Why this drug is interesting
Magnesium appears in three quite separate emergency situations — a malignant arrhythmia, an obstetric emergency, and severe asthma — with three different regimens, and it is the only drug in this collection where the units themselves are a recognised source of error.
The Resuscitation Council specifies millimoles. Obstetric guidance specifies grams. The ampoule is labelled as a percentage. All three describe the same substance, and a clinician who cannot convert between them at speed is a clinician who will eventually give the wrong dose.
The second distinctive feature: in torsades, magnesium works whether or not the serum magnesium is low. It is being used as a membrane stabiliser, not as replacement therapy, and waiting for a level before giving it is a mistake.
Pharmacology
Mechanism
Magnesium is the second most abundant intracellular cation and a cofactor for hundreds of enzymes, but its emergency actions come from a small number of membrane effects:
- Physiological calcium antagonism — magnesium competes with calcium at channels and binding sites, reducing calcium influx. This underlies both the smooth muscle relaxation in asthma and the suppression of early afterdepolarisations in torsades
- Membrane stabilisation — reducing the triggered activity that initiates torsades de pointes
- Presynaptic inhibition of acetylcholine release at the neuromuscular junction — the basis of both its anticonvulsant effect in eclampsia and its dose-limiting toxicity
- Cerebral vasodilatation and reduced vasospasm, contributing to the eclampsia effect
- NMDA receptor blockade — magnesium is the physiological pore blocker of the NMDA channel
Kinetics
- Onset, IV
- Immediate
- Distribution
- Rapid; most of the body's magnesium is intracellular or in bone, so serum levels are a poor guide to total body stores
- Elimination
- Almost entirely renal
- Implication
- Renal impairment causes accumulation and toxicity — reduce the dose and monitor closely
Torsades de pointes and cardiac use
The RCUK 2025 adult tachyarrhythmia algorithm is explicit for polymorphic VT with QT prolongation:3
- Give Mg²⁺ 8 mmol IV over 10 minutes
- Consider isoprenaline or temporary pacing to increase the heart rate
- Avoid amiodarone
Alongside magnesium
- Stop the offending drug and review everything the patient is taking for QT-prolonging agents
- Correct potassium and calcium, aiming for a high-normal potassium
- Defibrillate if the rhythm degenerates or the patient is pulseless
- Identify congenital long QT if there is a suggestive personal or family history
Magnesium is also used adjunctively in some refractory ventricular arrhythmias and in digoxin toxicity, where hypomagnesaemia potentiates glycoside effects — see Digoxin.
Eclampsia and severe pre-eclampsia
Magnesium sulphate is indicated for the control and prevention of seizures in severe pre-eclampsia, and control and prevention of recurrent seizures in eclampsia.1 It is not a general-purpose anticonvulsant, and it outperforms both diazepam and phenytoin in this specific setting.
Regimens
| Component | Regimen |
|---|---|
| Loading dose | 4 g IV over 5 minutes (usually as a 20% solution) |
| Maintenance — intravenous | 1 g/hour, continued for 24 hours after the last fit |
| Maintenance — intramuscular (Pritchard) | 5 g IM into the upper outer quadrant of each buttock, then 5 g IM every 4 hours for 24 hours after the last fit |
| Maximum infusion rate | 2 g/hour (8 mmol Mg²⁺/hour) — must not be exceeded |
Close monitoring for ECG changes is also required, and the infusion should be slowed or stopped if the cardiac condition changes.1 Obstetric and anaesthetic involvement should be immediate; delivery remains the definitive treatment.
Severe asthma and other uses
Severe or life-threatening asthma
A single intravenous dose of 1.2–2 g over 20 minutes is used in acute severe asthma that has not responded to initial bronchodilator therapy. The mechanism is smooth muscle relaxation through calcium antagonism.
Hypomagnesaemia
Indicated for treatment of magnesium deficiency where the oral route is inappropriate.1 Worth remembering that hypomagnesaemia causes refractory hypokalaemia and hypocalcaemia — a potassium that will not correct despite replacement is a prompt to check and replace magnesium.
Other
- Fetal neuroprotection in anticipated preterm birth — an obstetric-led indication
- Adjunct in some refractory arrhythmias and in digoxin toxicity
- Occasionally in severe tetanus and in specific poisonings, under specialist advice
Toxicity, contraindications and interactions
Contraindications and cautions
- Severe renal impairment — the dominant caution; reduce dose and monitor levels
- Myasthenia gravis — magnesium impairs neuromuscular transmission and may precipitate a crisis
- Heart block and significant bradycardia
- Hypocalcaemia
- Hepatic coma with a risk of renal failure
Interactions
- Neuromuscular blocking agents — magnesium markedly potentiates them; a relevant consideration if the eclamptic patient needs intubation. See Sugammadex
- Calcium channel blockers — additive hypotension
- Digoxin — caution with concurrent calcium administration; see Digoxin
- Other CNS depressants — additive sedation
Critical appraisal
- The eclampsia evidence is exceptionally strong. The Collaborative Eclampsia Trial and the MAGPIE trial together established magnesium as superior to diazepam and phenytoin for recurrent seizures, and as effective prophylaxis in severe pre-eclampsia. This is one of the better-evidenced drug choices in emergency medicine and is not controversial.
- The torsades evidence is weaker but the recommendation is sound. It rests on case series and mechanistic reasoning rather than randomised trials — an acceptable basis for a treatment given once, in a rhythm that kills quickly, with a wide safety margin at that dose.
- The asthma evidence is genuinely mixed. Intravenous magnesium reduces admissions in severe presentations, but the effect is modest and heterogeneous across trials; nebulised magnesium has largely not delivered. Presenting it as an established asthma therapy overstates it.
- Units remain the practical risk. Guidelines quote millimoles, grams and percentage solutions interchangeably, and the same drug is used at 2 g and at 4 g loading in adjacent parts of the same department. Written, unit-explicit protocols matter more here than clinician recall.
- Serum magnesium is a poor guide. Most magnesium is intracellular, so a normal level does not exclude deficiency — and in torsades the level is irrelevant to the decision to treat.
References
- 1Magnesium Sulfate 50% w/v Solution for Injection or Infusion — Summary of Product Characteristics. electronic Medicines Compendium. Sections 4.1, 4.2, 4.4. Verified 20 Aug 2026.
- 2Magnesium sulfate — dosing and safety monograph. BNF, NICE. bnf.nice.org.uk
- 3Resuscitation Council UK. Adult tachyarrhythmia algorithm, 2025. resus.org.uk — mirrored at lifesupport.resusdoc.uk. Polymorphic VT with QT prolongation: give Mg²⁺ 8 mmol IV over 10 min; consider isoprenaline or temporary pacing; avoid amiodarone.
- 4The Eclampsia Trial Collaborative Group. Which anticonvulsant for women with eclampsia? Evidence from the Collaborative Eclampsia Trial. Lancet 1995;345(8963):1455–63.
- 5The Magpie Trial Collaborative Group. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet 2002;359(9321):1877–90.
- 6NICE NG133. Hypertension in pregnancy: diagnosis and management. National Institute for Health and Care Excellence.
- 7British Thoracic Society / SIGN. British guideline on the management of asthma. brit-thoracic.org.uk