Hyperkalaemia is a perennial exam favourite because it combines ECG interpretation, a clear emergency protocol and a long list of drug causes — all testable in a single vignette. This guide covers the essentials as examiners frame them, to the current UK Kidney Association (UKKA) standard. Follow local protocols and current guidance in practice; figures reflect UKKA guidance as of mid-2026.
Definition and severity
Hyperkalaemia is a serum potassium above the normal range, graded by the UKKA as mild (5.5 to 5.9 mmol/L), moderate (6.0 to 6.4 mmol/L) and severe (6.5 mmol/L or above). Severity guides urgency, but the presence of ECG changes escalates any level to an emergency.
Why it matters and how it presents
Potassium sets the resting membrane potential, so a high level destabilises cardiac conduction and can cause fatal arrhythmias. Patients are often asymptomatic, or report only non-specific weakness, so it is frequently found on bloods rather than clinically — which is why the ECG and the potassium value drive management. The danger is disproportionate to the symptoms: a patient can feel almost well with a potassium high enough to cause cardiac arrest. Causes cluster into three groups that examiners expect you to be able to list: reduced excretion (acute kidney injury and chronic kidney disease, the commonest setting; Addison's disease; and the drugs noted below), a shift of potassium out of cells (acidosis, including DKA; tissue breakdown such as rhabdomyolysis, tumour lysis or extensive burns; and insulin deficiency), and, more rarely, a genuinely increased intake — usually only when excretion is already impaired.
The ECG
Examiners expect the classic progression, roughly in order of rising potassium: tall, tented T waves first; then flattening and loss of P waves with PR prolongation; then widening of the QRS complex; and finally a sine-wave pattern preceding ventricular fibrillation or asystole. Any of these changes makes hyperkalaemia a cardiac emergency regardless of the number. A normal ECG does not exclude dangerous hyperkalaemia, and the changes do not always appear in a neat sequence — so the potassium value and the ECG are interpreted together, and treatment of a high value is not deferred simply because the trace looks unremarkable. Bradyarrhythmias and conduction block can also occur.
Management to the UKKA standard
Think in three steps: protect the heart, shift potassium into cells, and remove potassium from the body.
Protect the heart: in cardiac arrest, peri-arrest, or any patient with ECG changes, give intravenous calcium — commonly 30 mL of 10% calcium gluconate over 10 minutes with cardiac monitoring, repeated if the changes persist. Calcium stabilises the myocardium within minutes but does not lower potassium — a point examiners test directly. Calcium chloride is an alternative in haemodynamic instability; use caution in patients taking digoxin. Calcium must not be given through a line containing bicarbonate, as it precipitates, and its protective effect lasts only 30 to 60 minutes, so the potassium-shifting and potassium-removing steps must follow promptly.
Shift potassium into cells: the mainstay is an insulin–glucose infusion — 10 units of soluble insulin in 25 g of glucose — for moderate and severe hyperkalaemia, followed by a 10% glucose infusion to prevent the delayed hypoglycaemia this commonly causes. Nebulised salbutamol (10 to 20 mg) is a useful adjunct but should not be used as the sole treatment, as a proportion of patients do not respond to it.
Remove potassium: stop the offending drugs and potassium sources, treat the underlying cause, and consider a potassium binder such as sodium zirconium cyclosilicate. Definitive removal — dialysis — is needed for severe or refractory hyperkalaemia, especially in established renal failure. Throughout, the cause is treated in parallel: rehydration and treatment of any acute kidney injury, correction of acidosis, and review of every contributing drug. Mild hyperkalaemia without ECG changes can often be managed by addressing the cause and the diet alone, reserving the emergency protocol for moderate or severe levels and for any ECG change. Sodium bicarbonate is not recommended for routine treatment.
High-yield exam points and traps
- Calcium is cardioprotective, not potassium-lowering: it buys time, while insulin–glucose and salbutamol actually shift potassium.
- Pseudohyperkalaemia: a haemolysed or delayed sample can give a spuriously high result — repeat before treating an asymptomatic patient with a normal ECG. Common causes of a spurious result include a difficult or prolonged venepuncture, a delay in the sample reaching the laboratory, and a very high platelet or white cell count.
- Drug causes are heavily tested: ACE inhibitors and ARBs, potassium-sparing diuretics (spironolactone, eplerenone, amiloride), NSAIDs, trimethoprim, and potassium supplements or salt substitutes.
- Delayed hypoglycaemia after insulin–glucose is common — monitor capillary glucose for several hours afterwards.
- Salbutamol is an adjunct, not monotherapy.
- The shifting agents are temporary, so the potassium can rebound and require repeat treatment or definitive removal.
- The ECG, not just the number, dictates urgency.
A few common questions
What potassium level counts as severe hyperkalaemia? 6.5 mmol/L or above, per the UKKA; 5.5 to 5.9 is mild and 6.0 to 6.4 is moderate — but ECG changes escalate any level.
Does calcium lower potassium? No — intravenous calcium stabilises the myocardium and protects against arrhythmia but does not reduce the potassium level; insulin–glucose and salbutamol do that.
What is the immediate treatment for hyperkalaemia with ECG changes? Intravenous calcium to protect the heart, followed immediately by an insulin–glucose infusion to shift potassium into cells.
What are the common ECG changes? Tented T waves, then flattened or absent P waves and a widened QRS, progressing to a sine wave and arrest.
What are the main causes of hyperkalaemia? Reduced renal excretion (acute or chronic kidney injury, Addison's disease, certain drugs), a shift of potassium out of cells (acidosis, tissue breakdown such as rhabdomyolysis or tumour lysis), and, rarely, excessive intake when excretion is already impaired. Always check whether an unexpected result fits the clinical picture, as a spurious reading is common.
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