Insulin, beta agonists and alkalosis drive potassium into cells
Expansion
Total body potassium is about 3500 mmol, of which only about 2 per cent is extracellular. Small shifts therefore produce large changes in serum concentration.
Into cells (lowering serum potassium)
- Insulin, by stimulating the sodium-potassium ATPase
- Beta-2 agonists such as salbutamol
- Alkalosis
- Refeeding, and rapid cell production after treating B12 deficiency
Out of cells (raising serum potassium)
- Acidosis, particularly mineral acidosis
- Insulin deficiency and hyperglycaemia
- Beta blockers
- Cell lysis: rhabdomyolysis, tumour lysis, haemolysis, burns
- Suxamethonium, dangerously so in burns, denervation and prolonged immobility
- Digoxin toxicity, by inhibiting the pump
The consequence is that a patient in diabetic ketoacidosis may have a normal or high serum potassium with a total body deficit of hundreds of millimoles, and treatment with insulin will unmask it.
Conversely, pseudohyperkalaemia from haemolysed samples, a tight tourniquet, delayed processing, or very high platelet or white cell counts should always be considered before treating an unexpected result.