Acute severe hypokalaemia and hypomagnesaemia: ECG, repletion, and refractory causes

Also known as Hypokalaemia · Low potassium · Hypomagnesaemia · Potassium repletion · Refractory hypokalaemia · Gitelman syndrome

Hypokalaemia (K <3.5 mmol/L) is common in ICU (diuretics, GI loss, drugs). SEVERE (<2.5) → polymorphic VT risk. ECG changes: T-wave flattening, ST depression, U waves, prolonged QT. Hypomagnesaemia (Mg <0.7 mmol/L, defined as under 1.7 mg/dL in cohort studies) met 52 percent of medical-ICU admissions and was present in 42 percent of hypokalaemic inpatients — always check + replace Mg in refractory hypokalaemia (ROMK channel). Repletion: ORAL salts preferred; IV potassium chloride only as a diluted, monitored infusion (in critical care usually up to 40 mmol/h) — never an undiluted push. Torsades: stop QT-prolonging drugs, IV magnesium sulfate 1 to 2 g, keep K in the high-normal range, overdrive pace if recurrent. Causes: diuretics, GI loss, DKA insulin, refeeding, β2-agonists, mineralocorticoid excess, cisplatin/amphotericin, PPIs (Mg), Gitelman/Bartter.

high45 referencesUpdated 26 July 202616 min readSource-verified · Sept 2026

Checked against its sources on 3 Sept 2026

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8 MCQs

The one-line answer

Severe hypokalaemia (K under 2.5 mmol/L) is where the arrhythmia risk bites — sustained polymorphic VT was most likely below this level in a monitored post-arrest cohort, and urgency follows severity, symptoms and the ECG, not the number alone. Refractory hypokalaemia means REPLACE MAGNESIUM FIRST — hypomagnesaemia coexists in 42 percent of hypokalaemic inpatients, and K repletion stays refractory until the Mg deficit is corrected (intracellular Mg normally plugs the ROMK channel). Repletion: oral potassium salts preferred; IV potassium chloride only as a diluted, monitored infusion — in critical care usually up to 40 mmol/h — never an undiluted push. Hypomagnesaemia (under 0.7 mmol/L) met 52 percent of medical-ICU admissions, where it tracked with higher mortality, ventilation and hypocalcaemia.^[29]^[2]^[13]^[12]^[3]^[28]^[45]

Meet the patient

A 56-year-old chronic alcoholic with 5 days of profuse vomiting and diarrhoea is admitted with dizziness and weakness. Heart rate 108, blood pressure 88/52, proximal and respiratory muscle weakness, positive Chvostek sign. Potassium 1.9, magnesium 0.32, ionised calcium 0.86, phosphate 0.45, pH 7.50 (metabolic alkalosis). ECG: QTc 580 ms, U waves merging with T waves, and a 20-second run of Torsades de Pointes with a pulse. She is on chronic omeprazole and has been given IV erythromycin and haloperidol on the ward.^[1]

Two cubicles down, a 64-year-old with bladder cancer on day 4 of his third cycle of cisplatin is in ICU with weakness and tremor. He has received repeated infusions of IV KCl but the potassium stays at 2.6. Magnesium is 0.35. The ECG shows a prolonged QTc with ventricular ectopics — cisplatin lowers serum magnesium and potassium in nearly all exposed patients, with hypomagnesaemia persisting in 60 percent short-term.^[20]^[34]

The two questions that decide the next hour are the same on every hypokalaemic patient: how low is the K, and what is the ECG doing? (drives the urgency and the route), and why is the K not rising? (the answer is almost always magnesium). Hold those two and the rest of the topic slots into place.^[1]

References45Show

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