ECG in Ischaemia and Infarction
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Direct answer
ST-segment shift is the ECG's ischaemia alarm, and its direction encodes depth: elevation means full-thickness (transmural) injury from an occluded artery, while horizontal or downsloping depression of at least 1 mm means subendocardial ischaemia. Localisation follows lead groups — II, III and aVF watch the inferior wall (usually the right coronary artery), V1-V4 the anteroseptal wall (left anterior descending), I, aVL and V5-V6 the lateral wall (circumflex), and isolated ST depression in V1-V3 actually faces a posterior infarction, so V7-V9 and V4R complete the picture. Q waves thicker than 40 ms in two contiguous leads declare completed infarction, and the sequence — hyperacute T waves, then ST elevation, then Q waves, then T inversion — timestamps the event for the reporting technologist.
What you must remember
- Lead-artery map: inferior II, III, aVF (RCA in about 80 per cent); anteroseptal V1-V4 (LAD); lateral I, aVL, V5-V6 (circumflex); right ventricle V4R; posterior V7-V9 (ST elevation 0.5 mm or more is diagnostic there).
- Reciprocal changes: ST depression in leads facing the injured wall from opposite sides (I and aVL mirror the inferior wall) — their presence raises specificity for true STEMI.
- Evolution clock: hyperacute peaked T waves first, ST elevation within minutes, Q waves typically by 6-14 hours, T-wave inversion over the first day or two; persistent ST elevation weeks later suggests aneurysm.
- ST depression grammar: horizontal or downsloping of 1 mm or more, measured 60-80 ms after the J point, is significant; upsloping depression is weaker evidence.
- Right ventricular infarct: ST elevation in V4R with an inferior STEMI; nitrates and diuretics can crash preload-dependent filling — fluid is the treatment, and the technologist who flags V4R changes early changes management.
- Posterior infarct disguise: tall R waves with upright T waves and ST depression in V1-V3 are the mirror image; the diagnosis is made in V7-V9, not dismissed.
- Two named patterns worth quoting: Wellens syndrome (deep inverted or biphasic T waves in V2-V3 in a pain-free patient with critical proximal LAD stenosis — never stress-test them) and the De Winter pattern (upsloping ST depression with tall symmetric T waves in V1-V6, equally proximal-LAD).
One inferior STEMI, read properly
A 55-year-old with 40 minutes of crushing central chest pain produces ST elevation of 3 mm in II, III and aVF with reciprocal depression of 1.5 mm in I and aVL. The technologist immediately records V4R; ST elevation there adds right ventricular involvement, which warns against nitrates. The artery is the right coronary artery in roughly four of five such cases. Half an hour later a run of Wenckebach appears — predictable, because the RCA feeds the AV node, and this block is usually atropine-responsive. Print serial 12-leads: the Q waves that appear next morning confirm full-thickness necrosis, and the deep T inversions that follow weeks later are the "age indeterminate" pattern candidates must date on paper.
Contrast this with the diabetic woman whose effort chest pain produces only 1 mm of horizontal ST depression in V5-V6 during a treadmill test: subendocardial ischaemia from a tight circumflex or LAD stenosis — a non-ST-elevation picture managed with antiplatelets, anticoagulation and risk stratification, not a thrombolytic clock.
Where the exam sets its traps
Three recycling traps. First, reciprocal depression in I and aVL during an inferior STEMI is not a second infarct — it is the mirror, and students who report "inferolateral infarction" because of it lose the mark. Second, the tall R in V1: candidates reach for right ventricular hypertrophy, but with upright T waves and ST depression in V1-V3 the answer being probed is posterior infarction, and only V7-V9 settles it. Third, timing: Q waves within the first hour do not "age" the infarct, and ST elevation that never resolves points to aneurysm or pericarditis — the diffuse saddle-shaped elevation with PR depression and no reciprocal changes being the pericarditis signature that spares the patient a thrombolytic.
Frequently asked questions
Which leads localise an inferior infarct and which artery is usually guilty?
Leads II, III and aVF, with the right coronary artery responsible in about 80 per cent of cases. Record V4R to look for right ventricular extension before nitrates or diuretics are given.
What ECG finding suggests posterior wall infarction?
ST depression with tall R waves and upright T waves in V1-V3, the mirror image of posterior ST elevation. Confirming requires posterior leads V7-V9, where 0.5 mm or more of ST elevation is diagnostic.
When do Q waves appear and what do they signify?
Pathological Q waves — 40 ms wide or deeper than a quarter of the following R wave — typically develop by 6-14 hours and represent electrically dead, transmurally infarcted myocardium. New Q waves date the event; old Q waves alone mean "age indeterminate".
Why must a patient with Wellens syndrome not undergo a stress test?
Deep inverted or biphasic T waves in V2-V3 with preserved R progression signal a critical proximal LAD stenosis with a threatened anterior wall. Stressing such a patient can precipitate occlusion and catastrophic infarction.
What distinguishes pericarditis ST elevation from STEMI?
Pericarditis gives diffuse concave saddle-shaped ST elevation with PR-segment depression, no reciprocal changes and no territorial pattern, often with a rub and pleuritic positioning. STEMI is regional, evolves towards Q waves, and shows reciprocals.