Synopsis
Recognise potassium-related neuromuscular and cardiac risk, locate the loss or shift, and replace potassium without causing rebound hyperkalaemia.
- Severity is not the concentration alone: rate of fall, heart disease, digoxin, QT-prolonging medicines, magnesium depletion and acid–base disturbance determine arrhythmic risk.
- Differentiate true body depletion from intracellular shift; insulin, beta-2 agonists, alkalosis, refeeding and periodic paralysis can lower serum potassium without the same total-body deficit.
- Gastrointestinal loss usually produces appropriate renal potassium conservation, while diuretics, mineralocorticoid excess, renal tubular disease and magnesium depletion cause inappropriate urinary wasting.
Key red flags
Fatigue, cramps, proximal weakness and reduced reflexes can progress to flaccid paralysis or ventilatory failure when potassium falls rapidly or profoundly.
Investigation priorities
Confirm severity, define kidney handling constraints and establish a baseline for replacement.
Management branches
A blood test shows low potassium or the clinical presentation suggests potassium-related weakness or arrhythmia.
- Assess ABCDE, symptom onset, heart disease, digoxin and QT-risk medicines, obtain an ECG and repeat potassium with renal, magnesium and acid–base tests.
- Move severe concentration, ECG change, arrhythmia, respiratory weakness, paralysis or ongoing rapid loss to a monitored area and call senior medical support.
Key medicines
Oral potassium chlorideSelect the licensed preparation and divided dose from the current BNF and local formulary according to concentration, symptoms, deficit, ongoing loss and renal function; review the next potassium before automatic continuation.
Intravenous potassium chlorideUse only a ready-diluted licensed infusion at the concentration and pump-controlled rate authorised by the current local potassium chart; exceptional central concentrations or higher rates require critical-care, pharmacy and continuous ECG safeguards.