Hypokalemia in heart failure: A low or a high point?

Hypokalemia occurs commonly in chronic heart failure consequent to neurohormonal activation and diuretic therapy.1 Clinicians chase potassium levels with potassium supplementation, risking hyperkalemia when renal dysfunction ensues. Scientific rigor is lacking to define the optimal potassium level, the appropriate pace of correction and whether such correction influences outcome. In the absence of randomized trial data, the current European Society of Cardiology guidelines are unable to provide specific recommendations regarding potassium supplementation for hypokalemia.2 Several mechanisms contribute to hypokalemia in chronic heart failure (Figure 1).3 First, reduced renal perfusion activates the renin-angiotensin-aldosterone system; aldosterone release facilitates sodium retention and potassium excretion. Second, stimulation of the β2 adrenergic receptor by upregulated circulating catecholamines promotes sodium reabsorption, potassium excretion, and shifts potassium to the intracellular compartment. Third, loop diuretics or a combination of loop and thiazide diuretics induce further renal potassium losses. Loop diuretics inhibit the Na+-K+-2Cl– co-transporter in the loop of Henle. Sodium is therefore delivered to the distal tubule, where it is reabsorbed at the expense of greater potassium and acid excretion, resulting in hypokalemia and contraction alkalosis. Low intracellular magnesium also worsens renal potassium wasting by releasing inhibition of the renal outer medullary potassium (ROMK) channel; combined magnesium and potassium supplementation is necessary to increase tissue potassium levels.4 As heart failure progresses in severity, greater neurohormonal and pharmacological derangements occur and may result in worsening risk of hypokalemia.