Hyperkalaemia is defined as serum potassium concentration greater than 5.5 mmol/l. Its prevalence in the general population is unknown, but it is thought to occur in 1-10% of patients admitted to hospital.1 The rate of morbidity and mortality associated with hyperkalaemia has risen greatly with the use of drugs that target the renin-angiotensin system, and since publication 10 years ago of a randomised trial that showed that adding an aldosterone receptor antagonist to usual treatment for congestive failure improved outcomes.2 3 4 5

Potassium is the most abundant cation in the human body and has key roles in the excitatory properties needed for conduction of nerve impulses and muscle contraction. Ninety eight per cent of the body’s potassium is in the intracellular fluid (concentration about 140 mmol/l), with only 2% in extracellular fluid (3.8-5.0 mmol/l). A complex interplay of regulatory mechanisms is needed to maintain normal potassium balance, which involves the transfer of potassium between the extracellular and intracellular compartments (fig 1)⇓. In the long term potassium homoeostasis is mainly governed by regulation of renal potassium excretion, notably by the actions of aldosterone (fig 2)⇓. These mechanisms ensure that although total daily potassium intake could range from 40 mmol to 200 mmol per day, potassium levels in serum remain within the relatively narrow normal range. Derangements in potassium regulation, and resultant changes in serum potassium concentration, may alter membrane excitability. Disorders of plasma potassium can therefore have profound effects on nerve, muscle, and cardiac function.