ECG changes in hypercalcemia: Mechanism

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ECG changes in hypercalcemia: Mechanism

ECG changes in hypercalcemia: ST segment shortens when the serum calcium or specifically the level of ionized calcium rises. This leads to shortening of the QT interval in hypercalcemia. In severe hypercalcemia, the shortening of ST segment is so much that it appears to be almost absent and T wave starts almost at the end of QRS complex. Calcium channels act mainly in the phase 2 of the myocardial action potential. Hence the effect of hypercalcemia is confined to the ST segment with very little effect on the T wave which is during phase 3 of cardiac action potential and therefore dependant on movements of potassium ions.

It may be noted that about 50% of serum calcium is bound to serum proteins and it is the unbound or ionized calcium which determines the physiological effects of hypercalcemia and hence the ECG changes. For the same reason, changes in blood pH can alter the physiological effect of hypercalcemia. Alkalosis reduces the level of ionized calcium and acidosis increases the level of ionized calcium due to reciprocal changes in protein binding.

Rare cases of ST segment elevation mimicking acute myocardial infarction has been reported along with hypercalcemia and resolving after control of hypercalcemia.1,2 Since the QT interval is shortened in hypercalcemia, initial upslope of the T wave which starts immediately after the QRS complex mimics the hyperacute phase of acute myocardial infarction, especially if the T waves are a bit taller than usual.


  1. Nishi SP, Barbagelata NA, Atar S, Birnbaum Y, Tuero E. Hypercalcemia-induced ST-segment elevation mimicking acute myocardial infarction. Journal of Electrocardiology. 2006;39:298-300.
  2. Donovan J, Jackson M. Hypercalcaemia Mimicking STEMI on Electrocardiography. Case Rep Med. 2010; 2010: 563572.

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