About This Page
This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- K⁺ >5.5 mmol/L = hyperkalaemia. >6.5 mmol/L or ECG changes = SEVERE — immediate treatment required
- Commonest causes: AKI/CKD, ACEi/ARBs, potassium-sparing diuretics (spironolactone), NSAIDs, adrenal insufficiency, rhabdomyolysis, metabolic acidosis
- ECG changes (progressive): tall tented T waves → flattened P waves → widened QRS → sine wave → VF/cardiac arrest
- Emergency treatment: 1) IV calcium gluconate 10% 10 mL (cardioprotection — stabilises myocardium), 2) insulin 10 U + glucose 50 mL 50% (shifts K⁺ intracellularly), 3) nebulised salbutamol
- Definitive: treat cause, stop K⁺-retaining drugs, calcium resonium/sodium zirconium cyclosilicate (oral K⁺ binders), dialysis if refractory
Overview
Hyperkalaemia is defined as a serum potassium concentration >5.5 mmol/L. It is one of the most dangerous electrolyte disturbances because of its potential to cause lethal cardiac arrhythmias. Potassium homeostasis depends on renal excretion (~90%), with cellular uptake regulated by insulin and catecholamines. Causes include reduced renal excretion (AKI, CKD, drugs — ACEi, ARBs, spironolactone, NSAIDs), increased cellular release (rhabdomyolysis, tumour lysis syndrome, haemolysis, acidosis, burns), and excessive intake (rarely). Pseudohyperkalaemia (artefactual) from haemolysed samples or prolonged tourniquet time is common and must be excluded.
Epidemiology
Hyperkalaemia occurs in approximately 1–10% of hospitalised patients. It is the commonest lethal electrolyte disturbance. Risk is highest in patients with CKD (especially stages 4–5), those on ACEi/ARB + spironolactone combinations, and in AKI. Drug-induced hyperkalaemia accounts for a significant proportion of cases. It is a major contributor to cardiac arrest in renal patients.
Clinical Features
Symptoms
Often asymptomatic — detected on blood tests
Muscle weakness (especially lower limbs, can progress to paralysis)
Paraesthesiae (tingling)
Palpitations
Nausea, vomiting, diarrhoea
Cardiac arrest (VF or asystole) — may be the first presentation in severe hyperkalaemia
Signs
May have no abnormal signs
Muscle weakness or flaccid paralysis
Bradycardia or irregular pulse
Hyporeflexia
Investigations
First-line
Serum potassium (venous blood gas for rapid result)Mild: 5.5–5.9 mmol/L. Moderate: 6.0–6.4 mmol/L. Severe: ≥6.5 mmol/L or ANY level with ECG changes
12-lead ECGURGENT — assess for hyperkalaemic changes. Progressive: tall tented T waves (earliest) → loss of P waves → prolonged PR → widened QRS → sine wave pattern → VF/asystole
Exclude pseudohyperkalaemiaHaemolysed sample, prolonged tourniquet, thrombocytosis, leucocytosis. If in doubt, repeat sample with free-flowing venepuncture
Second-line
U&EsRenal function (AKI/CKD), sodium, bicarbonate (acidosis drives K⁺ out of cells)
VBG/ABGRapid potassium + acid-base status. Acidosis causes extracellular K⁺ shift
Medication reviewACEi, ARB, spironolactone, amiloride, trimethoprim, NSAIDs, potassium supplements, digoxin
CKIf rhabdomyolysis suspected (crush injury, collapse, statins + acute illness)
Specialist
Cortisol/ACTHIf adrenal insufficiency suspected (Addison disease: hyperkalaemia + hyponatraemia + hypotension + hyperpigmentation)
1
Immediate — severe hyperkalaemia (≥6.5 or ECG changes)
- 1. CARDIOPROTECTION: IV calcium gluconate 10% 30 mL (3 × 10 mL) over 5–10 minutes. Does NOT lower potassium — stabilises cardiac membrane. Repeat ECG after 5 min; may repeat dose
- 2. SHIFT K⁺ INTO CELLS: 10 units Actrapid insulin IV with 25 g glucose (50 mL 50% dextrose) over 15–30 min. Onset 15–30 min, lasts 4–6 h. Monitor BMs hourly for 6 hours (hypoglycaemia risk)
- 3. Nebulised salbutamol 10–20 mg (shifts K⁺ intracellularly — additive effect with insulin-dextrose)
- 4. Correct acidosis if pH <7.2: IV sodium bicarbonate 8.4% 50 mL (drives K⁺ into cells via H⁺/K⁺ exchange)
- 5. Cardiac monitoring throughout
2
Remove potassium from body
- Stop ALL potassium-retaining drugs (ACEi, ARB, spironolactone, NSAIDs, K⁺ supplements)
- Oral/rectal potassium binders: sodium zirconium cyclosilicate (Lokelma) — fast onset; or calcium resonium (slower)
- IV furosemide (40–80 mg) if adequate renal function — promotes urinary K⁺ excretion
- Dialysis: for refractory hyperkalaemia, especially in AKI/CKD or if life-threatening
3
Treat underlying cause
- AKI: IV fluids, relieve obstruction, treat sepsis
- Drug-induced: stop/switch offending agent
- Addison disease: IV hydrocortisone 100 mg stat
- DKA: insulin infusion (corrects K⁺ shift — but monitor as K⁺ may fall rapidly)
Complications
- Cardiac arrest: VF or asystole from severe hyperkalaemia — the most feared complication
- Fatal arrhythmias: Heart block, ventricular tachycardia, ventricular fibrillation
- Muscle paralysis: Ascending weakness — can affect respiratory muscles
- Iatrogenic hypoglycaemia: From insulin-dextrose treatment — must monitor glucose hourly for 6 hours
UKMLA Exam Tips
- 1ECG changes in order: tall tented T waves → flat P waves → wide QRS → sine wave → VF/asystole
- 2Calcium gluconate does NOT lower potassium — it STABILISES the myocardium. Always give first in severe hyperkalaemia
- 3Insulin-dextrose: SHIFT K⁺ into cells temporarily (4–6 h). Must also remove K⁺ from the body (binders, furosemide, dialysis)
- 4Classic drug combination causing hyperkalaemia: ACEi + spironolactone (both reduce K⁺ excretion). Very common exam scenario
- 5In DKA: total body potassium is LOW (renal losses), but serum K⁺ may be HIGH (acidosis shifts K⁺ out of cells). K⁺ falls rapidly with insulin — must replace aggressively
- 6Addison disease: hyperkalaemia + hyponatraemia + hypotension + hyperpigmentation — aldosterone deficiency
- 7Always check ECG BEFORE any clinical decision — the ECG changes determine urgency, NOT just the number
practicetest your knowledge on hyperkalaemiaApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — renal and beyond.
open q-bank