• P Glover.
• Department of Critical Care Medicine, Flinders Medical Centre, Adelaide, SA, Australia.
• Crit Care Resusc. 1999 Sep 1;1(3):239-51.

ObjectiveTo review the metabolism and function of potassium and causes and management of hypokalaemia.Data SourcesA review of studies reported from 1966 to 1998 and identified through a MEDLINE search of the English-language literature of hypokalaemia.Summary Of ReviewPotassium is predominantly an intracellular ion that contributes to approximately 50% of the intracellular fluid osmolality and is largely responsible for the resting membrane potential. The latter accounts for its influence on the excitability of muscle and nervous tissue. Hypokalaemia is defined as a serum potassium of less than 3.5 mmol/L or plasma potassium less than 3.0 mmol/L and may be asymptomatic. Clinical features associated with hypokalaemia include abnormalities of cardiovascular, neurological and metabolic function and may be treated with oral potassium salts, although tachycardia and muscle weakness are the two life threatening disorders which may require rapid intravenous correction. The potassium salts of chloride, phosphate and acetate are often used, although the choice is often guided by the presence of an associated hypochloraemic alkalosis, non-anion gap acidosis or hypophosphataemia, indicating treatment with potassium chloride, potassium acetate, or potassium phosphate, respectively. The infusion rates of intravenous therapy depends upon the salt used. Potassium chloride is usually infused at a rate up to 40 mmol/h, whereas potassium acetate and potassium monohydrogen or dihydrogen phosphate are usually infused up to 5 mmol/h and 2 mmol/h respectively.ConclusionsHypokalaemia can be asymptomatic or it may cause cardiovascular, neurological or skeletal muscle dysfunction. If intravenous potassium therapy is required, then correction with potassium chloride, acetate, or phosphate salts are usually guided by the presence of a metabolic acidosis, alkalosis or hypophosphataemia.

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