Thus, it may prove beneficial to pay more attention to hypokalemia and to maintain plasma potassium levels in the upper normal range. Interestingly, drugs with a proven significant positive effect on mortality and morbidity rates in heart failure patients all increase plasma potassium concentration. In cardiovascular patients, hypokalemia is often caused by nonpotassium-sparing diuretics, insufficient potassium intake and a shift of potassium into stores by increased potassium uptake stimulated by catecholamines, beta-adrenoceptor agonists and insulin. Moreover, due to the large number of Na +/K + pumps and K + channels, the skeletal muscles possess a huge capacity for potassium exchange. However, skeletal muscles play an important role in short-term potassium homeostasis, primarily because skeletal muscles contain the largest single pool of potassium in the body. Long-term potassium homeostasis depends on renal potassium excretion. Hypokalemia is associated with increased risk of arrhythmia in patients with cardiovascular disease, as well as increased all-cause mortality, cardiovascular mortality and heart failure mortality by up to 10-fold. Importantly, inadequate management of hypokalemia was found in 24% of hospitalized patients. Furthermore, up to 20% of hospitalized patients and up to 40% of patients on diuretics suffer from hypokalemia.
Hypokalemia is present in 7% to 17% of patients with cardiovascular disease. Thus, hypokalemia and, also, more transient reductions in plasma potassium concentration are of importance. Disturbed potassium homeostasis among heart cells is an example of such a trigger. These deaths often emerge from a complex interplay of substrates and triggers. Worldwide, approximately three million people suffer sudden cardiac death annually.
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