Diagnosis of hyperkalemia is usually based on laboratory studies, although the electrocardiogram (ECG) may contain changes suggestive of hyperkalemia. Typical ECG findings in hyperkalemia progress from tall, “peaked” T waves and a shortened QT interval to lengthening PR interval and loss of P waves, and then to widening of the QRS complex culminating in a “sine wave” morphology and death if not treated.
1–3 Treatment of life-threatening hyperkalemia focuses on blocking the effects on myocyte transmembrane potential and cardiac conduction, as well as decreasing extracellular potassium levels.
3 Calcium (intravenous calcium chloride or gluconate) can effectively block the effect of extracellular potassium elevation on cardiac myocytes within minutes by restoring a more appropriate electrical gradient across the cellular membrane.
2 Sodium bicarbonate, beta-2 adrenergic agonists, and the combination of glucose and insulin all drive potassium intracellularly and lower the extracellular serum potassium level.
3 Finally, excessive body potassium can be removed with sodium polystyrene sulfonate (Kayexalate), whereas hemodialysis represents the definitive method to reduce serum potassium levels.
2,3