Hypokalaemia and hyperkalaemia — viva

Opening (must-hit)

"This is severe hyperkalaemia with cardiotoxic ECG changes — a widened QRS and peaked T waves — and it is a cardiac emergency. My first action is to give intravenous 10 percent calcium gluconate at 0.5 mL per kilogram, maximum about 10 mL, slowly over 5 minutes with continuous cardiac monitoring, to stabilise the myocardium. This does not lower the potassium, so I immediately follow with a shifting agent — nebulised salbutamol and insulin-dextrose — and I arrange definitive removal of potassium, likely dialysis given the acute kidney injury. I do not wait for a repeat potassium; the ECG tells me to act now." [2][3]

Examiner: "Why calcium first, and what exactly does it do?"

"Calcium gluconate raises the threshold potential of the cardiac myocyte membrane. In hyperkalaemia the extracellular potassium is high, so the resting membrane potential becomes less negative, which partially inactivates the fast sodium channels and slows conduction — that is the widened QRS and the risk of asystole. Calcium does not remove potassium; it counteracts the membrane effect within minutes and buys time for the shifting agents to work. I use calcium gluconate peripherally because it is less vesicant than calcium chloride if it extravasates, and I give it slowly because rapid calcium itself can cause arrhythmia." [2][4]

Examiner: "Give me your shifting agent doses and the key safety issue."

"I give nebulised salbutamol 2.5 mg for a child under 25 kg and 5 mg for a child over 25 kg — beta-2 agonism activates the sodium-potassium ATPase and drives potassium into cells within about 30 minutes. I combine it with intravenous insulin 0.1 unit per kilogram and glucose 0.5 g per kilogram, for example 5 mL per kilogram of 10 percent dextrose. The key safety issue is iatrogenic hypoglycaemia: the insulin-dextrose and hypoglycaemia association is well documented, occurring in roughly 10 to 20 percent of treatments, so I check blood glucose every 15 to 30 minutes for at least two hours. The evidence from Kemper and McClure supports salbutamol in children, and the Crnobrnja data underpin the glucose and monitoring requirement." [5][7][8]

Examiner: "Now turn it around — a child with refractory hypokalaemia. Why does it not correct?"

"The answer is almost always hypomagnesaemia. Low magnesium disinhibits the ROMK channel in the distal nephron, which increases potassium secretion, so the kidney keeps wasting potassium no matter how much I replace. I check the magnesium and replace it — magnesium sulfate 25 to 50 mg per kilogram — before or alongside the potassium, because the hypokalaemia will not resolve until magnesium is restored. This is one of the most reliable single-right-answer stems in electrolyte medicine." [4]

Examiner: "How would you give intravenous potassium safely?"

"Potassium chloride, never as an undiluted bolus, always via an infusion pump, at a maximum of 0.2 mmol per kilogram per hour through a peripheral line — 0.4 mmol per kilogram per hour centrally, only with cardiac monitoring. The peripheral concentration should not exceed about 40 mmol per litre. I reassess the serum potassium frequently. The reason for the rate limit is that fast potassium causes ventricular fibrillation and cardiac arrest — it is the mechanism of lethal injection, which is why an undiluted bolus is never given." [4][3]

Examiner: "Final corner — Bartter versus Gitelman at the table."

"Both are inherited salt-wasting tubulopathies with hypokalaemic metabolic alkalosis and normal-to-low blood pressure. Bartter is a thick ascending limb defect that mimics a loop diuretic — it presents early, often antenatally with polyhydramnios, and shows hypercalciuria with a risk of nephrocalcinosis. Gitelman is a distal convoluted tubule defect that mimics a thiazide — it presents later, in adolescence, often with tetany, and shows hypomagnesaemia and hypocalciuria. The calcium direction is the tie-breaker: Bartter is hypercalciuria, Gitelman is hypocalciuria. Both are managed with lifelong potassium and magnesium supplementation, potassium-sparing diuretics, and in Bartter, prostaglandin inhibition." [4]

Closing summary

"In summary: hyperkalaemia with ECG changes — calcium first, then shift with salbutamol and insulin-dextrose, then remove with dialysis, and watch the glucose. Refractory hypokalaemia — it is the magnesium. Intravenous potassium — pump, diluted, 0.2 mmol/kg/hour peripheral. Bartter versus Gitelman — follow the calcium." [2][4]