The potassium comes back at 7.1 mmol/L. Is it real? Is the patient about to arrest? What do you give first — and why does the first drug not lower potassium at all?
Hyperkalaemia (spelled hyperkalemia in the US) is one of the few lab results that can kill within minutes, and it's a favourite in exams and on call. This guide walks through it in the order you'd actually think on the ward: confirm it, check the EKG, protect the heart, shift potassium into cells, then remove it.
What counts as hyperkalaemia?
| Severity (adult, common UK/international grading) | Serum K⁺ |
|---|---|
| Normal | 3.5–5.0 mmol/L (lab-dependent) |
| Mild | 5.5–5.9 mmol/L |
| Moderate | 6.0–6.4 mmol/L |
| Severe | ≥ 6.5 mmol/L |
Any level with EKG changes is treated as an emergency, whatever the number.
First: is it real? (pseudohyperkalaemia)
A haemolysed sample, a delayed sample, a tight tourniquet with fist clenching, or very high white cell or platelet counts can falsely raise potassium. If the patient is well and the EKG is normal, repeat urgently — but never delay treatment in an unwell patient or one with EKG changes while waiting for a repeat. A blood gas gives a fast potassium.
Hyperkalaemia EKG changes (in order)
| Stage | EKG change |
|---|---|
| Early | Tall, narrow, peaked T waves |
| Progressing | PR prolongation, flattened or absent P waves |
| Severe | QRS widening, bradycardia, conduction blocks |
| Pre-arrest | Sine-wave pattern → VF, asystole or PEA |
Two important points: the EKG does not reliably match the potassium level (a patient can have a high K⁺ and a near-normal EKG), and changes can jump stages quickly. For a full approach to reading the trace, see our step-by-step EKG guide.
Causes of hyperkalaemia
Reduced excretion
- Acute kidney injury and chronic kidney disease
- Drugs: ACE inhibitors, ARBs, spironolactone and other potassium-sparing diuretics, trimethoprim, NSAIDs, heparin, calcineurin inhibitors
- Hypoaldosteronism, including Addison's disease
Shift out of cells
- Diabetic ketoacidosis and other metabolic acidosis (insulin deficiency)
- Tissue breakdown: rhabdomyolysis, tumour lysis syndrome, burns, haemolysis
- Drugs: non-selective beta-blockers, digoxin toxicity, suxamethonium
Increased intake
- Potassium supplements or IV potassium, usually only significant when excretion is also impaired
Beta-blockers appear here for a reason — they reduce potassium uptake into cells. More on their side effects in our beta-blocker cheat sheet. And because acidosis drives potassium out of cells, always look at the blood gas — see how to interpret an ABG.
Connect the dots between drugs, kidneys and the EKG
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See the Complete Edition – $59Emergency management of hyperkalaemia
Think in four steps: protect the heart, shift potassium into cells, remove potassium from the body, monitor. Treat with the patient on a cardiac monitor.
Management table (adult, standard textbook doses — check local protocol)
| Step | Treatment | Typical adult dose | Onset / duration | Key point |
|---|---|---|---|---|
| Protect the heart | Calcium gluconate 10% | 30 mL IV over 5–10 min (UK guidance); many US protocols give 10 mL (1 g) and repeat as needed | 1–3 min / 30–60 min | Stabilises the myocardium; does not lower K⁺. Give if EKG changes. Repeat if changes persist |
| Protect the heart | Calcium chloride 10% (alternative) | 10 mL IV, ideally via a central/large vein | 1–3 min / 30–60 min | About 3× the calcium of gluconate; irritant to veins |
| Shift K⁺ into cells | Insulin–dextrose | 10 units soluble (regular) insulin IV with 25 g glucose (e.g. 50 mL of 50% or 250 mL of 10%) | 15–30 min / 4–6 h | Main shifting treatment. Monitor glucose closely for at least 6 h — hypoglycaemia is common |
| Shift K⁺ into cells | Salbutamol (albuterol) nebulised | 10–20 mg nebulised | ~30 min / 2–4 h | Adjunct to insulin, not a substitute; caution in tachyarrhythmia/ischaemic heart disease |
| Shift K⁺ into cells | Sodium bicarbonate | Per local protocol | Variable | Only in significant metabolic acidosis; not routine |
| Remove K⁺ | Potassium binders: sodium zirconium cyclosilicate or patiromer | Per product / local protocol | Hours | Removes K⁺ via the gut |
| Remove K⁺ | Loop diuretic (e.g. furosemide) | Per local protocol | Variable | Only if the patient passes urine and is not volume depleted |
| Remove K⁺ | Haemodialysis | — | Fastest definitive removal | Refractory hyperkalaemia, severe AKI/ESKD |
Don't forget
- Stop the cause: potassium supplements, ACE inhibitors/ARBs, spironolactone, NSAIDs, trimethoprim.
- Recheck potassium about 1 hour after shifting treatment, then regularly — the shift wears off, so potassium rebounds unless it is removed.
- Treat the underlying cause: AKI, DKA, rhabdomyolysis.
- Digoxin toxicity: seek senior/toxicology advice before giving calcium.
Emergencies make sense when you know why
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Get the Complete EditionHyperkalaemia in one line
C BIG K DROP, a common memory aid: Calcium, Beta-agonist (salbutamol), Insulin + Glucose, Kayexalate/binders, Diuretics/Dialysis — but note the order on the ward is protect, shift, remove.
Frequently asked questions
What are the first EKG changes in hyperkalaemia?
Tall, narrow, peaked T waves are usually the first change. As potassium rises further, the PR lengthens, P waves flatten, the QRS widens and finally a sine-wave pattern appears.
Why is calcium given in hyperkalaemia if it doesn't lower potassium?
Calcium stabilises the cardiac cell membrane and reduces the risk of arrhythmia within minutes. It buys time while insulin–dextrose and other treatments lower the potassium.
How does insulin lower potassium?
Insulin activates the sodium–potassium ATPase pump, moving potassium into cells. Glucose is given alongside it to prevent hypoglycaemia.
What potassium level is dangerous?
A level of 6.5 mmol/L or above is usually classed as severe, but any level with EKG changes is an emergency.
What drugs cause hyperkalaemia?
Common causes include ACE inhibitors, ARBs, spironolactone and other potassium-sparing diuretics, trimethoprim, NSAIDs, heparin and non-selective beta-blockers.
Keep going
- How to read an EKG: a step-by-step system
- How to interpret an ABG in 6 steps
- Beta-blocker side effects: the high-yield cheat sheet
Revise smarter, not longer
21 doctor-written guides, 15 practice exams, the ABG handbook and a 12-week study plan. The Med Notes Guide Complete Edition, $59.
Get the Complete Edition – $59Educational content only. Not medical advice. Doses are standard adult textbook doses; always check your local guidelines and protocols.