The ECG is widely treated as the arbiter of whether a raised potassium needs urgent treatment, and it is not reliable enough for that role. A substantial proportion of patients with potassium above 6.5 mmol/L have no diagnostic ECG change, and peaked T waves are neither sensitive nor specific — tall T waves are common in healthy young people and absent in many patients heading for arrest.
What actually predicts danger is the rate of rise and the context. A dialysis patient at 6.8 who lives between 5.5 and 6.5 is in a different position from a patient with acute kidney injury who was 4.2 yesterday. Ask when the last potassium was and what it was.
Treat on the number and the trajectory. Calcium gluconate or chloride stabilises the myocardium and does nothing to the potassium; insulin with glucose and a nebulised beta-agonist shift it; only dialysis, a binder or renal excretion remove it. The commonest error is stopping after the shifting agents and not arranging removal — potassium shifted intracellularly comes back within a few hours, usually after the team has changed over.
- Do not use a normal ECG to downgrade urgency in a potassium above 6.5 mmol/L.
- Ask for the previous potassium and its date — the rate of rise matters more than the absolute value.
- Give calcium first if there are any ECG changes; it buys time and does not lower potassium.
- Always plan removal, not just shifting, and hand over the recheck time explicitly.
- Stop the contributors: ACE inhibitors, ARBs, spironolactone, trimethoprim, NSAIDs and potassium-containing salt substitutes.
Why it matters
The ECG is routinely used to decide how urgent a raised potassium is, and it is not a test that can carry that decision.
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