Myocardial infarction: the ECG, the wall and the culprit artery

1. How the twelve leads look at the heart

Each lead is a viewpoint. II, III and aVF look up at the inferior wall; I, aVL, V5 and V6 at the lateral wall; V1 and V2 at the septum; V3 and V4 at the anterior wall; aVR looks into the cavity from the right shoulder. Tap a lead or a colour on the ECG: the wall it faces lights up on the heart.

Surgeon’s corner: STEMI: new ST elevation at the J point in two contiguous leads, ≥ 1 mm — in V2–V3 ≥ 2 mm in men from 40, ≥ 2.5 mm in younger men, ≥ 1.5 mm in women (not valid with LVH or left bundle branch block). With ongoing ischaemic symptoms, bundle branch block, a paced rhythm, posterior and de Winter patterns are treated like STEMI. Within 12 h of onset: primary PCI if it can be done within 120 min of the diagnosis; otherwise fibrinolysis within 10 min, then transfer.

2. Anterior STEMI: the LAD

ST elevation from V1 to V4 (often to V6) is the anterior wall: the LAD. Elevation in I and aVL as well means a proximal occlusion, before the first diagonal; the ST depression in II, III and aVF is the mirror image. The larger the territory — septum, anterior wall, apex — the higher the risk of heart failure, ventricular septal rupture and apical thrombus.

Surgeon’s corner: Before the ST rises, the first sign can be tall, broad, "hyperacute" T waves in V2–V4. De Winter pattern (upsloping ST depression with tall T waves in V1–V6) is also an LAD occlusion: treat it as a STEMI.

3. Lateral STEMI: circumflex or diagonal

ST elevation in I, aVL, V5 and V6 is the lateral wall: the circumflex (its obtuse marginal branches) or a diagonal of the LAD. Reciprocal ST depression in III and aVF. A high lateral infarct (I and aVL only) is easy to miss: the elevation can be small, and the inferior ST depression is often the clue.

Surgeon’s corner: The circumflex is the "electrically silent" artery: many circumflex occlusions show no clear ST elevation on the standard twelve leads. Refractory pain or instability needs an immediate invasive strategy (< 2 h) even without STEMI criteria — and V7–V9 can reveal the occlusion.

4. Inferior STEMI: right coronary or circumflex?

ST elevation in II, III and aVF is the inferior wall. It is the right coronary artery in about 80%: ST elevation larger in III than in II, with ST depression in I and aVL. A circumflex culprit tends to give II ≥ III, an isoelectric or raised lead I (with less aVL depression), and often ST elevation in V5–V6 or ST depression in V1–V3.

Surgeon’s corner: In every inferior STEMI ask two questions: is the right ventricle involved (record V4R) and is there posterior extension (ST depression in V1–V3)? Watch for bradycardia and AV block.

5. Right ventricular infarction: record V4R

An occlusion of the right coronary artery before its acute marginal branches infarcts the right ventricle too: ST elevation ≥ 0.5 mm in V3R and V4R (≥ 1 mm in men under 30; V4R is the V4 position on the right side of the chest). ST elevation in V1 with an isoelectric or depressed V2 is a clue. At the bedside: low blood pressure, distended neck veins and clear lungs.

Surgeon’s corner: The infarcted right ventricle lives on preload: avoid nitrates, morphine and diuretics, give fluid carefully and reperfuse fast. The V4R elevation fades within hours — record it at once.

6. Posterior STEMI: look from behind

The basal inferolateral wall (the old "posterior" wall) has no lead facing it. Its infarction shows as a mirror image in V1–V3 (often to V4): horizontal ST depression with upright T waves; tall, broad R waves appear later, as the equivalent of Q waves. Put V7–V9 on the back at the level of V6 (posterior axillary line, tip of the scapula, beside the spine): ST elevation ≥ 0.5 mm (≥ 1 mm in men under 40) confirms it.

Surgeon’s corner: ST depression maximal in V1–V3 (or V4) with upright T waves is a posterior STEMI until proven otherwise: emergency reperfusion, not the NSTEMI pathway.

7. aVR up, everything else down

ST elevation in aVR (often in V1 too) with ST depression ≥ 1 mm in eight or more leads means diffuse subendocardial ischaemia: left main stem or proximal LAD stenosis, or three-vessel disease — or severe ischaemia from another cause such as shock, anaemia or a fast arrhythmia.

Surgeon’s corner: This is not a STEMI in itself; with haemodynamic instability or refractory pain, go to immediate angiography. Many of these patients need bypass surgery rather than stents.

8. After the infarction: Q waves

Hours to days later, Q waves appear (the dead wall no longer depolarises, so the lead looks through it into the cavity), the R waves shrink, the ST segment comes back down and the T waves invert. ST elevation that persists for weeks suggests a left ventricular aneurysm.

Surgeon’s corner: Pathological Q waves: any Q > 0.02 s (or QS) in V2–V3, or Q ≥ 0.03 s and ≥ 1 mm deep (or QS) in two contiguous leads among I, II, aVL, aVF and V4–V6. A small Q in III or aVR alone is normal. Poor R-wave progression from V1 to V4 can be the only trace of an old anterior infarction.

9. Wellens: the warning before the infarct

Deep symmetrical (or biphasic) T inversion in V2–V3, recorded when the pain has gone, with little or no ST elevation, preserved R waves, no pathological Q waves and a normal or only mildly raised troponin: a critical proximal LAD stenosis that has opened again. Untreated, many of these patients have a large anterior infarction within days to weeks.

Surgeon’s corner: Never send a Wellens patient to an exercise test: it can trigger the infarction. Admit, treat as high-risk acute coronary syndrome and arrange early angiography.

10. Mechanical complications: the wall gives way

In the first week after a large infarction, before the scar is firm (free-wall rupture also within the first 24 hours), the softened wall can rupture: the free wall (tamponade, sudden loss of output), the septum (ventricular septal defect: new loud systolic murmur and shock) or a papillary muscle (acute mitral regurgitation, pulmonary oedema). Late reperfusion and a first, large infarction raise the risk.

Surgeon’s corner: Any sudden deterioration after an infarction: bedside echo at once. All three usually need surgery. Free wall: pericardiocentesis or mechanical support as a bridge to emergency surgery. Septal rupture: mechanical circulatory support, then surgery (or percutaneous closure in selected patients). Papillary muscle: urgent surgery, or edge-to-edge repair in selected inoperable patients.