10 Heart Diseases and Their ECG Findings

1. ST-Elevation Myocardial Infarction (STEMI)

• Hyperacute T waves - tall, broad, peaked T waves (earliest change, minutes after onset)
• ST-segment elevation - >1 mm in 2 contiguous limb leads or >2 mm in 2 contiguous precordial leads
• Reciprocal ST depression - in leads "opposite" the infarct territory
• Pathological Q waves - develop within hours; width >40 ms, depth >25% of R wave (indicates transmural necrosis)
• T-wave inversion - follows ST normalization (reperfusion phase)

• Wellens syndrome - deep biphasic/inverted T waves in V2-V3 = critical LAD stenosis (preinfarction)
• De Winter sign - upsloping ST depression + peaked T in V1-V6 = LAD occlusion without classic elevation
• Sgarbossa criteria - used to diagnose AMI in the presence of LBBB

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

• Horizontal or downsloping ST depression - >0.5 mm, typically in multiple leads (indicates subendocardial ischemia)
• T-wave inversion - new symmetric T-wave inversion, especially >1 mm deep
• Transient ST changes - correlate with pain episodes
• ECG may be normal in up to 1-6% of confirmed NSTEMIs

3. Acute Pericarditis

• ST elevation is diffuse (involves most leads, not territory-specific)
• ST morphology is concave upward ("saddle-shaped"), not convex
• PR depression is the hallmark finding
• No reciprocal changes (except in aVR and V1)
• No Q waves

4. Hypertrophic Cardiomyopathy (HCM)

• Left ventricular hypertrophy (LVH) - high-voltage QRS (Sokolow-Lyon: S in V1 + R in V5/V6 >35 mm)
• Deep, narrow Q waves in inferolateral leads (II, III, aVF, V4-V6) - called "septal Q waves," reflect hypertrophied septum
• Giant negative T waves in mid-precordial leads (V3-V5) - characteristic of apical HCM (Yamaguchi variant)
• ST-segment depression and T-wave inversions in lateral leads
• Left atrial enlargement - broad notched P wave (P mitrale)
• Atrial fibrillation - common in advanced disease
• LVH pattern + inferolateral Q waves in an athlete strongly favors HCM over athlete's heart

5. Pulmonary Embolism (PE)

• ECG is abnormal in ~70% of cases but non-specific - a normal ECG does not exclude PE
• Sinus tachycardia - most common finding
• S1Q3T3 pattern - deep S wave in lead I, Q wave in lead III, inverted T in lead III (present in only ~20%, but classic sign of acute right heart strain)
• New right bundle branch block (RBBB) - complete or incomplete - indicates right ventricular strain/overload
• T-wave inversions in V1-V4 (right precordial leads) - reflects RV strain
• Right axis deviation
• P pulmonale - tall peaked P waves in inferior leads (>2.5 mm) = right atrial overload
• Atrial fibrillation or flutter - occasional
• ST depression in inferior/lateral leads - from RV ischemia

6. Atrial Fibrillation (AF)

• Absent P waves - replaced by rapid irregular fibrillatory baseline ("f" waves at 350-600/min)
• Irregularly irregular RR intervals - the defining feature; no two RR intervals are alike
• QRS is typically narrow (unless aberrant conduction or bundle branch block is present)
• Ventricular rate is variable: typically 100-180/min if uncontrolled; <60/min if rate-controlled

• AF with WPW - can produce wide, irregular, very rapid QRS complexes (pre-excited AF) - life-threatening
• AF with LBBB - wide complex irregular rhythm mimicking VT

7. Complete (Third-Degree) Heart Block

• P waves and QRS complexes are completely dissociated (independent rhythms)
• Atrial rate is regular and faster than ventricular rate (normal sinus rate ~60-100/min)
• Ventricular escape rhythm - QRS at 20-40/min (wide, bizarre if junctional escape is below His)
• If the escape pacemaker is junctional (above bifurcation): narrow QRS at 40-60/min
• If the escape pacemaker is ventricular: wide QRS at 20-40/min
• PP intervals are regular; RR intervals are regular - but they are independent of each other

8. Wolff-Parkinson-White Syndrome (WPW)

• Short PR interval (<120 ms) - impulse bypasses the AV node via accessory pathway
• Delta wave - slurred upstroke at the beginning of the QRS (initial pre-excitation of ventricular myocardium)
• Widened QRS (>120 ms) - due to fusion of normal conduction + accessory pathway activation
• ST-T changes - secondary repolarization abnormalities opposite to the delta wave direction
• Pseudo-infarct patterns - negative delta waves in inferior or precordial leads can mimic Q waves of MI

9. Long QT Syndrome (LQTS)

• Prolonged QTc interval - corrected QT (Bazett formula: QT/√RR):
  • Normal: <440 ms (men), <460 ms (women)
  • Borderline: 440-470 ms
  • Abnormal/diagnostic: >500 ms (high risk for Torsades)
• T-wave morphology varies by subtype:
  • LQT1 - broad-based T wave (exercise-triggered arrhythmias)
  • LQT2 - notched, bifid T wave (triggered by auditory stimuli/startle)
  • LQT3 - late-onset, peaked T wave with long isoelectric ST segment (arrhythmias at rest/sleep)
• Torsades de Pointes (TdP) - polymorphic VT with QRS axis rotating around the baseline; may degenerate to VF
• Prominent U waves - occasionally seen (more typical of hypokalemia-induced QTc prolongation)

10. Left Ventricular Hypertrophy (LVH) / Hypertensive Heart Disease

• High-voltage QRS - the primary marker:
  • Sokolow-Lyon criteria: S(V1) + R(V5 or V6) >35 mm
  • Cornell criteria: R(aVL) + S(V3) >28 mm (men) or >20 mm (women)
• Left axis deviation - QRS axis between -30° and -90°
• "LV strain" pattern - asymmetric ST depression and T-wave inversion in lateral leads (I, aVL, V5-V6); reflects subendocardial ischemia from increased wall stress
• Left atrial enlargement (P mitrale) - broad, notched biphasic P wave in V1 (negative terminal component >1 mm deep and >40 ms wide)
• Prolonged QRS duration - near LBBB threshold in advanced disease
• Increased QRS duration + large voltages = increased LV mass confirmed on echo

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