Hyperkalaemia Pharmacotherapy

Hyperkalaemia pharmacotherapy protects the heart, shifts potassium into cells and removes it from the body. Mild hyperkalaemia is 5.5 to 5.9 mmol/L, moderate 6.0 to 6.4 mmol/L and severe 6.5 mmol/L or more, or any level with ECG changes. Causes include kidney failure, drugs, adrenal insufficiency, tissue breakdown and acidosis.

Classification. Membrane stabilisers (calcium); shift agents (insulin with glucose, salbutamol, sodium bicarbonate); removal agents (loop diuretics, potassium binders, dialysis).

Mechanism. Calcium raises the threshold potential and protects against arrhythmia within minutes. Insulin and beta-agonists drive potassium into cells through the sodium-potassium pump. Binders trap potassium in the gut. Diuretics and dialysis remove it from the body.

Stop contributors. Hold ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs, trimethoprim, heparin and potassium supplements. Do not delay protection while repeating the blood test.

Treat the cause. Relieve obstruction, treat adrenal insufficiency (hydrocortisone), and restore volume.

• First-line. Calcium for ECG changes; insulin with glucose; salbutamol as an adjunct; then a binder or loop diuretic.
• Alternative. Binders alone for mild hyperkalaemia; low-potassium diet; loop or thiazide diuretics in chronic kidney disease.
• Specialist. Haemodialysis; long-term binders to continue renin-angiotensin blockers; fludrocortisone in hypoaldosteronism.
• Emergency. ECG changes (peaked T waves, wide QRS, loss of P waves, sine wave), arrhythmia, severe weakness.

Selection. Treat the heart first, shift next, remove last. Insulin with glucose is the most reliable shift therapy. Do not rely on bicarbonate alone.

Contraindications. Calcium in digoxin toxicity (caution; use slowly); insulin without glucose monitoring; resins and binders in bowel obstruction or ileus; salbutamol in severe tachyarrhythmia; bicarbonate in volume overload.

Serious adverse effects.

• Hypoglycaemia up to 6 hours after insulin, especially in kidney failure.
• Tachycardia and tremor with salbutamol; volume overload with bicarbonate.
• Gut ischaemia and necrosis with polystyrene resins; oedema and hypokalaemia with zirconium cyclosilicate.
• Constipation and low magnesium with patiromer.

Major interactions. Digoxin with calcium; beta-blockers blunt salbutamol; binders reduce absorption of other oral drugs (separate by 2 to 6 hours); insulin with sulfonylureas.

Common prescribing errors.

• Giving insulin without glucose, or without hourly glucose checks.
• Not giving calcium when the ECG is abnormal.
• Treating only the number and not the cause.
• Giving potassium-containing fluids to a hyperkalaemic patient.
• Failing to repeat potassium after treatment.

Special groups.

• Pregnancy: use the usual adult measures; avoid resins if possible.
• Breastfeeding: compatible.
• Children: weight-based dosing; seek paediatric advice.
• Older adults: more at risk of hypoglycaemia and arrhythmia.
• Kidney: the commonest cause; halve insulin dose and plan dialysis early.
• Liver: monitor glucose closely.
• East Africa: sodium zirconium cyclosilicate and patiromer are costly and usually not stocked, and calcium resonium may be the only binder; dialysis may be distant, so move the patient early; hyperkalaemia from trimethoprim-sulfamethoxazole and from tissue breakdown is a plausible exposure.

Monitoring. Continuous ECG, potassium at 1, 2, 4 and 6 hours, glucose hourly for 6 hours, urine output, creatinine and blood gas.

Referral and escalation. ECG changes, potassium over 6.5 mmol/L, oliguria, failure to respond, or need for dialysis.

Comparison with alternative classes. Calcium works fastest but does not lower potassium. Insulin and salbutamol shift potassium for hours. Binders and dialysis are the only ways to remove it.