Adam Wells
Because of the widespread use of diuretics and neuro humoral activation, hypokalemia is a common electrolyte disorder among heart failure patients, contributing to an increased risk of ventricular arrhythmias and sudden cardiac death. Recent experimental studies suggest that hypokalemia-induced arrhythmias are initiated by decreased Na+ /K+ATPase activity, which then leads to Ca2+ overload, Ca2+/Calmodulin-dependent kinase II (CaMKII activation, and the development of afterdepolarizations). The current mechanistic evidence of hypokalemia-induced triggered arrhythmias is reviewed in this article, and we discuss how molecular changes in heart failure may lower the threshold for these arrhythmias. Finally, we discuss how recent discoveries regarding hypokalemia-induced arrhythmias may have implications for future antiarrhythmic treatment strategies.