Hypomagnesemia

Torsades is the crisis. Hypomagnesemia is a named risk factor for QT prolongation and polymorphic VT. For hemodynamically unstable torsades, give magnesium sulfate 2 to 4 g IV and cardiovert, correct potassium and calcium at the same time, and remove the inciting drug. Amiodarone is the wrong reach - it prolongs the QT further. For recurrent episodes, raise the underlying rate with isoproterenol or transvenous pacing.

Get a QTc before you reach for QT-prolonging drugs. A baseline 12-lead is worth it in the at-risk patient - alcohol use disorder, chronic diuretics, long-term PPI, chronic diarrhea. QTc above 500 ms carries a two- to three-fold increase in torsades risk. Ondansetron, droperidol, haloperidol, methadone, and macrolides all add to it, so pick the antiemetic accordingly.

ECG findings. Widening of the PR interval, widening of the QRS, and peaked T waves are the described changes, on top of the QT prolongation.

You cannot fix the potassium until you fix the magnesium. Refractory hypokalemia is the classic tell - low magnesium disinhibits the ROMK channel and the kidney keeps wasting potassium no matter how much you replace. Calcium behaves the same way, because magnesium depletion suppresses PTH release. Send a magnesium level with the potassium and calcium rather than chasing them separately.

Repletion dosing. Hemodynamically unstable: 1 to 2 g magnesium sulfate over about 15 minutes. Symptomatic but stable: 1 to 2 g over an hour. Non-emergent adult repletion: 4 to 8 g slowly over 12 to 24 hours. Pediatric: 25 to 50 mg/kg, maximum 2 g. Serum levels rise quickly but intracellular stores lag, so continue repletion for two days after the level normalizes. With creatinine clearance under 30 mL/min/1.73 m2, halve the dose and follow levels - these patients tip into hypermagnesemia.

Neuromuscular blockade cuts both ways. Untreated, hypomagnesemia removes competitive inhibition at the neuromuscular junction, so more acetylcholine is released and the patient is irritable - tremor, hyperreflexia, spasm, tetany. Once you replete, magnesium blocks calcium influx at the nerve terminal and reduces acetylcholine release, which potentiates non-depolarizing NMB. If you have given magnesium, expect a longer block, titrate to TOF, and confirm recovery before extubation. In myasthenia gravis, neuromuscular function worsens at magnesium concentrations that would be unremarkable in anyone else.

CNS irritability. Hypomagnesemia can produce seizures, tremor, and generalized weakness; vertical nystagmus and tetany may be found on exam. Do not write off new seizure activity or unexplained weakness in the PACU without a magnesium level.

Citrate chelates magnesium during transfusion. Rapid transfusion, above about 6 units per hour in an adult, chelates calcium and magnesium and produces hypotension, myocardial depression, QT prolongation, heart block, laryngospasm and tetany, and coagulopathy. Slow the transfusion rate so the liver can clear the citrate and replete calcium and magnesium. Hepatic dysfunction, hypoalbuminemia, hypothermia, and pediatric patients all make it worse.

Magnesium is the second most abundant intracellular cation after potassium and a cofactor across glycolysis, the Krebs cycle, and neuromuscular transmission. Normal serum runs 1.46 to 2.68 mg/dL; hypomagnesemia is below 1.46 mg/dL and typically stays silent until the level falls under about 1.2 mg/dL. Alcohol use disorder, gastrointestinal and renal losses, diuretics, long-term proton pump inhibitors, and critical illness are the usual causes - prevalence reaches 65% in ICU patients against 2.5% to 15% in the general population.

The perioperative problem is electrical. Low magnesium inhibits renal outer medullary potassium channels, wasting potassium in the urine and depleting it intracellularly, which lowers the threshold for a cardiac action potential and prolongs repolarization. It also blunts magnesium-dependent cAMP generation, cutting PTH release and dropping calcium. The result is an irritable myocardium sitting on a long QT.