Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Hyperkalaemia
Endocrinology and metabolism · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Time-critical presentation
Serum potassium at least 6.5 mmol/L, hyperkalaemic ECG change, rapid rise, paralysis or clinical instability is life-threatening. Obtain an urgent ECG, continuous monitoring, senior and renal help, and use the current UK Kidney Association hospital algorithm. Give intravenous calcium immediately for toxic ECG changes while potassium-shifting and removing measures are prepared; cardiac arrest follows the RCUK hyperkalaemia algorithm.
Overview
Confirm and risk-stratify raised potassium, stabilise cardiac membranes, shift potassium safely and secure definitive removal with rebound surveillance.
Extracellular potassium controls myocardial and skeletal-muscle membrane potential. As it rises, conduction slows and excitability becomes unstable, producing peaked T waves, PR prolongation, P-wave loss, QRS widening, sine-wave morphology, ventricular fibrillation or asystole. ECG progression is not reliably sequential, and a lethal concentration may have little warning on one tracing.
True hyperkalaemia reflects impaired renal excretion, cellular release or redistribution, or excessive administration. Acute kidney injury, advanced CKD, hypoaldosteronism, acidosis, insulin deficiency, rhabdomyolysis, tumour lysis and medicines that inhibit the renin–angiotensin–aldosterone system are common. Pseudohyperkalaemia arises from haemolysis, difficult collection, thrombocytosis, extreme leucocytosis or sample delay.
Emergency treatment has three distinct aims: protect the heart with calcium, move potassium into cells with insulin–glucose and beta-agonist, and remove potassium from the body or stop ongoing release. Exact products, timing and repeat criteria must follow the current UKKA and RCUK algorithms. Dialysis access failure, pregnancy, digoxin toxicity and poisoning require immediate specialist adaptation.
Key points
Aetiology
01
Impaired renal excretion
Acute kidney injury, advanced chronic kidney disease, hypoaldosteronism or missed dialysis limits removal of the daily potassium load.
02
Cellular release or redistribution
Acidosis, insulin deficiency, rhabdomyolysis, tumour lysis, burns or prolonged seizures move or release potassium into extracellular fluid.
03
Medicine-related accumulation
Renin-angiotensin-aldosterone inhibitors, potassium supplements, trimethoprim and NSAIDs can combine with dehydration or renal decline to raise potassium.
04
Pseudohyperkalaemia
Haemolysis, difficult sampling, sample delay or extreme platelet and white-cell counts can create a high laboratory value without equivalent plasma exposure.
Pathophysiology
1
Extracellular potassium rises
Reduced excretion, cellular leakage or transcellular shift increases potassium around excitable muscle and nerve membranes as the process continues.
2
Membrane potential becomes unstable
The altered potassium gradient changes myocardial depolarisation and repolarisation, progressively slowing conduction and potentially culminating in malignant arrhythmia or asystole.
3
Cardiac conduction may fail
Peaked T waves, atrioventricular delay, QRS widening, sine-wave change or ventricular arrhythmia may develop, but progression is not reliably sequential.
Clinical features and red flags
Electrical toxicityRed flag
Peaked T waves, prolonged PR, flattened or absent P waves, widening QRS, bradycardia, sine wave or ventricular arrhythmia demands immediate calcium treatment.
Neuromuscular effectRed flag
Paraesthesia, ascending weakness, flaccid paralysis or ventilatory compromise can accompany severe hyperkalaemia and should not be mistaken for a primary neurological disorder.
Renal failure contextRed flag
Oliguria, acute kidney injury, missed dialysis or access dysfunction predicts impaired removal and lowers the threshold for urgent renal replacement planning.
Cell breakdownRed flag
Crush injury, prolonged seizure, burns, rhabdomyolysis, tumour lysis or haemolysis can release potassium continuously and cause rapid rebound after temporary shifting.
Medicine accumulation
ACE inhibitors, angiotensin-receptor blockers, mineralocorticoid antagonists, potassium supplements, trimethoprim and NSAIDs interact strongly with renal decline and dehydration.
Pseudohyperkalaemia
Haemolysis flag, prolonged tourniquet, fist clenching, extreme cell counts or discordant plasma and serum values can create an artefact but require prompt controlled confirmation.
Investigations
01Urgent twelve-lead ECGFirst step
Why
Detect cardiac membrane toxicity and determine the immediate need for intravenous calcium.
Interpretation and limitations
Perform at potassium 6.0 mmol/L or above in hospital; any characteristic change escalates treatment, while a normal tracing never excludes progression.
02Repeat lithium-heparin plasma potassium
Why
Confirm a surprising result rapidly and reduce clotting or sample artefact.
Interpretation and limitations
Use an appropriate rapidly analysed sample without fist clenching; treat immediately if the first result and ECG are dangerous rather than waiting for confirmation.
03Glucose before insulin and serially afterwards
Why
Plan glucose protection and detect the common delayed complication of insulin-mediated potassium shift.
Interpretation and limitations
A baseline below 7 mmol/L triggers the UKKA additional 10% glucose infusion, and all treated patients need scheduled checks through at least six hours.
04Renal profile, bicarbonate and venous gas
Why
Define excretory failure, acidosis, insulin deficiency and the likelihood that dialysis or cause-specific treatment is needed.
Interpretation and limitations
Oliguric renal failure or persistent severe acidosis reduces confidence in temporary medical measures and warrants early renal or critical-care escalation.
Differential diagnosis
01
Pseudohyperkalaemia
A haemolysis flag, difficult collection or extreme cell count with a clinically discordant result supports artefact, but controlled confirmation must be prompt.
02
Acute kidney injury
Oliguria and a rising creatinine indicate impaired removal, often with medicines and acidosis contributing to a genuine rapid increase.
03
Cell breakdown
Muscle pain, markedly raised creatine kinase, tumour-lysis features or major tissue injury point to continuing intracellular release and rebound risk.
04
Mineralocorticoid deficiency
Hypotension, hyponatraemia or adrenal history with reduced renal potassium excretion suggests adrenal insufficiency or hypoaldosteronism when biochemical results match the presentation.
Management
01ConfirmRisk-stratify without delaying rescueFirst stepA laboratory or point-of-care result shows raised potassium or the ECG suggests hyperkalaemia.+
1Use ABCDE, repeat potassium appropriately, obtain an urgent 12-lead ECG at 6.0 mmol/L or above and establish continuous monitoring for UKKA high-risk categories.
2Review renal output, acid–base state, glucose, medicines, cell injury and dialysis history while stopping exogenous potassium and avoidable causal agents.
3If severe potassium or toxic ECG change is present, activate the hospital algorithm immediately and call senior, renal and critical-care teams before confirmation delays treatment.
02ProtectStabilise the myocardiumThe ECG shows hyperkalaemic toxicity or cardiac arrest is attributed to hyperkalaemia.+
1Use calcium chloride in
Complications
01
Fatal arrhythmia
Severe electrical instability can progress abruptly to ventricular fibrillation, pulseless rhythms or asystole without a predictable ECG sequence.
02
Neuromuscular paralysis
Membrane dysfunction can cause paraesthesia, ascending weakness and flaccid paralysis; respiratory-muscle involvement may eventually compromise ventilation.
03
Post-treatment rebound
Intracellular shifting therapies wear off while total-body potassium remains high, allowing recurrence unless potassium is removed or ongoing release stops.
04
Treatment-related hypoglycaemia
Insulin used to shift potassium can lower glucose for several hours, especially in kidney impairment or when glucose monitoring is incomplete.
Monitoring and follow-up
Repeat potassium at 1, 2, 4, 6 and 24 hours after treatment under UKKA guidance, shortening the schedule for ongoing release, dialysis delay or clinical deterioration.
Use continuous cardiac monitoring for potassium at least 6.5 mmol/L, any toxic ECG change or an unwell patient at 6.0–6.4 mmol/L with possible rapid rise.
After insulin–glucose, record blood glucose at baseline, 30, 60, 90, 120 minutes and hourly through six hours, extending observation after repeat dosing or late hypoglycaemia risk.
Repeat ECG after calcium and when potassium or clinical status changes; recurrence of widening or bradycardia may precede the next laboratory result.
Track urine output, creatinine, bicarbonate, CK and tumour-lysis markers when relevant, because temporary serum improvement does not stop continued tissue release or excretory failure.
At discharge, assign repeat potassium and renal testing after medicine adjustment, binder initiation or acute kidney recovery and communicate explicit sick-day advice.
Special situations
Calcium protects but conceals
ECG improvement after calcium confirms membrane effect, not potassium clearance; deterioration can recur as calcium wears off while serum concentration remains high.
ECG absence is not safety
Some patients retain a deceptively normal trace at severe concentrations, so UKKA treatment and monitoring thresholds do not depend on classic progression.
Insulin complication is delayed
Potassium shift begins quickly, but hypoglycaemia can occur several hours later, especially in renal failure; a normal one-hour glucose does not end surveillance.
Haemolysis needs context
Repeating an artefactual sample is correct, but using the possibility of haemolysis to ignore broad QRS complexes and oliguria is dangerous.
Removal determines durability
Insulin and salbutamol redistribute potassium; urine, binders or dialysis must clear it, or rebound follows as cellular effects fade.
RAAS treatment can sometimes survive
Correcting dehydration, acidosis, dietary excess and monitoring barriers may permit valuable kidney or heart therapy to resume under specialist care.
Common pitfalls
01
Waiting for a repeat laboratory sample before treating a patient with potassium 7.1 mmol/L and broadening QRS complexes.
02
Giving intravenous calcium and documenting the hyperkalaemia as treated without insulin–glucose, removal planning or repeat potassium.
03
Using salbutamol alone in severe hyperkalaemia despite variable response and lack of membrane stabilisation or potassium removal.
04
Failing to provide and monitor the extra glucose pathway when pretreatment glucose is below 7 mmol/L, causing predictable iatrogenic hypoglycaemia.
05
Checking potassium after one hour but not at later rebound points when shift therapies wear off or tissue breakdown continues.
06
Stopping all renin–angiotensin and heart-failure medicines permanently without documenting the cause, benefit trade-off and monitored alternative plan.
Practice
Two practice questions
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Question 1 of 2
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Endocrinology and metabolismOriginal SBA
Calcium purpose in hyperkalaemia
An adult with potassium 7.0 mmol/L has a widening QRS and absent P waves. What is the best immediate treatment principle?
Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
UKKA defines hyperkalaemia from 5.5 mmol/L and recommends an urgent 12-lead ECG for every hospitalised adult with potassium at least 6.0 mmol/L.
Use continuous three-lead monitoring at 6.5 mmol/L or above, with any hyperkalaemic ECG feature, or at 6.0–6.4 mmol/L when the patient is unwell or a rapid rise is expected.
Repeat a potentially haemolysed or surprising sample promptly, but never delay treatment when the ECG, potassium and clinical context indicate genuine severe toxicity.
Intravenous calcium stabilises the myocardium within minutes but does not lower serum potassium; potassium-shifting and removal treatment must proceed alongside it.
UKKA’s standard insulin–glucose regimen is 10 units soluble insulin with 25 g glucose, with extra glucose infusion when pretreatment glucose is below 7 mmol/L and scheduled monitoring for six hours.
Nebulised salbutamol is an adjunct, not monotherapy for severe disease, and response may be limited in patients taking non-selective beta-blockers.
Shift therapies wear off: repeat potassium at 1, 2, 4, 6 and 24 hours under UKKA guidance and arrange definitive gastrointestinal or dialysis removal when indicated.
After stabilisation, preserve beneficial renin–angiotensin or heart-failure therapy where possible through cause correction, dietary review and specialist potassium binders rather than automatic permanent withdrawal.
05
Creatine kinase, blood count and cause-directed studies
Why
Identify rhabdomyolysis, tumour lysis, haemolysis or extreme cell counts causing true or spurious elevation.
Interpretation and limitations
Interpret CK, urate, phosphate, calcium and cell counts with clinical timing; ongoing tissue release predicts recurrence after the first potassium fall.
06Medication and dialysis reconciliation
Why
Locate potassium intake, interacting medicines, missed sessions or vascular-access failure.
Interpretation and limitations
Confirm last doses and actual dialysis delivery; do not assume a prescribed session or stopped tablet means its physiological effect has ended.
cardiac arrest
or the peri-arrest resuscitation setting and calcium gluconate for other patients, following the exact UKKA dose and administration time.
2Repeat the ECG after calcium and consider further protocol dosing if toxic changes persist, recognising that protection lasts only about 30–60 minutes.
3Begin potassium-shifting and removal measures concurrently because calcium alters excitability but does not change the serum potassium concentration.
03ShiftMove potassium intracellularly safelyDefinitiveModerate or severe true hyperkalaemia requires rapid temporary reduction while definitive removal is arranged.+
1Give 10 units soluble insulin with 25 g glucose through the UKKA prescription, adding 10% glucose at 50 mL/hour for five hours when baseline glucose is below 7 mmol/L.
2Add nebulised salbutamol at the algorithm dose when suitable, but never rely on it alone for severe disease and anticipate tachycardia and variable response.
3Check glucose at the UKKA timed schedule through six hours and potassium at 1, 2, 4, 6 and 24 hours, treating hypoglycaemia and rebound promptly.
04RemoveSecure definitive potassium clearanceDefinitiveThe cause persists, renal excretion is poor or potassium remains severe or rebounds after shifting treatment.+
1Use a current locally approved potassium binder when the UKKA indication fits, checking bowel, sodium-load and medicine-spacing cautions for the selected product.
2Contact renal services urgently for severe refractory hyperkalaemia, oliguric kidney failure, dialysis dependence or ongoing tissue breakdown, ensuring vascular access and transfer are feasible.
3After recovery, review diet with renal expertise and redesign necessary RAAS or heart-failure treatment with monitoring rather than applying an unexplained permanent stop.
Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
Stabilises cardiac cell membranes rapidly while separate measures shift and remove potassium from the body.
Intravenous calcium salts for ECG toxicity
UKKA recommends 30 mL calcium gluconate 10% over 10 minutes for non-arrest patients, or 10 mL calcium chloride 10% over 5 minutes in cardiac arrest or peri-arrest; reassess the ECG and repeat only through the algorithm.
Calcium does not lower potassium and its protection is temporary. Confirm the salt and concentration because elemental calcium differs, use a secure line, avoid extravasation and obtain expert toxicology advice when digoxin poisoning is suspected.
Temporarily lowers serum potassium by stimulating cellular uptake, buying time for renal, gastrointestinal or dialysis removal.
Soluble insulin with glucose
Give 10 units soluble insulin with 25 g glucose under UKKA guidance; if pretreatment glucose is below 7 mmol/L, follow with 10% glucose at 50 mL/hour for five hours and titrate to the monitored glucose target.
Check glucose before treatment and at 0, 30, 60, 90, 120, 180, 240, 300 and 360 minutes. Hypoglycaemia risk is increased by renal failure, low body weight, non-diabetes and repeat dosing; treat lows immediately.
Adds beta-2-mediated intracellular potassium shift to insulin–glucose but does not provide membrane stabilisation or body removal.
Nebulised salbutamol
UKKA uses 10–20 mg nebulised salbutamol as adjunctive therapy for moderate or severe acute hyperkalaemia; administer through the local algorithm and assess heart rate and potassium response.
Do not use as monotherapy in severe disease. Response can be reduced by non-selective beta-blockade; anticipate tremor, tachycardia, ischaemia and hyperglycaemia and use extra caution in significant cardiac disease.