ECG changes in hypocalcemia – Mechanism

ECG changes in hypocalcemia – Mechanism

Prolongation of ST segment contributing to prolonged QT interval and corrected QT interval is the hallmark ECG change in hypocalcemia. Hypocalcemia prolongs phase 2 of the myocardial action potential, thereby prolonging the ST segment. T waves are not generally affected in hypocalcemia because phase 3 of the myocardial action potential is not affected by calcium ions. Calcium channels close at the end of phase 2, with phase 3 being mostly related to potassium channel activity.

Cases are on record in which severe hypocalcemia has mimicked ST elevation myocardial infarction in the emergency department. Coronary angiography showed patent coronary arteries and ECG changes reverted after correction of hypocalcemia with calcium supplementation.1

Associated electrolyte abnormalities can alter the ECG findings of hypocalcemia as occurs in renal failure, in which hypocalcemia is often associated with hyperkalemia. Yet intravenous calcium which is often given for treatment of hyperkalemia in acute renal failure is useful in treatment of associated hypocalcemia as well.

It may be noted that half of the serum calcium is bound to plasma proteins, of which 80% is bound to albumin. 5 to 10% of the calcium is bound to plasma anions like phosphates and citrates. Only about half of the calcium is in the ionized form with physiological activity. Ionized calcium can be reduced in alkalosis as alkalosis enhances calcium binding to albumin.

Reference

  1. Ilveskoski E, Sclarovsky S, Nikus K. Severe hypocalcemia simulating ST-elevation myocardial infarction. Am J Emerg Med. 2012;30:256.e3-6.