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ECG in Myocardial Infarction
Pathophysiology of ECG Changes
Acute ischemia lowers the resting membrane potential and shortens action potential duration in affected myocardium. This creates a voltage gradient between normal and ischemic zones, generating "currents of injury" that manifest as ST-segment deviations on the surface ECG.
Fig A: Subendocardial ischemia - ST vector points inward -> overlying leads show ST depression. Fig B: Transmural (epicardial) ischemia - ST vector points outward -> overlying leads show ST elevation.
Sequential ECG Changes in STEMI
MI evolves through a predictable ECG sequence:
| Stage | Timing | ECG Finding |
|---|
| Hyperacute | Minutes | Tall, broad ("hyperacute") T waves |
| Acute injury | Hours | ST-segment elevation; T wave may still be upright |
| Evolving | Hours to days | T-wave inversion in same leads; Q waves appear |
| Old/chronic | Weeks to months | Persistent Q waves; ST may normalize; T waves may normalize or remain inverted |
Anterior STEMI - Acute and Evolving
Top row: Acute phase with ST elevations in anterior leads and reciprocal ST depressions inferiorly. Bottom row: Evolving phase with Q waves and T-wave inversions developing.
Inferior STEMI - Acute and Evolving
Top row: Acute inferior STEMI with ST elevation in inferior leads. Bottom row: Evolving changes with Q waves in inferior leads and ST depressions in anterior precordial leads (reciprocal changes).
Localization by Lead Distribution
(From Tintinalli's Emergency Medicine)
| Territory | Leads with ST Elevation | Artery Usually Involved |
|---|
| Anteroseptal | V1, V2, (V3) | LAD (proximal) |
| Anterior | V1-V4 | LAD |
| Anterolateral | V1-V6, I, aVL | LAD or LCx |
| Lateral | I, aVL | LCx or diagonal |
| Inferior | II, III, aVF | RCA (80%) or LCx |
| Inferolateral | II, III, aVF, V5, V6 | RCA + LCx |
| True posterior | Tall R in V1-V2, R/S ≥1, ST depression V1-V3 (reciprocal) | LCx or RCA-PL |
| Right ventricular | II, III, aVF + ST elevation in V3R-V6R | Proximal RCA |
Tip: Inferior STEMI (II, III, aVF) always mandates right-sided ECG leads to detect concurrent RV infarction, which is present in ~40% of inferior MIs. ST elevation in V4R is the most sensitive sign.
Reciprocal Changes
Reciprocal ST depressions are mirror-image changes seen in leads electrically opposite to the infarct zone. They strongly support the diagnosis of true STEMI:
- Anterior STEMI: reciprocal ST depression in II, III, aVF
- Inferior STEMI: reciprocal ST depression in I, aVL, and often V1-V3
- Posterior STEMI: no direct ST elevation in standard leads - the entire picture IS the reciprocal: ST depression + tall R in V1-V2 (flip V1-V3 upside down to see the "elevation")
Q Waves
Pathological Q waves indicate myocardial necrosis and loss of depolarization forces:
- Width ≥ 0.04 s (1 mm) and depth ≥ 25% of the following R wave
- Previously thought to indicate transmural infarction exclusively - this is no longer considered accurate; Q waves can occur with subendocardial infarcts and may be absent in transmural infarcts
- May persist permanently or regress over months in some patients
Wellens Syndrome (High-Risk NSTEMI Pattern)
Deep, symmetric T-wave inversions in V1-V4 (sometimes V1-V6, I, aVL) indicate critical LAD stenosis even without current ST elevation. This is a pre-infarction warning.
Deep symmetric T-wave inversions across precordial leads - the Wellens T-wave sign, typically indicating high-grade LAD stenosis.
STEMI Diagnostic Criteria (Standard Thresholds)
- New ST elevation at the J-point in ≥2 contiguous leads:
- ≥ 2.5 mm in men <40 years in V2-V3; ≥ 2.0 mm in men ≥40 years; ≥ 1.5 mm in women in V2-V3
- ≥ 1 mm in all other leads
- New LBBB with typical ischemic symptoms is treated as STEMI equivalent
- Sgarbossa criteria help identify MI in the presence of LBBB:
- Concordant ST elevation ≥1 mm in leads with positive QRS (5 points)
- Concordant ST depression ≥1 mm in V1-V3 (3 points)
- Discordant ST elevation ≥5 mm (2 points); modified: use ST/S ratio >0.25
NSTEMI / Ischemia ECG Changes
- ST depression (horizontal or downsloping) ≥0.5 mm in ≥2 contiguous leads
- T-wave inversion ≥1 mm (symmetric, in leads with dominant R waves)
- Transient ST changes (≥0.5 mm) during symptoms are highly specific
- A normal ECG does not exclude NSTEMI - serial ECGs and troponins are required
Emerging Concept: OMI Paradigm
Recent literature (2024-2025) highlights the Occlusion MI (OMI) framework, which recognizes that the traditional STEMI/NSTEMI binary misses ~25-40% of patients with acute coronary occlusion who lack classic ST elevation. The OMI model incorporates:
- De Winter T-waves: upsloping ST depression with tall, symmetric T waves in V1-V4 (LAD occlusion without ST elevation)
- Hyperacute T-waves: broad, bulky, asymmetric T waves as the earliest sign
- Posterior MI patterns: ST depression in V1-V3 as the only finding
- Wellens patterns: as described above
ECG Limitations
- A single normal ECG does not exclude MI - repeat every 15-30 minutes if initial is non-diagnostic
- LBBB, pacemaker rhythm, WPW can mask ischemic changes
- Many conditions mimic MI: pericarditis, early repolarization, LVH, Brugada pattern, hyperkalemia, myocarditis, takotsubo cardiomyopathy
Sources: Harrison's Principles of Internal Medicine 22E (2025), Tintinalli's Emergency Medicine (9th Ed)