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Kjeldsen K. Hypokalemia and sudden cardiac death. Exp Clin Cardiol. 2010;15(4):e96-9
Kjeldsen, K. (2010). Hypokalemia and sudden cardiac death. Experimental and clinical cardiology, 15(4), e96-9.
Kjeldsen, Keld. "Hypokalemia and sudden cardiac death." Experimental and clinical cardiology vol. 15,4 (2010): e96-9.
Kjeldsen K. Hypokalemia and sudden cardiac death. Exp Clin Cardiol. 2010;15(4):e96-9. PMID: 21264075; PMCID: PMC3016067.
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Exp Clin Cardiol. 2010;15(4):e96-9.

Hypokalemia and sudden cardiac death.

Experimental and clinical cardiology

Keld Kjeldsen

Affiliations

  1. Laboratory for Molecular Cardiology, Medical Department B, The Heart Centre, Copenhagen University Hospital (Rigshospitalet) and Danish National Research Foundation Centre for Cardiac Arrhythmia, University of Copenhagen, Copenhagen, Denmark.

PMID: 21264075 PMCID: PMC3016067

Abstract

Worldwide, approximately three million people suffer sudden cardiac death annually. These deaths often emerge from a complex interplay of substrates and triggers. Disturbed potassium homeostasis among heart cells is an example of such a trigger. Thus, hypokalemia and, also, more transient reductions in plasma potassium concentration are of importance. Hypokalemia is present in 7% to 17% of patients with cardiovascular disease. Furthermore, up to 20% of hospitalized patients and up to 40% of patients on diuretics suffer from hypokalemia. Importantly, inadequate management of hypokalemia was found in 24% of hospitalized patients. 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. Long-term potassium homeostasis depends on renal potassium excretion. 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. Moreover, due to the large number of Na(+)/K(+) pumps and K(+) channels, the skeletal muscles possess a huge capacity for potassium exchange. 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. Interestingly, drugs with a proven significant positive effect on mortality and morbidity rates in heart failure patients all increase plasma potassium concentration. Thus, it may prove beneficial to pay more attention to hypokalemia and to maintain plasma potassium levels in the upper normal range. The more at risk of fatal arrhythmia and sudden cardiac death a patient is, the more attention should be given to the potassium homeostasis.

Keywords: Arrhythmia; Hypokalemia; Na+/K+-ATPase; Potassium; Sudden cardiac death

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