5 Ischemia, Infarction, and ECG Mimics

Learn how to recognize ischemia and possible acute coronary occlusion on ECG, distinguish infarction from ischemia, identify important mimics, and understand risk-based emergency assessment.

Interpret the ECG in clinical context

In suspected acute coronary syndrome (ACS), interpret the ECG together with symptoms, examination, prior tracings, and the clinical course. Obtain and interpret a 12-lead ECG within 1010 minutes of first medical contact. If the first tracing is nondiagnostic but suspicion remains, repeat ECGs, especially during persistent or recurrent symptoms, and consider additional leads. A normal or nonspecific ECG does not exclude ACS.

means inadequate myocardial blood flow and may produce dynamic ST-segment or T-wave changes. is myocardial injury due to ; establish it by integrating clinical evidence with a rise or fall in cardiac troponin. ECG findings can support the diagnosis but do not establish by themselves.

is an initial working diagnosis that identifies patients who may need immediate reperfusion. Not every patient with a -pattern ECG ultimately has an , and acute coronary occlusion can occur without meeting classic thresholds.

Recognize acute ischemic patterns

First check tracing quality, calibration, rate, and rhythm, and compare with prior ECGs when available. Then assess for new or dynamic changes in anatomically , which view neighboring regions of the heart. Interpret ST elevation, ST depression, and T-wave changes in the context of symptoms and reciprocal changes.

For adults with suspected ACS, conventional ST-elevation criteria are new J-point elevation in at least two :

  • At least 1 mm1\,\text{mm} in leads other than V2–V3.

  • In V2–V3, at least 2 mm2\,\text{mm} in men aged 4040 or older, 2.5 mm2.5\,\text{mm} in men younger than 4040, or 1.5 mm1.5\,\text{mm} in women.

These thresholds support recognition but do not replace clinical judgment. An ECG that falls short of the thresholds may still show dangerous occlusion.

Other ischemic patterns include new horizontal or downsloping ST depression and significant T-wave inversion in . ST depression in V1–V3, particularly with upright terminal T waves, may be the mirror image of posterior injury rather than simply anterior .

A consists of deep, symmetric T-wave inversion or biphasic T waves in V2–V3 during a pain-free interval. It is associated with critical LAD disease; avoid exercise stress testing and seek urgent specialist assessment.

Identify occlusion patterns without classic elevation

Some patterns can indicate acute coronary occlusion even without classic ST elevation. The label “ equivalent” is not a substitute for clinical assessment because guideline and clinical usage vary. Recognize possible occlusion patterns and seek urgent expert assessment and consideration of a reperfusion pathway.

  • : ST depression in V1–V3 may be reciprocal change. If suspicion persists, obtain posterior leads V7–V9; ST elevation in these leads supports posterior injury.

  • Right-ventricular : In suspected inferior , obtain right-sided leads, especially V3R–V4R. Elevation may indicate right-ventricular involvement.

  • De Winter pattern: Upsloping ST depression at the J point across the precordial leads with tall, symmetric T waves can indicate acute LAD occlusion.

  • LBBB or ventricular pacing: These patterns make ordinary ST-elevation interpretation difficult. Apply validated or modified and integrate symptoms and hemodynamic status. New LBBB alone is not diagnostic of MI.

  • Diffuse ST depression with ST elevation in aVR and/or V1: This can signal extensive subendocardial , including multivessel or left-main disease, especially in an unstable patient; it is not specific to one culprit artery.

Persistent ischemic symptoms or instability can justify urgent escalation even when the standard 12-lead ECG is equivocal.

Consider without dismissing risk

ST elevation is not specific to acute coronary occlusion. Consider the whole pattern, symptoms, prior ECGs, serial tracings, and bedside assessment; no single visual clue safely rules ACS in or out. include several distinct patterns and conditions:

  • Early repolarization: Often stable on prior ECGs and commonly seen in younger, well patients. A stable tracing does not exclude new ACS when symptoms are concerning.

  • Acute pericarditis: Often has widespread, relatively concave ST elevation with PR depression and typically lacks a single coronary-territory pattern. Clinical features matter.

  • LVH or bundle-branch block: Secondary ST–T changes may be discordant with the main QRS direction and obscure . Compare with prior ECGs and use appropriate criteria.

  • Brugada pattern: Characteristic right-precordial ST elevation, typically in V1–V3; assess for its characteristic morphology and clinical context.

  • Takotsubo syndrome: Can resemble ACS clinically and on ECG. ECG alone cannot reliably distinguish it from coronary occlusion.

Other conditions, including electrolyte abnormalities and myocarditis, may also alter ST segments or T waves. A suspected mimic should not delay emergency evaluation when acute coronary occlusion remains plausible.

Act on risk and escalate appropriately

Treatment decisions should reflect the overall risk rather than one tracing. These are emergency-care principles, not a substitute for clinician assessment; ACS care should follow current institutional pathways and be directed by qualified clinicians.

  1. Possible ACS: Obtain and interpret an ECG promptly, assess stability, and arrange urgent emergency evaluation. Repeat ECGs when symptoms persist, recur, or worsen; add posterior or right-sided leads when indicated.

  2. pattern or convincing occlusion pattern: Activate the local or reperfusion pathway and arrange immediate emergency cardiology care. Primary PCI is preferred when it can be delivered promptly. If timely PCI is unavailable, clinicians should assess fibrinolysis eligibility and follow established regional protocols. Do not wait for troponin results when the ECG and clinical picture call for immediate reperfusion.

  3. No persistent ST elevation but suspected NSTE-ACS: Use serial ECGs and cardiac troponin testing with clinical risk assessment. Dynamic ischemic changes, confirmed MI, or instability warrant urgent specialist evaluation and an invasive strategy according to risk and local protocols.

  4. Possible mimic: Reassess rather than dismiss. If symptoms, instability, or evolving ECG changes leave meaningful concern for coronary occlusion, seek urgent expert review.

The central principle is to read ECG findings in clinical context, compare prior and serial tracings, and recognize that may be dynamic or anatomically hidden. Classic ST-elevation thresholds are useful but do not capture every acute occlusion. Posterior, right-ventricular, de Winter, and selected conduction-pattern presentations deserve urgent attention; neither an apparent mimic nor a nondiagnostic ECG safely excludes ACS.