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Level 1 of 6Core

Disorders of potassium: hyperkalaemia and hypokalaemia

The core to-do list — diagnose and manage, at a glance

Diagnose— recognise it

  • Neither hyperkalaemia nor hypokalaemia has reliable clinical signs — the most important single statement on the subject: normal plasma potassium is 3.5–5.0 mmol/L, more than 98% of body potassium is inside cells, and severe hyperkalaemia may be entirely asymptomatic. You diagnose by sending the sample and looking at the ECG.
  • The thresholds that change what you do: potassium 6.5 mmol/L triggers emergency treatment irrespective of symptoms; 7.0 mmol/L is a medical emergency associated with ECG change and asystolic arrest. Hypokalaemia is below 3.5 mmol/L — mild 3.0–3.4, moderate 2.5–2.9, severe below 2.5, where weakness, flaccid paralysis, rhabdomyolysis and serious arrhythmia become expected.
  • Take a 12-lead ECG in every patient, interpret it personally, and repeat it after treatment. Hyperkalaemia: tented T waves, then P-wave loss with PR prolongation, then QRS widening, then a sine wave — a pre-arrest pattern. Hypokalaemia: T-wave flattening, ST depression, prominent U waves (most marked below 2.7 mmol/L). The ECG may be normal despite life-threatening hyperkalaemia — a potassium of 6.5 mmol/L or more without ECG changes is still managed aggressively. Use the ECG to escalate, never to reassure.
  • The rate of change determines toxicity as much as the absolute value (a dialysis patient at 6.2 mmol/L is far less endangered than a crush victim who climbed from 4.0 to 6.8 in six hours) — and reading the drug chart is the highest-yield diagnostic act: ACE inhibitors, ARBs, NSAIDs, spironolactone, amiloride, trimethoprim and their combinations raise potassium; diuretics, purgatives and potassium-free fluids lower it.
  • A blood-gas potassium returns within minutes — treat a gas-machine value as real until the laboratory contradicts it, sending a laboratory sample in parallel; add urea, creatinine and electrolytes, and serum magnesium in every hypokalaemic patient. Consider pseudohyperkalaemia (well patient, normal ECG, haemolysis flag, marked thrombocytosis or leucocytosis) — but never delay treatment for it in a patient with ECG changes.Not available at your setup — Arterial blood gas, Serum electrolytes.
  • Danger signs: in hyperkalaemia — any ECG change, muscle weakness, oliguria or anuria, potassium 6.5 mmol/L or more, a rapidly rising trend; in hypokalaemia — arrhythmia, concurrent digoxin, respiratory muscle weakness, potassium below 2.5 mmol/L.

Manage now— 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.
  • Calcium to protect the myocardium where there are ECG changes: 10% calcium gluconate 10 mL IV over 5 minutes, repeated every 15 minutes until the ECG improves (total 5–30 mL); onset 0–5 minutes, lasts only 30–60 minutes — repeat if the QRS re-widens. Child: 0.5 mL/kg over 5 minutes, max 20 mL. Calcium does not change the potassium concentration — an unchanged result is expected, not failure. Never give it through a line that has carried sodium bicarbonate.Doctor / Nurse
  • Soluble insulin with glucose, always together: insulin 10 units with 50% glucose 50 mL (25 g) IV over 10–15 minutes (20% glucose 125 mL or 10% glucose 250 mL deliver the same 25 g); acts in 15–60 minutes, lasts 4–6 hours. Measure capillary glucose at 15, 30 and 60 minutes then hourly for at least 6 hours — hypoglycaemia at 1–2 hours is the commonest iatrogenic complication. Child: insulin 0.1 unit/kg with 10% glucose 5 mL/kg over 30 minutes.Doctor / Nurse
  • Nebulised salbutamol 10–20 mg in 4 mL of 0.9% sodium chloride over 10 minutes, given at the same time as the insulin (different mechanisms, additive effects); acts in 15–30 minutes, lasts 2–4 hours. This is four to eight times the airway dose of 2.5 mg — the most commonly under-dosed drug in the sequence — and about one patient in five does not respond, so it is never sole therapy. Child: 2.5 mg if under 25 kg, 5 mg if 25 kg or over.
  • Remove potassium — ask early whether the patient is passing urine: if so, furosemide 40–160 mg IV with 0.9% sodium chloride to maintain volume (onset 0.5–2 hours); if not, no drug will remove potassium fast enough and dialysis becomes the treatment. Gut binders (onset 1–7 hours, none an emergency treatment): sodium zirconium cyclosilicate 10 g orally up to three times daily, patiromer 4.2–16.8 g, or polystyrene sulphonate 15 g orally three times daily with a laxative. In a patient not making urine, every shifting drug is a loan.Doctor / NurseNot available at your setup — Dialysis / renal replacement. No dialysis on site: repeat insulin–glucose and salbutamol to the timetable and arrange urgent transfer — shifting agents remove nothing and the potassium rebounds at 4–6 hours.
  • Re-dose to a timetable and stop the cause: calcium wears off at 30–60 minutes, salbutamol at 2–4 hours, insulin at 4–6 hours. Recheck potassium at 1 hour then at least two-hourly, and immediately if the rhythm changes; if still at or above 6.0 mmol/L at 1–2 hours, repeat insulin–glucose and salbutamol and reconsider removal. Stop potassium supplements and salt substitutes; suspend ACE inhibitors, ARBs, mineralocorticoid antagonists, NSAIDs, trimethoprim (documenting why); correct volume depletion; catheterise or image the renal tract where obstruction is possible.
  • 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 monitoring to avoid overshoot. For any patient on maintenance IV fluids add 20 mmol potassium per litre and check potassium at least daily. Children: potassium chloride 2–4 mmol/kg/day orally in divided doses.
  • IV potassium only for potassium below 3.0 mmol/L, arrhythmia, muscle weakness, severe DKA or an unusable gut: dilute in 0.9% sodium chloride — never in a glucose-containing solution — max 40 mmol/L in a peripheral vein, usual max rate 10 mmol/hour, up to 20 mmol/hour only with continuous cardiac monitoring, below 2 mmol/hour in poor renal function. Recheck after every 20–40 mmol. Never give concentrated potassium chloride as a bolus — the classic fatal drug error of hospital medicine. Use premixed bags; if an ampoule must be added, invert the bag at least ten times, label it and have a second person check.Doctor / Nurse
  • Replace magnesium in every hypokalaemic patient — failure to correct hypokalaemia is very often hypomagnesaemia: magnesium sulphate 2 g (8 mmol) in 100 mL of 0.9% sodium chloride IV over 20 minutes for symptomatic or arrhythmia-associated deficiency, over 1–2 hours if not arrhythmic, with dose reduction in renal impairment.Doctor / Nurse

Emergency hyperkalaemia sequence — onset and duration

StepDoseOnset / duration
10% calcium gluconate10 mL IV over 5 min, repeat q15min (total 5–30 mL)0–5 min / 30–60 min
Insulin + glucoseInsulin 10 units + 50% glucose 50 mL (25 g) over 10–15 min15–60 min / 4–6 h
Nebulised salbutamol10–20 mg in 4 mL saline over 10 min15–30 min / 2–4 h
Furosemide (if passing urine)40–160 mg IV with 0.9% saline0.5–2 h
Gut binders / dialysisNot emergency treatment / definitive if oliguric1–7 h / —

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, 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.

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