (unless aberrant conduction or bundle branch block present)
• Variable ventricular rate - typically 100-180 bpm if uncontrolled
• Undulating baseline best seen in V1

• Absent P waves + irregularly irregular rhythm = AF until proven otherwise
• Coarse AF: prominent fibrillatory waves (often seen in rheumatic heart disease)
• Fine AF: barely visible fibrillatory baseline (long-standing AF)

4. Atrial Flutter

• Sawtooth flutter waves - regular, negative deflections at ~300 bpm, best seen in II, III, aVF
• 2:1 AV conduction most common - ventricular rate ~150 bpm
• Regular ventricular rhythm (unlike AF)
• Narrow QRS (unless BBB present)
• Carotid sinus massage or adenosine can temporarily increase AV block and reveal flutter waves

5. Complete (Third-Degree) Heart Block

• Complete AV dissociation - P waves and QRS complexes are completely independent
• Regular P waves at normal or elevated atrial rate (60-100 bpm)
• Regular escape rhythm at slow ventricular rate:
  • Junctional escape: 40-60 bpm, narrow QRS
  • Ventricular escape: 20-40 bpm, wide QRS (>120 ms), bizarre morphology
• P wave "marches through" QRS - PR intervals constantly changing
• Bradycardia is prominent; symptoms include syncope (Stokes-Adams attacks)

6. Wolff-Parkinson-White (WPW) Syndrome

• Short PR interval (<120 ms) - impulse bypasses AV node delay
• Delta wave - slurred upstroke at start of QRS (slow accessory pathway conduction through ventricular muscle)
• Wide QRS (>120 ms) - due to pre-excitation + fusion
• Secondary ST-T changes - ST depression and T inversion opposite to delta wave polarity
• Pseudo-infarct patterns - negative delta waves can mimic Q waves
• During AVRT tachycardia: narrow complex (orthodromic, most common) or wide complex (antidromic)
• AF + WPW = extremely fast, irregular, wide-complex tachycardia - potentially fatal

7. Acute Pericarditis

• Stage 1 (acute): Diffuse concave ("saddle-shaped") ST elevations in most leads (I, II, aVL, aVF, V3-V6); PR segment depression (pathognomonic) in same leads; PR elevation in aVR
• Stage 2: ST segments normalize; T waves flatten
• Stage 3: Diffuse T wave inversions
• Stage 4: ECG returns to normal

8. Left Ventricular Hypertrophy (LVH)

• High-voltage QRS:
  • Sokolow-Lyon: S in V1 + R in V5 or V6 >35 mm
  • Cornell: R in aVL + S in V3 >28 mm (men), >20 mm (women)
• Left axis deviation (-30° to -90°)
• ST depression and T wave inversion in lateral leads (I, aVL, V5-V6) - the "strain pattern" (secondary repolarization abnormality)
• Left atrial enlargement - broad, notched P waves (P mitrale) or biphasic P in V1
• Prolonged QRS (up to 110 ms)
• Wide QRS transition zone
• In the T-wave panel above: "Left ventricular hypertrophy (V5-V6)" - symmetric T inversions, often very deep, with large R waves

9. Pulmonary Embolism (PE)

• Most common: Sinus tachycardia (most frequent, but nonspecific)
• S1Q3T3 pattern (classic but present in only ~20%): S wave in lead I + Q wave in lead III + T inversion in lead III
• Right heart strain signs:
  • New RBBB (complete or incomplete)
  • Right axis deviation
  • P pulmonale (peaked P waves in II indicating RAH)
  • ST depression/T inversion in V1-V4 (right precordial strain)
  • New atrial fibrillation or flutter
• Clockwise rotation of precordial leads (persistent S waves through V5-V6)
• Electrical alternans if pericardial effusion develops
• Normal ECG does NOT exclude PE

10. Hypertrophic Cardiomyopathy (HCM / HOCM)

• LVH voltage criteria (similar to hypertensive LVH but often more pronounced)
• Deep, symmetric T wave inversions - most characteristic, especially in V1-V5; often the "giant negative T waves" of apical HCM (Yamaguchi variant: >10 mm inverted T waves in V4-V5)
• Pathological Q waves - narrow, deep Q waves in lateral leads (I, aVL, V5-V6) and inferior leads - due to hypertrophied septum, can mimic old MI
• Left atrial enlargement - broad P waves
• Nonspecific ST changes
• In the T-wave image above: "Hypertrophic cardiomyopathy - Symmetric T wave inversions, most commonly in V1-V3. Often very deep and accompanied by large R waves."

Quick Reference Summary Table

Clinical note: ECG interpretation must always be correlated with clinical context, symptoms, and biomarkers. No single ECG finding is pathognomonic in isolation. When in doubt, compare with prior tracings and involve a senior clinician.