ReviewAnnals of cardiac anaesthesia2026
Electrophysiological Mechanisms of ST Segment and T-Wave Changes: Insights into Ischemia, Conduction Delay, Hypertrophy, and Electrolyte Disturbance.
Review in Annals of cardiac anaesthesia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
abstractST-T abnormalities are commonly encountered in cardiology, cardiac surgical, critical care, and emergency settings. ST segment depression refers to displacement of the ST segment below the PR-segment (baseline), whereas ST segment elevation refers to displacement above this baseline. A downward displacement greater than 0.5 mm below the baseline or an upward displacement exceeding 0.1 mV in the limb leads or 0.2 mV in the precordial leads, measured 40 ms after the J point relative to the baseline, is considered significant. ST-T abnormalities can be primary or secondary. Primary ST-T changes are repolarization abnormalities seen in myocardial ischemia, electrolyte disturbances, tachycardia, increased sympathetic activity, and adverse drug effects. Secondary ST-T changes are activation (depolarization) abnormalities observed with bundle branch block, left ventricular hypertrophy, pre-excitation, ventricular ectopics, and pacemaker-stimulated complexes. Primary ST-T abnormalities due to acute myocardial ischemia, evolving myocardial infarction, and hyperkalemia represent life-threatening emergencies and require urgent medical intervention. Secondary ST-T abnormalities signal underlying structural or conduction disease and warrant evaluation and management. Cardiac anesthesiologists, cardiologists, and emergency physicians are frequently involved in the care of patients presenting with such cardiac emergencies. It is crucial to distinguish ST-T abnormalities caused by acute myocardial ischemia, evolving myocardial infarction, and hyperkalemia from those due to other conditions, as timely recognition and treatment can be lifesaving. This narrative review describes the electrophysiological basis of ST-T changes in various clinical contexts and outlines how to differentiate acute myocardial ischemia and hyperkalemia from other causes of ST-T abnormalities.
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