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.
- Check magnesium early because hypomagnesaemia promotes renal potassium loss and makes apparently adequate potassium replacement ineffective.
- ECG changes may include T-wave flattening, ST depression, prominent U waves, apparent QT or QU prolongation, ectopy and tachyarrhythmia, but a normal tracing does not exclude danger.
- Use oral potassium when the patient is stable, able to absorb treatment and does not need rapid correction; split doses and review tolerability and concurrent intake.
- Reserve intravenous potassium for severe, symptomatic or non-enteral situations, using a ready-diluted licensed bag, pump, approved access and organisation-specific concentration and rate.
- Recheck during replacement and after the cause changes, because renal recovery, stopped losses or reversal of an intracellular shift can turn continued supplementation into hyperkalaemia.
Key red flags
Fatigue, cramps, proximal weakness and reduced reflexes can progress to flaccid paralysis or ventilatory failure when potassium falls rapidly or profoundly.
Palpitations, syncope, ventricular ectopy or tachyarrhythmia is especially concerning with ischaemia, heart failure, digoxin or concurrent magnesium depletion.
Episodic profound weakness with little urinary loss suggests familial or thyrotoxic intracellular shift; aggressive replacement can cause dangerous rebound and warrants specialist input.
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.
- Stop or reduce the precipitating medicine or loss when safe, but preserve essential therapy through a documented alternative rather than indiscriminate discontinuation.