Calcium does not lower serum potassium. It directly antagonises the membrane effects of hyperkalaemia. Hyperkalaemia decreases the resting membrane potential (makes it less negative), bringing it closer to the threshold potential. This causes initial hyper-excitability followed by inexcitability (conduction blocks, asystole). Calcium raises the threshold potential, restoring the normal voltage gap between resting and threshold, thereby stabilising the myocardium. Think of it as raising the bar that the membrane potential must cross to fire - the potassium is still high, but the heart is temporarily protected.

Calcium Gluconate 10% (10 mL = 93 mg elemental Ca) is preferred via peripheral IV because it causes less tissue necrosis on extravasation. Calcium Chloride 10% (10 mL = 272 mg elemental Ca) delivers three times more elemental calcium and is preferred in cardiac arrest or peri-arrest situations via a central line. In Indian ICUs, both are available. The choice depends on IV access and clinical urgency.

Insulin drives potassium into cells by stimulating the Na+/K+-ATPase pump. Dextrose is purely to prevent hypoglycaemia. The standard is 10 Units Actrapid with 25g Dextrose (100 mL of 25% Dextrose). Expected potassium reduction is 0.5 to 1.2 mEq/L within 15 to 30 minutes, lasting 4 to 6 hours. Delayed hypoglycaemia peaks at 2 to 3 hours and is the commonest complication of hyperkalaemia treatment. Mandatory GRBS monitoring: every 30 minutes for 2 hours, then hourly for a further 4 hours.

Nebulised salbutamol (10 to 20 mg - note this is 4 to 8 times the bronchodilator dose) reduces potassium by 0.5 to 1.5 mEq/L. Onset is 15 to 30 minutes, duration 2 to 4 hours. Combined with insulin-dextrose, the effect is additive. However, approximately 20 to 40% of ESRD patients are resistant to the hypokalaemic effect. Significant tachycardia (heart rate increase of 15 to 25 bpm) and tremor are expected. Use with extreme caution in patients with ischaemic heart disease or existing tachyarrhythmias.

NaHCO3 shifts potassium intracellularly by correcting extracellular pH. It is effective only when significant metabolic acidosis is present (pH < 7.2). In the absence of acidosis, NaHCO3 alone does not meaningfully lower potassium and should NOT be relied upon. When indicated, administer 50 to 100 mL of 8.4% NaHCO3 IV over 5 minutes. Caution: each 50 mL ampoule delivers approximately 50 mEq of sodium - significant in heart failure patients.

ECG changes in hyperkalaemia follow a predictable but not always sequential progression. Some patients progress directly from peaked T waves to cardiac arrest without intermediate stages. ECG changes do not correlate perfectly with serum K levels - a patient with K 7.0 may have a normal ECG, while one with K 5.8 on digoxin may have advanced changes.

Dialysis is the definitive elimination therapy for hyperkalaemia. Haemodialysis removes 25 to 50 mEq of potassium per hour. Indications for emergent dialysis include:

• ESRD / Anuric patients: Loop diuretics and renal elimination are ineffective.
• Refractory hyperkalaemia: K remains ≥ 6.0 mEq/L after two cycles of full medical therapy (calcium + insulin-dextrose + salbutamol + diuretics).
• Persistent ECG changes: Life-threatening ECG changes (QRS widening, sine wave) unresponsive to calcium gluconate.
• Massive tissue breakdown: Rhabdomyolysis, tumour lysis syndrome, major burns, or crush injury where ongoing potassium release will exceed medical elimination capacity.
• Severe AKI with oliguria: When diuretic response is absent and K is rising despite shift therapies.