01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Potassium sets resting membrane potential in muscle and nerve. A low extracellular concentration hyperpolarises cells and disrupts cardiac repolarisation, causing weakness, cramps, ileus and arrhythmia. Serum concentration represents only a small extracellular fraction, so an apparently modest fall can accompany substantial depletion, while a redistribution event can look severe without equivalent loss.
Causes can be organised as reduced intake, gastrointestinal loss, renal loss and transcellular shift. Poor intake alone is rarely sufficient unless combined with illness. Vomiting causes renal potassium loss indirectly through chloride depletion and aldosterone. Diarrhoea loses potassium directly. Loop and thiazide diuretics, mineralocorticoid excess, renal tubular acidosis, aminoglycosides and hypomagnesaemia increase urinary loss.
Treatment is a controlled replacement and diagnostic exercise, not a race to a reference interval. The amount retained depends on ongoing loss, magnesium, acid–base state and renal function. Concentrated potassium products are high-risk medicines; exact dilution, route and rate must come from the live BNF, SmPC and local infusion policy with pharmacy or critical-care support for exceptional rates.
Key points
- 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.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Gastrointestinal loss
Diarrhoea directly removes potassium, while vomiting causes chloride depletion, secondary aldosterone activity and additional renal potassium wasting.
Renal potassium wasting
Loop or thiazide diuretics, mineralocorticoid excess, renal tubular disorders, aminoglycosides and low magnesium increase urinary potassium loss.
Transcellular shift
Insulin, beta-adrenergic stimulation and alkalosis move potassium into cells, sometimes producing a rapid serum fall without equivalent total-body depletion.
Low intake with illness
Poor intake alone is rarely sufficient, but it reduces replacement while gastrointestinal, renal or treatment-related losses continue.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Extracellular potassium falls
Net loss or intracellular redistribution reduces the potassium concentration around excitable nerve, skeletal-muscle and cardiac cells.
- 2Cell membranes hyperpolarise
A larger transmembrane gradient makes depolarisation more difficult, producing weakness, cramps, reduced gut motility and impaired respiratory muscle function.
- 3Cardiac repolarisation destabilises
Low potassium prolongs and disperses repolarisation, creating ectopy and atrial or ventricular arrhythmia, especially with digoxin or low magnesium.
- 4Ongoing losses prevent correction
Continued diarrhoea, diuresis, aldosterone effect or magnesium deficiency causes replacement to be lost before intracellular stores recover.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
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.
Constipation, abdominal distension and ileus may reflect smooth-muscle dysfunction, but obstruction and surgical disease still require independent assessment.
Diarrhoea, vomiting, nasogastric drainage, fistula, high-output stoma, laxatives or diuretics commonly reveal a continuing deficit that replacement alone cannot overcome.
A sudden fall after insulin, nebulised beta-agonist, acute alkalosis or refeeding can rebound when the stimulus ends and therefore needs cautious dosing.
Episodic profound weakness with little urinary loss suggests familial or thyrotoxic intracellular shift; aggressive replacement can cause dangerous rebound and warrants specialist input.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Repeat serum potassium and renal profileFirst step - Why
- Confirm severity, define kidney handling constraints and establish a baseline for replacement.
- Interpretation and limitations
- Repeat unexpected results rapidly without delaying treatment of arrhythmia or paralysis; falling estimated GFR or oliguria sharply reduces the safety margin for continued dosing.
- 02
Twelve-lead ECG and rhythm monitoring - Why
- Detect repolarisation abnormality and ventricular irritability requiring monitored correction.
- Interpretation and limitations
- Flattened T waves, ST depression, U waves and ectopy support toxicity, but ECG sensitivity is incomplete and high-risk context can justify monitoring despite a normal trace.
- 03
Serum magnesium, calcium and phosphate - Why
- Find companion deficits that cause symptoms, refractory potassium loss or a broader refeeding syndrome.
- Interpretation and limitations
- Low magnesium must be corrected to reduce renal potassium wasting; low phosphate after nutrition or DKA treatment may explain respiratory or muscle weakness independently.
- 04
Venous blood gas or serum bicarbonate - Why
- Identify acidosis or alkalosis that narrows gastrointestinal, renal and shift mechanisms.
- Interpretation and limitations
- Metabolic alkalosis fits vomiting, diuretics or mineralocorticoid effect; normal-gap acidosis with urinary wasting raises renal tubular acidosis, while diarrhoea causes extrarenal bicarbonate loss.
- 05
Spot urine potassium with creatinine or timed urinary assessment - Why
- Decide whether kidneys are conserving potassium appropriately during depletion.
- Interpretation and limitations
- Use a locally accepted ratio or excretion measure with nephrology advice; ongoing diuretics, changing replacement and low urine output can make a single value misleading.
- 06
Blood pressure, renin and aldosterone pathway - Why
- Investigate renal potassium wasting with hypertension and metabolic alkalosis.
- Interpretation and limitations
- Correct potassium and review interfering medicines before specialist endocrine testing, because diuretics and renin–angiotensin drugs materially distort results.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Redistribution rather than depletion
Recent insulin, beta-agonist use or alkalosis with rapid onset suggests cellular shift, carrying different rebound risk from prolonged whole-body loss.
Gastrointestinal loss
Diarrhoea, vomiting or stoma output with appropriately low urinary potassium supports an extrarenal source when combined with the history and other findings.
Renal wasting
Inappropriately high urinary potassium during hypokalaemia, interpreted with acid-base status and medicines, indicates kidney loss when supported by the history and examination.
Mineralocorticoid excess
Hypertension, metabolic alkalosis and renal potassium loss with suppressed renin suggest aldosterone or another mineralocorticoid mechanism.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01RiskIdentify the monitored patientFirst stepA blood test shows low potassium or the clinical presentation suggests potassium-related weakness or arrhythmia.+
- 1Assess ABCDE, symptom onset, heart disease, digoxin and QT-risk medicines, obtain an ECG and repeat potassium with renal, magnesium and acid–base tests.
- 2Move severe concentration, ECG change, arrhythmia, respiratory weakness, paralysis or ongoing rapid loss to a monitored area and call senior medical support.
- 3AlternativeStop or reduce the precipitating medicine or loss when safe, but preserve essential therapy through a documented alternative rather than indiscriminate discontinuation.
02ReplaceChoose enteral or intravenous potassiumTrue depletion or clinically significant hypokalaemia requires active correction.+
- 1Use oral potassium for stable patients with a functioning gut, selecting preparation and divided dose from the BNF and local formulary and addressing nausea or adherence.
- 2For severe symptoms, very low potassium or unavailable enteral route, prescribe a ready-diluted intravenous product through the approved pump, access, concentration and rate chart with rhythm monitoring when required.
- 3Correct magnesium and continuing gastrointestinal or renal losses in parallel, and reassess before every additional dose rather than estimating the whole deficit once.
03ExplainSeparate loss from shiftHypokalaemia recurs, is unexpectedly resistant or lacks an obvious acute cause.+
- 1Construct a timeline of diarrhoea, vomiting, stoma or tube losses, nutrition, insulin, beta-agonists, diuretics, laxatives, antimicrobials and blood-pressure medicines.
- 2Interpret acid–base status, blood pressure, magnesium and urinary potassium to distinguish extrarenal loss, renal wasting, mineralocorticoid effect and transcellular movement.
- 3Refer recurrent renal loss, hypertension with alkalosis, suspected periodic paralysis or inherited tubulopathy to endocrine or renal specialists for controlled testing.
04StopPrevent replacement overshootPotassium approaches target, renal function changes or the precipitating shift or loss resolves.+
- 1Recheck potassium at the interval appropriate to route and rate, review urine output and stop intravenous replacement when the indication no longer outweighs risk.
- 2Reduce planned doses after magnesium correction, renal decline, cessation of diarrhoea or insulin and beta-agonist effect, anticipating delayed redistribution from cells.
- 3At discharge, communicate the causal medicine decision and repeat-test date rather than leaving long-term supplementation without monitoring.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Oral potassium chloride
Select 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.Oral products can cause nausea, ulceration and poor adherence and differ in mmol content. Avoid uncontrolled use in renal impairment, check interacting potassium-raising medicines, and do not rely on supplementation while an untreated continuing loss persists.
Intravenous potassium chloride
Use 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.Never administer by intravenous push and never add concentrate casually to a ward fluid bag. Confirm renal output, line route, bag concentration and pump, monitor potassium and rhythm, and stop promptly when renal function or redistribution changes.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Cardiac arrhythmia
Electrical instability can cause ectopy, atrial arrhythmia, ventricular tachyarrhythmia or cardiac arrest, particularly with structural heart disease.
Neuromuscular weakness
Progressive potassium depletion can produce flaccid weakness, paralysis, rhabdomyolysis and respiratory failure through impaired skeletal-muscle excitability.
Ileus
Reduced smooth-muscle excitability slows intestinal motility, causing constipation, abdominal distension, nausea and occasionally functional bowel obstruction.
Rebound hyperkalaemia
Aggressive replacement during a temporary cellular shift or after renal function changes can overshoot once potassium redistributes outward.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Repeat potassium after oral doses according to severity and before each further intravenous prescription; shorten intervals for severe disease, rapid infusion or changing renal function.
- Use continuous ECG monitoring for arrhythmia, important ECG change, profound hypokalaemia or infusion rates that the local policy restricts to a monitored environment.
- Trend magnesium and replace it concurrently when low, because potassium can continue leaking renally despite large replacement if magnesium remains deficient.
- Measure urine output and creatinine throughout intravenous treatment; oliguria or acute kidney injury requires immediate rate and cumulative-dose reassessment.
- Record diarrhoea, stoma, drain, nasogastric and urinary losses and whether the causative medicine remains active so replacement matches the current, not historic, deficit.
- After recovery, recheck potassium after stopping supplements or changing diuretics and renin–angiotensin medicines to detect both recurrence and rebound elevation.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Vomiting causes renal potassium loss
Gastric fluid contains limited potassium, but chloride depletion, alkalosis and aldosterone drive substantial urinary wasting after prolonged vomiting.
Magnesium closes the renal leak
Low intracellular magnesium permits distal potassium secretion, explaining why isolated potassium treatment may barely change the serum result.
Apparent QT may be QU
A prominent U wave can fuse with the T wave and mimic major QT prolongation; either pattern flags repolarisation instability.
Shift disorders rebound
Total-body deficit is smaller in periodic paralysis or acute insulin effect, so large replacement becomes hazardous when potassium exits cells again.
Urine tests need timing
A sample after several replacement doses or while a diuretic remains active may not reflect the original renal response and needs cautious interpretation.
Chloride can be therapeutic context
Potassium chloride addresses both potassium and chloride depletion in vomiting-associated alkalosis, whereas another anion may fit phosphate depletion or acidosis differently.
11Common pitfallsFrequent interpretation and management errors.
- 01
Replacing potassium repeatedly without measuring magnesium and then describing the predictable renal wasting as treatment resistance.
- 02
Giving concentrated potassium by direct injection or adding it to a partly used fluid bag, creating fatal local concentration and dosing error.
- 03
Using a standard infusion rate despite oliguria, acute kidney injury or a rapidly reversing intracellular shift.
- 04
Reassuring from a normal ECG even though potassium is profoundly low and the patient has digoxin exposure or respiratory weakness.
- 05
Treating the laboratory value but leaving high-output diarrhoea, vomiting, stoma loss or a causal diuretic plan unaddressed.
- 06
Discharging with indefinite supplementation and no date to reassess potassium after the acute driver and renal function have changed.