Ecg changes in mi

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ECG changes in myocardial infarction ST elevation T wave Q wave

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Here is a comprehensive overview of ECG changes in myocardial infarction (MI):

ECG Changes in Myocardial Infarction

Pathophysiological Basis

Three major membrane abnormalities underlie the ECG changes in acute MI (Ganong's Review of Medical Physiology, Table 29-3):
Defect in Infarcted CellsCurrent FlowECG Change (leads over infarct)
Rapid repolarization (accelerated K⁺ channel opening)Out of infarctST segment elevation
Decreased resting membrane potential (loss of intracellular K⁺)Into infarctTQ depression → manifests as ST elevation
Delayed depolarizationOut of infarctST segment elevation
Ischemia lowers resting membrane potential and shortens action potential duration, creating a voltage gradient between normal and ischemic zones — these "currents of injury" appear on the surface ECG as ST deviation.

Chronological Evolution of ECG Changes

1. Hyperacute Phase (Minutes — First Hour)

  • Tall, peaked (hyperacute) T waves — earliest change; broad-based, asymmetric
  • Represents the very first electrical response to acute transmural ischemia before ST elevation develops

2. Acute Phase (Hours to Days) — STEMI

  • ST segment elevation in leads overlying the infarct
    • Transmural ischemia shifts the ST vector toward the epicardial/outer layers
    • Often convex ("tombstone") or coved morphology
  • Reciprocal ST depression in leads on the opposite side of the heart
  • Q waves begin forming as myocardial necrosis sets in — electrically silent dead tissue causes loss of R-wave forces

3. Evolving Phase (Days to Weeks)

  • T-wave inversions develop in the same leads as ST elevation (as ST returns toward baseline)
  • Pathological Q waves deepen and become permanent
  • R-wave loss / poor R-wave progression in precordial leads

4. Chronic Phase (Weeks to Months)

  • Persistent Q waves (marker of old infarct)
  • ST segment typically normalizes
  • T waves may remain inverted or gradually normalize
  • Persistent ST elevation (>4–6 weeks) suggests ventricular aneurysm

Current of Injury Diagram

Current of injury: subendocardial ischemia causes ST depression; transmural/epicardial ischemia causes ST elevation
Panel A: Subendocardial ischemia → ST vector directed inward → ST depression in overlying leads. Panel B: Transmural/epicardial ischemia → ST vector directed outward → ST elevation in overlying leads. — Harrison's Principles of Internal Medicine 22E, Fig. 247-11

STEMI vs NSTEMI

FeatureSTEMINSTEMI / Unstable Angina
ST changesElevation ≥1 mm (limb leads) or ≥2 mm (precordial)Depression or no change
Q wavesOften developUsually absent
T wavesHyperacute → inversionMay show inversion
TroponinElevatedElevated (NSTEMI) / normal (UA)
Reperfusion urgencyImmediate (PCI/thrombolysis)Urgent but tiered

Localization by Lead Distribution

TerritoryCulprit ArteryLeads with ST ElevationReciprocal Changes
AnteriorLAD (proximal)V1–V4II, III, aVF
AnterolateralLAD / LCxV3–V6, I, aVLII, III, aVF
LateralLCxI, aVL, V5–V6II, III, aVF
InferiorRCA (80%) / LCx (20%)II, III, aVFI, aVL
PosteriorRCA / LCxTall R in V1–V2 (reciprocal)ST↑ in V7–V9
Right ventricularProximal RCAV1, V4R
SeptalLAD (septal branches)V1–V2

Key Specific ECG Patterns

  • Wellens T-wave sign: Deep, symmetric T-wave inversions in V1–V4 (± I, aVL) → critical LAD stenosis, high risk for anterior STEMI
  • de Winter T-waves: Upsloping ST depression with tall, symmetric T waves in precordial leads → LAD occlusion equivalent (no classic ST elevation)
  • Posterior MI: Tall broad R waves and ST depression in V1–V2 (mirror image of posterior ST elevation); confirmed with posterior leads V7–V9
  • RV MI: ST elevation in V4R (right-sided chest lead); seen with inferior STEMI; important as nitrates are contraindicated
  • Bundle branch block: New LBBB with chest pain = STEMI equivalent. Sgarbossa criteria help identify STEMI with LBBB: (1) concordant ST elevation ≥1 mm, (2) concordant ST depression ≥1 mm in V1–V3, (3) discordant ST elevation ≥5 mm

Example ECG: Inferior STEMI

Inferior STEMI with ST elevation in leads II, III, aVF and reciprocal ST depression in aVL
ST elevation in inferior leads (II, III, aVF) with reciprocal ST depression in aVL; Q waves visible in inferior leads consistent with evolving/established infarction.

Important Limitations

  • A normal ECG does not exclude MI — serial ECGs are essential
  • LBBB, ventricular pacing, and WPW may mask ischemic changes
  • ST elevation mimics: pericarditis, early repolarization, Brugada pattern, takotsubo syndrome, hyperkalemia, myocarditis
  • Q wave mimics: LVH, LBBB, hypertrophic cardiomyopathy, WPW, myocarditis

Sources: Harrison's Principles of Internal Medicine, 22E (Chap. 247); Ganong's Review of Medical Physiology, 26E (Chap. 29)
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