Electrolytic Influences on the Depolarization/Repolarization Patterns

Abstract

Normal cardiac action potentials may be influenced by electrolyte imbalance, owing to changes in intra- and extracellular electrolyte concentrations. The ECG may be a way to estimate the severity of electrolyte imbalances and to judge whether there is a possible risk for life-threatening arrhythmias.

At a serum potassium level of 7.0–8.0 mEq/L, the ECG frequently shows peaked T waves; decreased amplitude of P waves; prolonged PR interval; sinoatrial, atrioventricular, and intraventricular conduction depression; widening of the QRS; and ST-segment elevation.

The hallmarks of hypokalemia-induced ECG changes are depressed ST segment and depressed or inverted T wave of low amplitude, prominent (deepened and broadened) U wave, prolonged QT interval, P wave increased amplitude and width, and prolonged PR interval (first-grade atrioventricular block).

Hypercalcemia and hypocalcemia influence predominantly the duration of the action potentials.

Increase of extracellular calcium concentration reduces the duration of the ventricular action potential by shortening phase 2. ECG changes secondary to hypercalcemia—shortened QT interval, prolonged QRS duration, bradycardia, all degrees of AV blocks, sinus node dysfunction and tachy-brady syndrome, ventricular tachycardia, ventricular fibrillation, and torsades de pointes—are also possible.

ECG changes secondary to hypocalcemia—prolonged QT interval, shortened QRS duration, AV block, sinus bradycardia, sinoatrial block, torsades de pointes, and ventricular fibrillation—are uncommon. However torsades de pointes cases have been observed in patients with QT prolongation due to hypomagnesemia. Severe hypermagnesemia can cause AV and IV conduction delays that can culminate in complete AV block.