Level 2 of 6Must-remember

Disorders of potassium: hyperkalaemia and hypokalaemia

Assess, manage and stay safe — enough on its own

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The card — assess, manage, caution

Assessment— look, ask, measure

Know the normal range: plasma potassium is 3.5–5.0 mmol/L; more than 98% of the body's 3500 mmol of potassium is inside cells, so the plasma value is a poor surrogate for the total store and small shifts across the cell membrane produce large changes in the number.
Hyperkalaemia thresholds that change what you do: hyperkalaemia is variously defined as above 5.0 mmol/L (Davidson's), above 5.2 mmol/L (CMDT) or at or above 5.5 mmol/L (Harrison's), but 6.5 mmol/L triggers emergency treatment irrespective of symptoms and 7.0 mmol/L is a medical emergency associated with ECG change and asystolic arrest.Not available at your setup — Serum electrolytes. Use a blood-gas potassium as an immediate estimate while the laboratory sample is processed.
Hypokalaemia thresholds: hypokalaemia is a potassium below 3.5 mmol/L, present in up to 20% of hospitalised patients, graded mild 3.0–3.4 mmol/L, moderate 2.5–2.9 mmol/L and severe below 2.5 mmol/L — the last being the level at which weakness, rhabdomyolysis and serious arrhythmia become expected rather than exceptional.Not available at your setup — Serum electrolytes. Use a blood-gas potassium as an immediate estimate while the laboratory sample is processed.
Neither disorder has reliable clinical signs — this is the most important single statement on the subject: hyperkalaemia below 6.5 mmol/L is usually silent, severe hyperkalaemia may be entirely asymptomatic, and the absence of symptoms is worth nothing.
Hyperkalaemic symptoms when they occur: muscle weakness, often profound and ascending, may be the only symptom; palpitations, presyncope, hypotension and bradycardia reflect developing conduction disturbance; Kussmaul respiration appears if a metabolic acidosis coexists; serious neuromuscular and conduction manifestations generally appear above 7.0 mmol/L but vary with the rapidity of the rise.
Hypokalaemic symptoms: 3.0–3.5 mmol/L is generally asymptomatic; below that expect weakness, fatigue, cramps and constipation; below 2.5 mmol/L expect marked weakness, flaccid paralysis that may involve the respiratory muscles, rhabdomyolysis with acute kidney injury, ileus and functional bowel obstruction, polyuria and polydipsia from impaired concentrating ability.
Take a twelve-lead ECG in every patient, interpret it personally, and repeat it after treatment: it defines urgency, not diagnosis.
The hyperkalaemic ECG sequence: tall, narrow-based, symmetrically peaked (tented) T waves best seen in the precordial leads, then reduction and loss of the P wave with PR prolongation, then ST depression, then progressive QRS widening, and finally merging of the widened QRS with the T wave into a sine wave — a pre-arrest pattern concerning for imminent ventricular fibrillation; bradycardia, complete heart block, ventricular tachycardia and undifferentiated broad-complex rhythms may appear at any stage.
The hypokalaemic ECG sequence: T-wave flattening, then ST depression and T-wave inversion, then prominent U waves, most marked below 2.7 mmol/L; a U wave following a flattened T is readily mistaken for a prolonged QT interval.
Never use the ECG to reassure: the ECG may be normal despite life-threatening hyperkalaemia, correlation between serum potassium and cardiac manifestations is poor, and a potassium of 6.5 mmol/L or more in the absence of ECG changes should still be managed aggressively. Use the ECG to escalate, never to reassure.
Danger signs in hyperkalaemia: any ECG change, muscle weakness, oliguria or anuria, a potassium of 6.5 mmol/L or more, and a rapidly rising trend.Not available at your setup — Serum electrolytes.
Danger signs in hypokalaemia: arrhythmia, concurrent digoxin, respiratory muscle weakness and a potassium below 2.5 mmol/L.Not available at your setup — Serum electrolytes.
The rate of change determines toxicity as much as the absolute value: a dialysis patient habitually at 6.2 mmol/L is far less endangered than a crush victim who has climbed from 4.0 to 6.8 mmol/L in six hours.Not available at your setup — Serum electrolytes.
Read the drug chart — it is the highest-yield diagnostic act: ACE inhibitors, angiotensin-receptor blockers, NSAIDs, spironolactone, eplerenone, finerenone, amiloride, triamterene, trimethoprim, pentamidine, heparin, calcineurin inhibitors and non-selective beta-blockers all raise potassium, and the combination of an ACE inhibitor with a potassium-sparing diuretic or an NSAID is particularly dangerous; diuretics, purgatives and potassium-free fluids lower it.
Bedside tests to send now: a blood-gas potassium returns within minutes and gives the pH, bicarbonate and base deficit as well — treat a gas-machine value as real until the laboratory contradicts it and send a laboratory sample in parallel; add urea, creatinine and electrolytes, and serum magnesium in every hypokalaemic patient.Not available at your setup — Arterial blood gas, Serum electrolytes. If a blood-gas analyser is unavailable, send an urgent laboratory sample and treat empirically on clinical grounds while waiting.
Consider pseudohyperkalaemia but never delay treatment for it: suspect it in a well patient with normal renal function, a normal ECG, no offending drugs, a haemolysis flag, or marked thrombocytosis (above 500 × 10⁹/L) or leucocytosis (above 100 × 10⁹/L) — confirm with a non-centrifuged whole-blood sample carried by hand to the laboratory, drawn from a fresh site with a wide-bore needle, without fist clenching and with the tourniquet released before sampling.
Special groups: neonates and small infants normally run a higher potassium than adults and haemolysed heel-prick samples are the rule, so repeat an abnormal value in a well infant by clean venepuncture but believe it in a sick, dehydrated or oliguric one; in older people presentation is non-specific (falls, confusion, immobility); in children gastroenteritis is by a wide margin the commonest cause of hypokalaemia and the potassium falls further as the acidosis corrects.

Management— do this, in order

Emergency treatment of hyperkalaemia is triggered by cardiac toxicity, muscle weakness, or a potassium above 6.5 mmol/L — calcium first, then insulin–glucose and nebulised salbutamol together, then removal, then stop the cause.Not available at your setup — Serum electrolytes.
Step 1, calcium to protect the myocardium where there are ECG changes: 10% calcium gluconate 10 mL intravenously over 5 minutes, repeated every 15 minutes until the ECG improves (total 5–30 mL); it works within 0–5 minutes and lasts only 30–60 minutes, so repeat it if the QRS re-widens.Doctor / Nurse
Calcium alternative: 10% calcium chloride 10 mL over 5–10 minutes delivers about three times the elemental calcium but is strongly vesicant — large vein or central line only.Doctor / NurseNot available at your setup — Central venous access. Give through a large peripheral vein only if a central line is genuinely unavailable, watching closely for extravasation.
Step 2, soluble insulin with glucose, always together: insulin 10 units with 50% glucose 50 mL (25 g) intravenously over 10–15 minutes; 20% glucose 125 mL or 10% glucose 250 mL deliver the same 25 g. It acts in 15–60 minutes (about a 1 mmol/L fall by 60 minutes) and lasts 4–6 hours.Doctor / Nurse
Guard against the hypoglycaemia that follows: measure capillary glucose at 15, 30 and 60 minutes and then hourly for at least 6 hours, keep further glucose available, and follow the bolus with a 10% glucose infusion if the pre-treatment glucose is below 7.0 mmol/L or the patient has chronic kidney disease, is malnourished or is not eating.
Step 3, nebulised salbutamol 10–20 mg in 4 mL of 0.9% sodium chloride over 10 minutes, given at the same time as the insulin because the mechanisms are different and the effects additive; it acts in 15–30 minutes and lasts 2–4 hours. Intravenous salbutamol 0.5 mg in 100 mL of 5% glucose over 15 minutes is rarely used.
Step 4, sodium bicarbonate only where there is significant metabolic acidosis: a 1.26% infusion for severe acidosis (pH below 6.9–7.1), or 8.4% 50–100 mmol intravenously slowly for emergency use only; onset 15–30 minutes, duration 1–2 hours. With a normal pH it achieves nothing.Doctor / NurseNot available at your setup — Arterial blood gas.
Step 5, remove potassium — ask early whether the patient is passing urine: if so give furosemide 40–160 mg intravenously with 0.9% sodium chloride to maintain volume (onset 0.5–2 hours); if not, no drug will remove potassium at the rate it is being generated and dialysis becomes the treatment.Doctor / Nurse
Gut binders (onset 1–7 hours, none of them an emergency treatment): sodium zirconium cyclosilicate 10 g orally up to three times daily (about 0.7 mmol/L per 10 g), patiromer 4.2–16.8 g once or twice daily, or polystyrene sulphonate resin 15 g orally three times daily with a laxative, or 30 g rectally.
Haemodialysis is definitive in oliguric acute kidney injury or established chronic kidney disease; the recognised indications for urgent dialysis are the AEIOU group — Acid–base disturbance, Electrolyte disturbance refractory to medical management, Intoxications, volume Overload unresponsive to diuretics, and Uraemic complications such as encephalopathy and pericarditis.Not available at your setup — Dialysis / renal replacement.
In every hyperkalaemic patient stop the cause: stop potassium supplements, potassium-containing fluids and salt substitutes; stop or suspend ACE inhibitors, ARBs, mineralocorticoid antagonists, amiloride, triamterene, NSAIDs, trimethoprim, heparin and calcineurin inhibitors, documenting why so they are not silently restarted; correct volume depletion; treat the acidosis; and catheterise or image the renal tract where obstruction is possible.
Re-dose to a timetable: the agents wear off in a predictable order — calcium at 30–60 minutes, salbutamol at 2–4 hours, insulin at 4–6 hours. Recheck the potassium at one hour and then at least two-hourly until it is falling and staying down, and immediately if the rhythm changes; if it remains at or above 6.0 mmol/L at 1–2 hours, repeat the insulin–glucose and salbutamol and reconsider removal rather than shifting.Not available at your setup — Serum electrolytes.
Children with hyperkalaemia (every dose needs an accurate weight): 10% calcium gluconate 0.5 mL/kg intravenously over 5 minutes (maximum 20 mL) for ECG change, repeated if changes persist; soluble insulin 0.1 unit/kg with 10% glucose 5 mL/kg intravenously over 30 minutes (0.5 g/kg glucose) with capillary glucose at 15, 30 and 60 minutes then hourly for 6 hours; nebulised salbutamol 2.5 mg if under 25 kg or 5 mg if 25 kg or over, over 10 minutes.Doctor / Nurse
Children, other measures: sodium bicarbonate 1 mmol/kg intravenously slowly (diluted 8.4%, or 1.26%) for documented significant acidosis only and never in the calcium line; calcium polystyrene sulphonate 0.5–1 g/kg orally or rectally up to four times daily with a laxative, avoided in ileus or obstruction.Doctor / Nurse
Hypokalaemia — oral replacement is the safest treatment for mild to moderate deficiency: withdraw the offending diuretic or purgative and give slow-release or effervescent potassium chloride; 20–40 mmol daily for dietary deficiency, 40–100 mmol/day over days to weeks for established hypokalaemia, replacing gradually over 24–48 hours with frequent monitoring to avoid overshoot into hyperkalaemia, given with food, using alkaline salts (potassium bicarbonate or citrate) where there is metabolic acidosis. For any patient on maintenance intravenous fluids add 20 mmol of potassium per litre and check potassium at least daily until 48 hours after supplementation stops.Not available at your setup — Serum electrolytes.
Hypokalaemia — intravenous replacement is reserved for a potassium below 3.0 mmol/L, cardiac arrhythmia, muscle weakness, severe diabetic ketoacidosis, or an unusable gut: dilute in 0.9% sodium chloride (0.45% acceptable), never in a glucose-containing solution, maximum 40 mmol/L in a peripheral vein, usual maximum rate 10 mmol/hour (10–15 mmol/hour peripherally with careful monitoring), up to 20 mmol/hour only with continuous cardiac monitoring, and below 2 mmol/hour in poor renal function with hourly potassium and ECG. Recheck potassium after every 20–40 mmol given.Doctor / NurseNot available at your setup — Infusion pump.
Replace magnesium in every hypokalaemic patient: magnesium sulphate 2 g (8 mmol) in 100 mL of 0.9% sodium chloride intravenously over 20 minutes for symptomatic or arrhythmia-associated deficiency, or over 1–2 hours if the patient is not arrhythmic, with dose reduction and close monitoring in renal impairment.Doctor / Nurse
Children with hypokalaemia: potassium chloride 2–4 mmol/kg/day orally in divided doses is the route of choice for almost every hypokalaemic child; if intravenous replacement is unavoidable give potassium chloride 0.5 mmol/kg (maximum 20 mmol) over 1–2 hours in 0.9% sodium chloride with continuous cardiac monitoring, never in a glucose-only solution and never above adult maximum rates.Doctor / Nurse

Caution— what harms

Never give concentrated potassium chloride as a bolus — it is the classic fatal drug error of hospital medicine and causes cardiac arrest. Use pre-mixed bags; if an ampoule must be added, invert the bag at least ten times, label it with the total potassium content, and have a second person check it.
Never give potassium in a glucose-containing solution — dextrose stimulates insulin release and drives the potassium further down.
Where sources diverge on infusion rate, take the slower option unless the patient is arrhythmic in front of you: the commonest fatal error in this topic is giving potassium too fast, and over-rapid replacement causes iatrogenic hyperkalaemia and phlebitis. Concentrations above 40 mmol/L cause pain and phlebitis and need central access.Not available at your setup — Infusion pump.
Calcium does not change the potassium concentration — an unchanged result after giving it is expected and is not treatment failure. It only buys the 30–60 minutes in which everything else works.
Never give calcium through a line that has just carried sodium bicarbonate and never mix the two — calcium carbonate precipitates and obstructs the cannula; calcium chloride extravasation causes tissue necrosis.
Salbutamol is the most commonly under-dosed drug in the sequence: the hyperkalaemia dose is 10–20 mg, four to eight times the airway dose of 2.5 mg. About one patient in five does not respond to beta-agonists at all, so salbutamol is never adequate as sole therapy; use it cautiously but do not withhold it in ischaemic heart disease or tachyarrhythmia, leaning instead on repeated insulin–glucose.
Hypoglycaemia is the commonest iatrogenic complication of hyperkalaemia treatment — it appears 1–2 hours later when the glucose bolus has been metabolised and the insulin has not, and is worse in renal impairment and malnutrition. Glucose alone is not a treatment in a non-diabetic patient: it does not generate the insulin concentrations required.
Sodium bicarbonate harms the wrong patient: 8.4% causes volume expansion from its sodium load and will precipitate pulmonary oedema in the fluid-overloaded anuric patient; it may be ineffective in end-stage kidney disease. Prefer the dilute 1.26% solution where available.
No gut binder is an emergency treatment. Polystyrene sulphonate resins may cause fluid overload (sodium salt) or hypercalcaemia (calcium salt), do not clearly increase excretion beyond the effect of the accompanying laxative, and are associated with colonic necrosis; the sodium salt is contraindicated in bowel obstruction and ileus.
In the patient who is not making urine, every drug given is a loan — shifting agents remove nothing from the body, and the potassium rebounds as insulin wears off at 4–6 hours. Only the kidney, gut binders and dialysis remove potassium.Not available at your setup — Dialysis / renal replacement.
In suspected digoxin toxicity calcium has traditionally been avoided for fear of provoking an intractable stone heart; modern evidence has largely failed to confirm this and opinion now favours giving it, diluted and slowly, where there are hyperkalaemic ECG changes — the definitive treatment being digoxin-specific antibody fragments rather than potassium-lowering therapy. What is not defensible is withholding calcium from a patient with a sine-wave ECG.
Never delay treatment to exclude pseudohyperkalaemia in a patient with ECG changes; equally, do not treat a spurious result — check the full blood count for thrombocytosis or leucocytosis and repeat the sample properly.
Redistributive hypokalaemia — periodic paralysis, theophylline toxicity, acute head injury — needs cautious replacement only, because the potassium returns to the extracellular compartment when the precipitant resolves, with a real risk of rebound hyperkalaemia; over-treatment of hyperkalaemia likewise produces rebound hypokalaemia.
Sequence acid–base correction correctly: in hypokalaemia with metabolic acidosis, potassium repletion takes precedence over alkali administration because correcting the acidosis shifts potassium into cells and lowers the extracellular concentration further; in diabetic ketoacidosis measure potassium before starting insulin, withhold it from the initial resuscitation fluid and whenever the potassium exceeds 5.5 mmol/L, add 40 mmol/L once the potassium lies between 3.5 and 5.5 mmol/L with adequate urine output, give additional replacement under continuous cardiac monitoring if it is below 3.5 mmol/L at presentation, and recheck at 1 hour, 2 hours and two-hourly thereafter, holding the potassium between 4.0 and 5.5 mmol/L.Not available at your setup — Serum electrolytes, Arterial blood gas.
Do not skip the monitoring: continuous cardiac monitoring for any potassium infusion above 10 mmol/hour, any potassium below 2.5 mmol/L, and any patient on digoxin; recheck potassium hourly to two-hourly after emergency hyperkalaemia treatment. Hypokalaemia in patients without cardiac disease is unlikely to cause serious arrhythmia, but with structural heart disease, recent infarction or digoxin it is genuinely dangerous.

Refer / escalate

Escalate urgently and arrange dialysis or transfer for any hyperkalaemic patient who is oliguric or anuric, has a potassium of 6.5 mmol/L or more, has any ECG change or a rapidly rising trend, or whose potassium remains at or above 6.0 mmol/L one to two hours after insulin–glucose and salbutamol; and for any hypokalaemic patient with arrhythmia, respiratory muscle weakness, a potassium below 2.5 mmol/L, or hypokalaemia on digoxin.

The card — assess, manage, caution

Disorders of potassium: hyperkalaemia and hypokalaemia — Level 1: CorePrevious Disorders of potassium: hyperkalaemia and hypokalaemia — Level 3: Core practiceNext

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