Hyperkalaemia ECG & Treatment Guide

Hyperkalaemia-related ECG changes are a series of progressive electrocardiographic abnormalities caused by rising serum potassium concentrations that directly alter cardiac membrane excitability and conduction velocity. Potassium is the principal intracellular cation, and even modest rises in extracellular potassium depolarise the resting membrane potential, altering the sodium channel kinetics responsible for cardiac action potentials. The ECG changes of hyperkalaemia follow a characteristic sequence correlated with potassium levels: peaked (tall, narrow, tent-shaped) T waves are the earliest and most sensitive finding, typically appearing at potassium >5.5 mmol/L; PR interval prolongation and P wave flattening occur at potassium >6.0–6.5 mmol/L; P wave disappearance (sinoventricular conduction replacing SA node activity) occurs at >6.5 mmol/L; progressive QRS widening and the development of a classic 'sine wave' pattern (merging of widened QRS with T waves) occurs at >7.0 mmol/L; and ventricular fibrillation or asystole may occur at potassium >8.0 mmol/L. However, the correlation between ECG findings and serum potassium is imperfect — rate of rise, concurrent medications, calcium levels, and pH all modulate cardiac sensitivity. Treatment of severe or symptomatic hyperkalaemia is a medical emergency and follows a structured sequence: membrane stabilisation with calcium gluconate or calcium chloride IV; intracellular potassium shifting with insulin+dextrose, salbutamol (albuterol) nebulisation, and sodium bicarbonate; enhanced potassium elimination with patiromer, sodium zirconium cyclosilicate, kayexalate, or haemodialysis.

1. 1Obtain a 12-lead ECG as soon as hyperkalaemia is suspected or confirmed — ECG findings determine the urgency of treatment and guide the sequence of interventions; do not wait for laboratory confirmation before obtaining an ECG in a symptomatic patient.
2. 2Assess ECG findings systematically: measure the T wave height and morphology (peaked = tall, narrow, symmetric, tent-shaped vs normal asymmetric); measure the PR interval (normal <200 ms); examine P wave presence and morphology; measure QRS duration (normal <120 ms); look for sine wave pattern or QRS-T merging.
3. 3Correlate ECG findings with the serum potassium level and assess for secondary causes: acute kidney injury, medications (ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs, trimethoprim, heparin), tumour lysis syndrome, rhabdomyolysis, haemolysis, or adrenal insufficiency (Addison's disease).
4. 4Initiate calcium gluconate (or calcium chloride) IV immediately for any of: potassium ≥6.5 mmol/L, QRS widening >120 ms, sine wave pattern, or loss of P waves — calcium stabilises cardiac membrane within 1–3 minutes but does not lower potassium; repeat after 5 minutes if ECG has not improved.
5. 5Administer potassium-shifting agents to move potassium intracellularly: insulin 10 units IV with 25 g (50 mL of 50%) dextrose (onset 15–30 min); salbutamol 10–20 mg nebulised (beta-2 effect, onset 30 min, lowers K by 0.5–1.0 mmol/L); sodium bicarbonate 50–100 mEq IV if concurrent metabolic acidosis (pH <7.2); these agents are temporising — potassium returns to serum within hours.
6. 6Initiate potassium elimination: patiromer (Veltassa) or sodium zirconium cyclosilicate (Lokelma) as oral/NG potassium binders for non-emergency elimination; kayexalate (sodium polystyrene sulphonate) is less preferred due to bowel necrosis risk; haemodialysis is the most effective and fastest method for severe refractory hyperkalaemia, particularly in renal failure.
7. 7Monitor potassium hourly for the first 4–6 hours after treatment and repeat ECG after each major intervention; identify and treat the underlying cause to prevent recurrence — the potassium shifting from insulin+salbutamol is transient (4–6 hours).