10 Common Heart Diseases: ECG Changes & Images

1. ST-Elevation Myocardial Infarction (STEMI)

ECG Changes

• Hyperacute T waves (earliest change — tall, peaked, asymmetric T waves)
• ST-segment elevation ≥1 mm in ≥2 contiguous limb leads, or ≥2 mm in ≥2 contiguous precordial leads (convex/tombstone morphology)
• Reciprocal ST-segment depression in opposite leads
• Pathological Q waves (>40 ms wide, >25% QRS height) — appear hours later, indicating necrosis
• T-wave inversions in the recovery phase

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

ECG Changes

• ST-segment depression (horizontal or down-sloping, ≥0.5 mm) in ≥2 contiguous leads
• T-wave inversions (symmetric, deep) — most prominent in the territory of ischemia
• No pathological Q waves (by definition — no transmural necrosis)
• Transient ST-T changes that may normalize between episodes
• The ECG may be normal in up to 6% of NSTEMI cases

Key distinction: Unlike STEMI, NO persistent ST elevation; treatment pathway differs (no immediate thrombolysis).

3. Atrial Fibrillation (AF)

ECG Changes

• Absent P waves — replaced by chaotic fibrillatory baseline (f-waves), best seen in V1
• Irregularly irregular R-R intervals (hallmark finding)
• Narrow QRS complexes (unless aberrant conduction/accessory pathway)
• Ventricular rate variable: 100–180 bpm (uncontrolled), 60–100 bpm (rate-controlled)
• Fibrillatory baseline most prominent in lead V1 and limb leads

4. Ventricular Fibrillation (VF)

ECG Changes

• Completely chaotic, disorganized waveforms with no identifiable P, QRS, or T waves
• Irregular undulations of varying amplitude and frequency
• Heart rate effectively undefined — no organized cardiac output
• Coarse VF: higher amplitude oscillations (often more recent onset, more responsive to defibrillation)
• Fine VF: low amplitude, difficult to distinguish from asystole

Medical emergency — requires immediate defibrillation (200J biphasic).

5. Ventricular Tachycardia (VT)

ECG Changes

• Wide QRS complexes (>120 ms) at a rapid rate (100–250 bpm)
• Regular rhythm (monomorphic VT) or irregular (polymorphic VT/Torsades)
• AV dissociation — P waves march independently from QRS (pathognomonic when seen)
• Fusion beats and capture beats (Dressler beats) — highly specific for VT
• Concordance across precordial leads (all positive = positive concordance, all negative = negative concordance)
• Axis: often superior (northwest axis)

Brugada criteria, Vereckei algorithm, and RWPT help differentiate VT from SVT with aberrancy.

6. Complete (Third-Degree) AV Block

ECG Changes

• Complete AV dissociation — P waves and QRS complexes are completely independent
• Regular P-P intervals (atrial rate: ~60–100 bpm)
• Regular R-R intervals but at a much slower rate (ventricular escape rate: 20–60 bpm)
• No consistent PR interval — P waves "march through" QRS complexes
• QRS morphology depends on escape focus:
  • Junctional escape (His bundle) → narrow QRS (~40–60 bpm)
  • Ventricular escape → wide, bizarre QRS (~20–40 bpm)

7. Pericarditis (Acute)

ECG Changes

• Spodick's sign: downsloping TP segment (highly specific for pericarditis)
• aVR reciprocal ST elevation and PR elevation
• Differentiated from STEMI by: diffuse distribution, concave morphology, PR depression, absence of Q waves, absence of reciprocal changes (except aVR)

8. Wolff-Parkinson-White (WPW) Syndrome

ECG Changes

1. Short PR interval (<120 ms) — due to bypass of AV node via accessory pathway
2. Delta wave — slurred upstroke at onset of QRS (pre-excitation of ventricular myocardium)
3. Widened QRS (>120 ms) — due to fusion of pre-excited and normally conducted impulses

• Secondary ST-T wave changes (opposite to QRS direction)
• Pseudo-Q waves in inferior leads (mimics inferior infarction)
• Accessory pathway localization by delta wave polarity (e.g., positive delta in V1 = left-sided pathway)
• Risk of AF with rapid ventricular response via the accessory pathway (life-threatening)

9. Right Bundle Branch Block (RBBB)

ECG Changes

• QRS duration ≥120 ms (complete RBBB); 100–119 ms (incomplete RBBB)
• rSR' pattern ("rabbit ears") in V1–V3 — the classic finding
• Wide, slurred S waves in leads I, aVL, V5, V6
• Secondary ST-T wave changes: T-wave inversions in V1–V3 (always secondary to conduction delay — not primary ischemia)
• Right axis deviation may be present
• Associated with: pulmonary embolism (new RBBB), right heart disease, post-cardiac surgery

New RBBB + anterior ST elevation = Sgarbossa criteria territory — possible LAD occlusion.

10. Hypertrophic Cardiomyopathy (HCM)

ECG Changes

• Left ventricular hypertrophy (LVH) voltage criteria:
  • Sokolow-Lyon: S(V1) + R(V5 or V6) >35 mm
  • Cornell: R(aVL) + S(V3) >28 mm (men), >20 mm (women)
• Deep, narrow Q waves ("dagger Q waves") in lateral leads (I, aVL, V5–V6) and inferior leads — due to septal hypertrophy
• Giant T-wave inversions (≥10 mm) in precordial leads V2–V5 — especially in apical HCM (Yamaguchi syndrome)
• LV strain pattern: ST depression + T-wave inversion in lateral leads
• Left axis deviation
• P-wave abnormality (left atrial enlargement): bifid P wave (P mitrale) or P >120 ms
• ECG is abnormal in 90–95% of HCM patients

Quick Reference Summary

Clinical pearl: Always interpret the ECG in the context of clinical history, symptoms, and hemodynamic status. ECG changes can overlap between conditions, and serial ECGs often provide more diagnostic value than a single tracing.