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The ECG in ischemia and infarction !

  • Measurement
  • Exam priority: medium

When heart muscle runs short of blood, the ST segment, T wave and Q wave change, and point to the wall and the artery involved.

Updated 2026-11-01

See it in 3D: LAD (anterior descending artery) · Right coronary artery · Circumflex artery · Left main coronary artery

What it is

Ischemia changes the resting potential and repolarization of the affected cells, and an injury current flows between healthy and injured tissue that shifts the ST segment. Subendocardial ischemia depresses the ST; transmural injury raises it in the leads facing the area. Necrosis leaves Q waves because that tissue no longer generates electrical forces.

How it works, step by step

  1. Without oxygen the Na⁺/K⁺-ATPase fails and K⁺ leaks out: ischemic cells sit less negative at rest.
  2. Their action potentials shorten and shrink: injured and healthy tissue end up at different voltages.
  3. An injury current flows between them; the ECG records it as a shift of the ST segment.
  4. If the injury is subendocardial, the vector points inward and the ST drops in the leads facing that wall.
  5. If the injury is transmural, the vector points toward the electrode and the ST rises; opposite leads show reciprocal depression.
  6. Necrotic tissue is electrically silent: the electrode looks through it into the cavity and records a Q wave.

Electrocardiogram: a normal beat in lead II

Electrocardiogram: a normal beat in lead II: 75 /min Lead II · 25 mm/s · 10 mm/mVPRQSTUPRSTQRSQTRhythm strip · 75 /minRR 0.80 s = 4 big boxes → 300 / 4 = 75 /min

HR 75 /minRR 0.80 sPR 0.16 sQRS 0.09 sQT 0.37 sQTc 0.41 s

Tap a wave (P, QRS, T, U), an interval (PR, ST, QT) or the RR.

  • ECG trace (lead II)
  • Small box: 0.04 s · 0.1 mV
  • Big box: 0.20 s · 0.5 mV
  • Selected part
Illustrative trace drawn by Durgical from smoothed waves (not a real recording); durations and amplitudes are approximate. Not for reading a clinical ECG.

Useful cutoffs

ParameterValueNote
ST elevation, most leads≥1 mm (0.1 mV)in two contiguous leads
ST elevation in V2–V3≥2 mm men ≥40 years; ≥1.5 mm womenJ point
Pathological Q wave≥0.04 s wide or ≥25% of the Rapprox.
TroponinAbove the lab's 99th percentilewith a rise or fall

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

Wall, leads and artery

WallLeadsUsual artery
Anteroseptal and anteriorV1–V4Left anterior descending
LateralI, aVL, V5–V6Circumflex or diagonal
InferiorII, III, aVFRight coronary (sometimes circumflex)
PosteriorST depression and tall R in V1–V3Right coronary or circumflex
Right ventricleV4RProximal right coronary

Clinical notes

  • Inferior MI with right ventricular involvement is preload-dependent: vasodilators can cause marked hypotension.
  • ST depression during an exercise test reflects inducible subendocardial ischemia (stable angina).
  • A new left bundle branch block can hide ST changes and is read with its own criteria.

Test yourself

Think of the answer, then tap the question to see it.

Why does subendocardial ischemia depress the ST while transmural injury raises it?

The injury current points toward the damaged zone: subendocardial injury points away from the surface electrode (ST down); transmural injury points toward it (ST up).

A patient has ST elevation in II, III and aVF. Which artery is suspected and which extra lead should you check?

The right coronary in most cases; V4R to look for right ventricular infarction.

What explains the Q wave of an infarct?

Necrotic myocardium generates no electrical force; the electrode "sees" through it the depolarization moving away in the opposite wall and records an initial negative deflection.

How do you tell acute pericarditis from ST-elevation MI on the ECG?

Pericarditis gives diffuse, concave elevation with PR depression and no reciprocal depression; MI follows one arterial territory and has reciprocal changes.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: Myocardial Infarction (StatPearls (NCBI Bookshelf), 2024); Stable Angina (StatPearls (NCBI Bookshelf), 2026); Pericarditis (StatPearls (NCBI Bookshelf), 2026); 19.2 Cardiac Muscle and Electrical Activity (OpenStax (Rice University), 2022); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 12). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.