Hyperkalaemia: ECG Changes and Emergency Management for Physicians

A 67-year-old man with diabetic kidney disease, on ramipril and spironolactone, comes in with two days of vomiting and generalised weakness. His pulse is 44 and the monitor shows broad, bizarre complexes. The laboratory phones a potassium of 7.4 mmol/L. Over the next few minutes the order in which you act matters more than the drugs you choose: stabilise the heart, shift potassium into cells, then remove it from the body.

Key points

• Severe hyperkalaemia is a potassium of 6.5 mmol/L or above (UK Kidney Association), but ECG change at any level is an emergency.
• The ECG is an insensitive guide; a normal tracing does not mean the patient is safe.
• Treatment has three steps: stabilise the myocardium with IV calcium, shift potassium with insulin–glucose and salbutamol, and remove potassium from the body.
• Calcium protects the heart but does not lower potassium; its effect lasts only a short time.
• Check for pseudohyperkalaemia, monitor glucose closely after insulin, and take care in digoxin toxicity.

Severity and when to act

UK Kidney Association guidance grades hyperkalaemia as mild (5.5–5.9 mmol/L), moderate (6.0–6.4 mmol/L) and severe (6.5 mmol/L or above). Emergency treatment is indicated for severe hyperkalaemia and for any level accompanied by ECG changes. The rate of rise, renal function and ongoing potassium load (rhabdomyolysis, tumour lysis, gastrointestinal bleeding) matter as much as the absolute number.

ECG progression

The classic sequence follows rising potassium, although individual patients do not read the textbook and changes may appear in any order or not at all:

1. Tall, narrow, peaked T waves.
2. PR prolongation and flattening, then loss, of P waves.
3. QRS widening, often with bizarre morphology.
4. Bradycardia, high-grade AV block or slow junctional and ventricular rhythms.
5. Sine-wave pattern, followed by ventricular fibrillation or asystole.

Any of these with a raised potassium should be treated immediately. Do not wait for a repeat sample if the ECG is abnormal.

Step 1: stabilise the myocardium

Give IV calcium gluconate 10%, 30 mL over 5–10 minutes, with cardiac monitoring. An alternative is calcium chloride 10%, 10 mL, which provides a similar amount of elemental calcium but is irritant to veins and is preferably given through a central line. Calcium raises the threshold potential and antagonises the membrane effects of potassium within minutes, but the effect wears off within about an hour.

Repeat the ECG after 5–10 minutes. If the changes persist, give a further dose. Some patients need more than one repeat dose before the complexes narrow.

Hyperkalaemia is one of the emergencies in our pillar guide to the 10 cardiac emergencies every physician must know, where it appears alongside complete heart block, one of its most common presentations.

Step 2: shift potassium into cells

Insulin–glucose is the most reliable shifting therapy. Give 10 units of soluble (regular) insulin with 25 g of glucose IV, typically over 15 minutes. The effect begins within about 15 minutes and lasts several hours.

Hypoglycaemia is the main hazard and is often delayed. It is more likely in patients with renal impairment, low body weight or a low pre-treatment glucose. UK Kidney Association guidance recommends a follow-on 10% glucose infusion when the pre-treatment glucose is below 7 mmol/L, and capillary glucose monitoring for at least six hours after insulin.

Nebulised salbutamol, 10–20 mg, is a useful adjunct to insulin–glucose but should not be used alone, because a proportion of patients do not respond. Use it cautiously in patients with tachyarrhythmias or active ischaemia.

IV sodium bicarbonate is not recommended routinely. It may have a role in severe metabolic acidosis, guided by specialist advice.

Step 3: remove potassium from the body

• Stop the cause: withhold ACE inhibitors, ARBs, mineralocorticoid receptor antagonists, potassium supplements, NSAIDs, trimethoprim and other potassium-raising drugs; treat dehydration and obstruction.
• Dialysis: the definitive treatment in refractory hyperkalaemia, particularly in anuric acute kidney injury or established kidney failure. Involve the renal team early; shifting therapy only buys time.
• Potassium binders: sodium zirconium cyclosilicate has a relatively rapid onset and is included in UK Kidney Association emergency pathways; patiromer acts more slowly and suits ongoing management. Older resins are slower and less predictable.
• Loop diuretic: appropriate where the patient is volume replete or overloaded and has residual renal function; avoid in hypovolaemia.

Recheck potassium within an hour or two of treatment and again over the following hours. Shifting therapy wears off, and rebound hyperkalaemia is common when the cause has not been dealt with.

The traps

Calcium does not lower potassium

After calcium the ECG may improve dramatically, and it is tempting to relax. The serum potassium is unchanged. Shifting and removal must follow without delay.

Pseudohyperkalaemia

A high potassium in a well patient with a normal ECG may be artefactual. Common causes are haemolysis during sampling, prolonged tourniquet time or fist clenching, delayed processing, contamination from an EDTA tube, and marked thrombocytosis or leucocytosis. Repeat the sample promptly, ideally with a blood-gas measurement, but do not delay treatment when the ECG is abnormal or the clinical picture fits.

Digoxin

Hyperkalaemia in acute digoxin toxicity reflects poisoning of the sodium–potassium pump and is a marker of severity. Digoxin-specific antibody fragments are the definitive treatment. The historical warning that IV calcium causes a “stone heart” rests on weak evidence, but many protocols still advise caution and slower administration; seek toxicology advice early.

Bradycardia that does not respond

Heart block and slow escape rhythms caused by hyperkalaemia often respond poorly to atropine and may need pacing, but correcting potassium is the priority. Combined AV nodal blockade, renal failure and hyperkalaemia can reinforce one another in a vicious circle; look for all three.

A one-minute checklist

1. ECG and continuous monitoring.
2. Abnormal ECG or potassium of 6.5 mmol/L or above: IV calcium now; repeat if the ECG does not improve.
3. Insulin 10 units with 25 g glucose; nebulised salbutamol as an adjunct.
4. Glucose monitoring for at least six hours.
5. Stop offending drugs, treat the cause, contact the renal team, and plan removal.
6. Repeat potassium within one to two hours and again later.

Physicians who want a structured way to master emergencies like this can join the 12-week Practical Cardiology Certificate for Physicians, whose founding cohort starts on 23 November 2026.

This article is educational content intended for registered medical practitioners. It does not replace clinical judgement. Always follow your local protocols and current national and international guidelines, including UK Kidney Association or equivalent local guidance, when managing patients.