Hyperkalaemia

Hyperkalaemia is a serum potassium above the reference range, and is one of the few electrolyte abnormalities capable of causing cardiac arrest within minutes.

Severity is conventionally graded as mild (5.5–5.9 mmol/L), moderate (6.0–6.4 mmol/L) and severe (≥6.5 mmol/L, or any level with ECG changes), though the rate of rise and the presence of ECG changes matter more than the number alone.

Causes fall into three groups: reduced excretion (acute kidney injury, chronic kidney disease, ACE inhibitors and ARBs, potassium-sparing diuretics, NSAIDs, trimethoprim, hypoaldosteronism), transcellular shift (metabolic acidosis, insulin deficiency, beta-blockers, digoxin toxicity, rhabdomyolysis, tumour lysis) and increased intake (supplements, transfusion of stored blood), usually only significant when excretion is already impaired.

• ECG is the most important immediate investigation and should be obtained before waiting for confirmatory bloods in any patient with suspected hyperkalaemia. The classic progression is: tall, peaked T waves → flattening and loss of P waves → PR prolongation → widening QRS → sine wave pattern → ventricular fibrillation or asystole. However, ECG changes correlate imperfectly with potassium level, and their absence does not make a high potassium safe
• Serum potassium, urea and creatinine, bicarbonate and glucose
• Exclude pseudohyperkalaemia before treating an unexpected result in a well patient with a normal ECG, particularly if there was a difficult venepuncture, a tourniquet held long, fist clenching, or a markedly raised white cell or platelet count
• Venous blood gas gives a rapid potassium result while awaiting the laboratory value, and simultaneously assesses acid-base status
• Review medications systematically, since drug-induced hyperkalaemia is common and frequently multifactorial — an ACE inhibitor plus spironolactone plus an NSAID in a patient with declining renal function is a familiar and preventable combination
• Consider digoxin toxicity, rhabdomyolysis (creatine kinase) and adrenal insufficiency where the picture fits

Treatment follows three sequential aims: protect the heart, shift potassium into cells, then remove it from the body. The first two buy time; only the third actually lowers total body potassium.

1. Cardiac protection:

• Intravenous calcium (calcium gluconate 10% 10–30 mL, or calcium chloride via central access) for any ECG changes or potassium ≥6.5 mmol/L. It does not lower potassium but stabilises the myocardium within minutes. The dose can be repeated if ECG changes persist
• Calcium is given with more caution in digoxin toxicity, though the historical concern about precipitating irreversible cardiac arrest is now considered overstated

2. Shift potassium intracellularly:

• Insulin with glucose: typically 10 units of soluble insulin in 25 g of glucose intravenously, lowering potassium by roughly 0.6–1.0 mmol/L over 15–30 minutes. Hypoglycaemia is the commonest complication and often occurs late, so glucose must be monitored for several hours afterwards and a glucose infusion considered
• Nebulised salbutamol (10–20 mg) as an adjunct, additive to insulin, though tachycardia limits its use in ischaemic heart disease
• Sodium bicarbonate has a limited role, and is reserved for significant metabolic acidosis rather than used routinely

3. Remove potassium:

• Loop diuretics with adequate volume status
• Potassium binders: sodium zirconium cyclosilicate or patiromer, which are effective and better tolerated than older resins and have made outpatient management of chronic hyperkalaemia considerably more feasible
• Haemodialysis is definitive, and is indicated in severe or refractory hyperkalaemia, established kidney failure, or where potassium continues to rise despite medical therapy

Alongside: stop all contributing drugs and potassium supplements, treat the underlying cause, and recheck potassium within 1–2 hours since shifting agents wear off and rebound is common. A patient treated with insulin and salbutamol alone, without removal, will frequently rise again.

Referral: nephrology urgently for refractory hyperkalaemia or where dialysis may be needed; critical care for arrhythmia or haemodynamic instability.