ECG Changes in Myocardial Infarction (STEMI & NSTEMI)

1. Pathophysiological Basis

2. Temporal Evolution of ECG Changes in STEMI

Phase 1 - Hyperacute T Waves (minutes)

• Tall, broad, peaked T waves appear over the ischemic zone
• This is the earliest ECG change, often missed as it is brief
• Due to rapid repolarization from K+ efflux

Phase 2 - ST Elevation (minutes to hours)

• ST segment becomes elevated (convex upward/coved) in leads overlying the infarct
• This is the diagnostic hallmark of STEMI
• Reciprocal ST depression appears in leads opposite the infarct, indicating subendocardial ischemia and predicts larger area of injury, greater severity of CAD, and higher mortality (Tintinalli's)

Phase 3 - Q Wave Formation (hours to days)

• Pathological Q waves develop as necrotic tissue becomes electrically silent
• Q wave is pathological when: width >40 ms (0.04 s) OR depth >25% of the QRS amplitude
• Non-Q-wave infarcts also occur (tend to be less severe but carry high risk of reinfarction)

Phase 4 - T Wave Inversion (hours to days)

• ST segment begins to normalize
• T waves invert symmetrically in the same leads as the prior ST elevation
• Deep T-wave inversions in V1-V4 with or without enzyme elevation suggest severe LAD obstruction ("Wellens T-wave sign")

Phase 5 - Resolution / Chronic Changes (weeks to months)

• ST segments return to baseline
• T waves may normalize or remain inverted
• Q waves may persist permanently as markers of old infarction (though may shrink)
• Failure of R-wave progression in precordial leads can be a late finding of anterior MI

3. STEMI Localization by Leads

Culprit Artery Clues (Tintinalli's, Table 49-5):

• ST elevation in III > II + ST depression in I/aVL = RCA occlusion (Sens 90%, Spec 71%)
• ST elevation in V1 or V4R with inferior STEMI = proximal RCA with RV infarction (Spec 100%)
• Inferior STEMI + ST elevation in lateral leads (V5/V6/aVL) with isoelectric/elevated ST in I = LCx occlusion
• ST elevation aVR > V1 = left main or proximal LAD occlusion

4. NSTEMI / Unstable Angina ECG Changes

• ST depression (horizontal or downsloping) in multiple leads
• T-wave inversion (symmetric, deep)
• ECG may be normal in ~25% of NSTEMI cases - diagnosis then depends on troponin elevation
• No pathological Q waves initially
• The key distinction: NSTEMI = elevated biomarkers without STEMI criteria; UA = no biomarker elevation

5. Special ECG Situations

Posterior MI

• No direct ST elevation in standard leads
• Diagnosed by reciprocal changes in V1-V3: ST depression + tall upright R waves + upright T waves
• Confirmed with posterior leads (V7-V9) showing ST elevation >0.5 mm

Right Ventricular MI

• Always occurs with inferior STEMI (proximal RCA occlusion)
• ST elevation in V4R (right-sided lead) is the most sensitive finding
• Clinically important: these patients are preload-dependent - nitrates and diuretics are contraindicated

LBBB and MI

• New LBBB can mask MI (and was formerly treated as STEMI equivalent)
• Sgarbossa criteria help diagnose MI in LBBB:
  • Concordant ST elevation ≥1 mm (in leads with positive QRS)
  • Concordant ST depression ≥1 mm in V1-V3
  • Discordant ST elevation ≥5 mm (excessively discordant)

Wellens Syndrome

• Deep symmetric T-wave inversions in V2-V3 (Type A: biphasic; Type B: deeply inverted)
• Indicates critical proximal LAD stenosis
• ECG changes occur during pain-free period; patient at high risk of anterior STEMI

6. Summary Table