Electrolyte changes and the electrocardiogram in diabetic acidosis

Abstract

Correlation of electrolyte and pH changes with serial electrocardiographic changes was made in thirteen patients during therapy for severe diabetic acidosis. Sagging of the S-T segments was a prominent feature of the electrocardiogram on entry when acidosis was marked. This change usually disappeared within twenty-four hours. In nineteen instances of depressed S-T segment, the pH or carbon dioxide combining power was low in sixteen (84 per cent). However, in 31 per cent of the patients whose records showed isoelectric S-T segments, the pH or Carbon dioxide combining power was low. Experimentally, depression of the S-T segment occurs with moderate elevation of the serum potassium but there was no correlation in our series with changes in serum potassium levels. The etiology of this change requires further study. Thirty-seven records showed prolonged Q-T intervals, many of these occurring one to four days after intensive therapy had been instituted. Sixteen (43 per cent) of these were associated with low total or ionized serum calcium or potassium. Twenty-one (57 per cent) of the patients whose records showed prolonged Q-T intervals had normal levels of serum calcium and potassium. There were seven patients in whom the Q-T interval was markedly prolonged; in six of these the serum calcium or potassium levels were below normal. These findings suggest that in some cases other factors than serum calcium and potassium depletion may be responsible for the prolongation of the Q-T interval. There was a high degree of correlation between low T waves and low serum potassium levels. The T waves increased in amplitude with return of the potassium to normal or elevated levels. The relationship of low serum magnesium to the electrocardiographic changes needs additional study. The complex nature of the factors present in diabetic acidosis which may affect the myocardium is discussed. These factors include the relationship between extracellular and intracellular electrolytes, cardiac nutrition in acidosis and ketosis, and the effects of anoxia and azotemia.