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.
Key points
- Mild 5.5–5.9, moderate 6.0–6.4, severe ≥6.5 mmol/L. Life-threatening if ECG changes present at ANY level
- ECG changes (progressive): tall tented T waves → flat P waves → widened QRS → sine wave → VF/asystole
- STEP 1 (cardiac protection): IV calcium gluconate 10% — 30 mL (3 ampoules) over 10 min with cardiac monitoring. Repeat if ECG changes persist
- STEP 2 (shift K⁺ into cells): insulin 10 units + 25 g glucose (50 mL of 50% or 125 mL of 20%) IV over 15 min. Also: salbutamol 10–20 mg nebulised
- STEP 3 (remove K⁺ from body): calcium resonium 15–30 g PO/PR, sodium zirconium cyclosilicate (Lokelma), or haemodialysis (definitive)
- Common causes: AKI/CKD, ACEi/ARB/spironolactone, rhabdomyolysis, tumour lysis, Addison's, massive transfusion, haemolysis (artefactual)
Overview
Hyperkalaemia is defined as a serum potassium above 5.5 mmol/L. It is a common and potentially life-threatening electrolyte emergency that can cause fatal cardiac arrhythmias. The most common causes are reduced renal excretion (AKI, CKD, obstructive uropathy), drugs that impair potassium excretion (ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs), and potassium release from cells (rhabdomyolysis, tumour lysis syndrome, haemolysis, burns, metabolic acidosis). Addison's disease causes hyperkalaemia from aldosterone deficiency. Pseudohyperkalaemia (artefactual elevation from haemolysis during blood draw, prolonged tourniquet time, or high WCC/platelet count) must be excluded before initiating treatment.
Epidemiology
Hyperkalaemia is one of the most common electrolyte abnormalities encountered in hospital practice, particularly in patients with renal impairment. Serum potassium >6.0 mmol/L is found in approximately 1–10% of hospitalised patients. It is the most common electrolyte cause of cardiac arrest. Risk is highest in patients on combination therapy with ACEi/ARB + spironolactone + NSAID (the "triple whammy") or those with AKI/CKD. Hyperkalaemia-related mortality is significant — severe hyperkalaemia with ECG changes carries immediate risk of cardiac arrest if untreated.
Clinical Features
Symptoms
Often asymptomatic — detected on routine bloods or ECG monitoring
Muscle weakness (may progress to flaccid paralysis)
Paraesthesiae
Palpitations (from arrhythmias)
Nausea, vomiting, diarrhoea
Cardiac arrest (VF or asystole) — may be the first presentation
Signs
ECG changes (in order of severity): tall tented T waves (earliest) → prolonged PR → flat/absent P waves → widened QRS → sine wave pattern → VF/asystole
Bradycardia or heart block
Hypotension (in severe cases)
Reduced or absent deep tendon reflexes
Muscle weakness (ascending, may mimic Guillain-Barré)
Investigations
First-line
Serum potassiumConfirm on venous blood gas (rapid) or laboratory sample. Exclude pseudohyperkalaemia (haemolysed sample — request repeat if suspected)
12-lead ECGAssess for changes: tented T waves, PR prolongation, QRS widening, sine wave. ECG changes mandate IMMEDIATE treatment regardless of K⁺ level
Second-line
U&Es, creatinine, eGFRAssess renal function — AKI/CKD is the commonest cause
Venous blood gasRapid K⁺ result, pH (acidosis worsens hyperkalaemia by shifting K⁺ out of cells), lactate
Blood glucoseCheck BEFORE insulin-dextrose (risk of hypoglycaemia). Monitor hourly for 6 h after insulin
Drug reviewACEi, ARB, spironolactone, eplerenone, amiloride, trimethoprim, NSAIDs, potassium supplements
Specialist
CKIf rhabdomyolysis suspected (trauma, crush injury, statins, prolonged immobility)
Cortisol / Synacthen testIf Addison's disease suspected (hyperkalaemia + hyponatraemia + hypotension + hyperpigmentation)
1
Step 1: Cardiac membrane stabilisation (if ECG changes or K⁺ ≥6.5)
- IV calcium gluconate 10%: 30 mL (3 × 10 mL ampoules) over 10 min with continuous cardiac monitoring
- This does NOT lower potassium — it stabilises the myocardium and protects against arrhythmias
- Onset: 1–3 min. Duration: 30–60 min. Repeat if ECG changes persist after 5 min
- Use calcium chloride (10 mL of 10%) if via central line — more rapid but caustic peripherally
2
Step 2: Shift potassium into cells (temporising measures)
- Insulin 10 units actrapid + 25 g glucose IV (50 mL of 50% dextrose via large vein or 125 mL of 20% dextrose) over 15 min
- Onset: 15–30 min. Duration: 4–6 h. Lowers K⁺ by ~0.5–1.0 mmol/L
- MUST monitor blood glucose hourly for 6 hours post-insulin (risk of hypoglycaemia — especially in CKD)
- If starting glucose >15 mmol/L: give insulin without glucose
- Salbutamol 10–20 mg nebulised: onset 15–30 min. Lowers K⁺ by ~0.5 mmol/L. Additive with insulin. Caution in IHD/tachycardia
- Sodium bicarbonate 8.4%: 50 mL IV over 10–20 min — ONLY if concurrent acidosis (pH <7.2). Not routine
3
Step 3: Remove potassium from the body
- Sodium zirconium cyclosilicate (Lokelma) 10 g PO TDS: potassium binder, onset 1 h. Preferred over calcium resonium
- Calcium resonium (polystyrene sulfonate) 15–30 g PO/PR: older binder, onset 4–24 h. Risk of GI necrosis — declining use
- Haemodialysis: definitive treatment for severe/refractory hyperkalaemia, especially in AKI/CKD. Most effective method
- Loop diuretic (furosemide 40–80 mg IV): if patient is not anuric — promotes renal K⁺ excretion
4
Ongoing management
- Stop/reduce causative drugs (ACEi, ARB, spironolactone, K⁺ supplements)
- Treat underlying cause: AKI, obstruction, Addison's, rhabdomyolysis
- Recheck K⁺ at 1, 2, 4, 6, and 24 hours. Repeat ECG
- Dietary potassium restriction (avoid bananas, oranges, potatoes, tomatoes, chocolate)
- Monitor blood glucose post-insulin for minimum 6 hours
Complications
- Cardiac arrest: VF or asystole — the most feared complication. Can occur rapidly without warning
- Bradycardia and heart block: AV block, complete heart block from impaired cardiac conduction
- Hypoglycaemia: After insulin-dextrose — must monitor glucose for 6 h. More common in CKD (reduced insulin clearance)
- Rebound hyperkalaemia: Temporising measures (insulin, salbutamol) only shift K⁺ intracellularly. It will return unless removed or cause treated
UKMLA Exam Tips
- 1ECG change progression: tall tented T → flat P → wide QRS → sine wave → VF/arrest. Know this sequence perfectly
- 2Calcium gluconate does NOT lower K⁺ — it stabilises the heart. First-line if ECG changes are present
- 3Insulin-dextrose: most effective temporising measure. ALWAYS give glucose with insulin (unless BG >15) and monitor for 6 h
- 4Salbutamol nebulised: useful adjunct to insulin-dextrose (additive K⁺ lowering). Use cautiously in cardiac patients
- 5"Triple whammy": ACEi + spironolactone + NSAID = high risk of hyperkalaemia. Classic prescribing error question
- 6Pseudohyperkalaemia: haemolysed sample, tight tourniquet, high WCC/platelets. Repeat sample before treating if clinically well with normal ECG
- 7Dialysis is the ONLY definitive way to remove potassium from the body in anuric patients
Put your reading into practice
Topic-specific question practice is not linked for this article yet.
Choose UKMLA questions from the existing bank. General exam practice covers your selected topics; it is not filtered to this article. Your usual question-bank access applies.
Choose UKMLA practiceAfter your session, return to this section to revisit the reading and choose your next review.
Verified Sources & References
related resources
Save your place and choose what comes next
Emergency Medicine · Article 5 of 13