A Systematic Approach
Rate, rhythm, axis, intervals, chambers, ischemia — in that order, every time.
Why Ischemia Changes the ECG
Myocardial ischemia alters the transmembrane action potential, shortening its duration and reducing resting membrane potential in the affected zone, which creates a voltage gradient (an "injury current") between ischemic and normal myocardium. Subendocardial ischemia generates a current vector directed away from the overlying epicardial leads, producing ST depression, while transmural injury shifts the vector toward those leads, producing ST elevation. Because the subendocardium is the last layer perfused and the first to become ischemic, ST depression is the more common early pattern, whereas ST elevation implies more severe, transmural injury requiring urgent reperfusion.
The 6-Step Framework
Every ECG deserves the same disciplined walk-through: (1) rate, (2) rhythm, (3) axis, (4) intervals (PR, QRS, QT/QTc), (5) chamber enlargement, (6) ischemia/infarction. Force yourself through all six even when the diagnosis appears obvious — the "obvious" STEMI hides a concurrent complete heart block often enough that you cannot afford to skip.Rate
At paper speed 25 mm/s, rate = 300 / (large boxes between R-R). For irregular rhythms, count QRS complexes over a 6-second strip and multiply by 10.
Rhythm
P before every QRS, QRS after every P, P upright in II with normal morphology → sinus. Irregularly irregular narrow-complex without organized P waves is atrial fibrillation until proven otherwise.
Axis
Normal: positive I and II. Left axis: positive I, negative II (LAFB, inferior MI, LVH). Right axis: negative I, positive II (RVH, LPFB, lateral MI, PE). Extreme axis: nearly always pathologic — hyperkalemia, VT, pacing.
Intervals
PR 120–200 ms. QRS <120 ms. QTc <450 ms (men) / <460 ms (women); >500 ms is a torsades risk.
Ischemia and Infarction
ST elevation is localizing: II/III/aVF inferior, V1–V4 anterior, V5/V6/I/aVL lateral, V7–V9 posterior. Reciprocal depression strengthens the diagnosis.
Common Pitfalls
Misplaced limb leads mimic infarct or axis deviation — a flat lead I with a normal-looking aVR is a clue to arm-lead reversal. Always read the rhythm strip before the 12-lead: a regular narrow complex at 150 bpm is atrial flutter with 2:1 block until proven otherwise.
STEMI-Equivalent Patterns: Wellens and De Winter
Some patterns look nothing like a classic ST-elevation MI but represent the same critical proximal LAD occlusion and should trigger the same urgency. Wellens' syndrome: deeply inverted or biphasic T waves confined to V2-V3 (sometimes extending to V1-V6) in a patient who is currently pain-free with normal or minimally elevated troponin — this is the ECG's memory of a recent critical LAD stenosis, and stress testing this pattern can precipitate an extensive anterior MI. De Winter T waves, seen in roughly 2% of acute LAD occlusions, show upsloping ST depression at the J point continuing into a tall, symmetric T wave in the precordial leads, without the ST elevation a clinician instinctively looks for — treat it as a STEMI equivalent requiring emergent reperfusion, not as NSTEMI.Clinical pearls
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Wellens' syndrome (biphasic or deeply inverted T waves V2–V3 in a pain-free patient) is a critical LAD lesion — do not stress test.
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De Winter T waves (upsloping ST depression with tall symmetric T waves in precordials) are a proximal LAD occlusion equivalent.
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Do not diagnose LVH by voltage alone in patients under 35 — thin chest walls generate misleading voltages.
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Isolated ST depression in V1-V3 with tall R waves and upright T waves should prompt posterior lead placement (V7-V9) to rule out posterior STEMI.
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Diffuse ST depression with ST elevation in aVR suggests left main or severe triple-vessel disease.
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A normal ECG does not exclude ACS; serial ECGs and troponins are warranted when clinical suspicion remains high.