Magnesium Sulfate

Therapeutic range - normal serum Mg²⁺ is 1.7–2.2 mg/dL; therapeutic levels for eclampsia/seizure prophylaxis are 4–7 mg/dL; toxic levels begin above 7–8 mg/dL.

Essential electrolyte - magnesium is a cofactor in over 300 enzymatic reactions and plays a critical role in neuromuscular transmission, membrane stabilization, and CNS excitability.

Reduced opioid requirements - produces dose-dependent antinociception and may reduce intraoperative and postoperative opioid requirements by 30–40%

Vasodilation - causes dose-dependent peripheral vasodilation and mild hypotension, particularly with rapid IV administration; treat with volume and vasopressors if needed.

Cardiac conduction - slows SA node automaticity and prolongs PR and QT intervals; high levels can cause complete heart block or cardiac arrest.

Mild negative inotropy - generally well tolerated in healthy patients; use with caution in patients with pre-existing cardiac dysfunction or on calcium channel blockers.

Bedside toxicity monitoring - assess patellar reflex, respiratory rate, and urine output (maintain ≥25 mL/hr) hourly in patients on continuous infusions.

Respiratory depression risk - loss of patellar reflexes (~7–10 mg/dL) precedes respiratory paralysis (~10–13 mg/dL); monitor reflexes in awake/unintubated patients. Serum levels above 12–15 mg/dL can cause respiratory arrest

Neuromuscular blockade potentiation - magnesium inhibits presynaptic acetylcholine release and reduces motor end-plate sensitivity, significantly potentiating both depolarizing and non-depolarizing NMBAs. Reduce initial NMBA dose by 25–50%. No need for defaciculating dose prior to Succinylcholine administration. Succinylcholine dose stays the same. Prior to extubation, confirm adequate NMB reversal with quantitative TOF monitoring (TOF ratio ≥0.9).

Precipitation Risk - Never administer in the same line as calcium salts, heavy metals, or phosphate-containing solutions — precipitation can occur.

Succinylcholine interaction - may blunt fasciculations and attenuate the rise in serum potassium; onset and duration of succinylcholine may be prolonged.

Flushing and warmth - common with bolus administration; secondary to vasodilation; generally benign but may be alarming to awake patients.

Nausea - can occur with rapid infusion; slow the rate if nausea develops.

Renal Patients - Accumulation risk is high in renal impairment; reduce maintenance infusion and monitor serum levels closely. Dialyzable.

Hypermagnesemia signs - nausea, lethargy, loss of deep tendon reflexes, respiratory depression, cardiac arrest.

Drug interactions - profoundly potentiates Non-depolarizing NMBAs. Magnesium in combination with calcium channel blockers will have additive effects on cardiovascular depression, hypotension, and AV block. Magnesium will have additive CNS depressant effects with opioids, benzodiazepines, neuraxial anesthetics, and volatile agents (anticipate lower MAC requirements).

OB - Magnesium is a first-line agent for seizure prophylaxis in preeclampsia/eclampsia (Pritchard protocol) and for neuroprotection of the preterm fetus. Magnesium is a tocolytic, used short-term to delay pre-term labor (which allows time for corticosteroids). NOT recommended for maintenance tocolysis. Tocolysis can also increase risks of postpartum hemorrhage. Magnesium crosses the placenta. Neonates born to mothers on mag infusions may exhibit respiratory depression, hypotonia, and poor feeding — NICU should be on standby. Magnesium potentiates spinal and epidural anesthesia; expect lower LA requirements and monitor for hypotension closely.

Magnesium relaxes the uterus, which can increase risks of postpartum hemorrhage.

IV magnesium inhibits the release of catecholamines after sympathetic stimulation but has no effect on postoperative pain levels.

If magnesium toxicity is suspected, give 10ml of 10% calcium gluconate

Absolute - Heart block, Myasthenia gravis, Hypermagnesemia, Anuric renal failure (relative absolute)

Relative - Severe renal impairment (CrCl <30 mL/min), Significant cardiac conduction abnormalities

Caution - Neuromuscular disease, Concurrent calcium channel blocker use, Digitalis toxicity, Respiratory compromise in non-intubated patients

Intraoperative Adjuct: 30–50 mg/kg bolus over 15 min before or at induction. Max 2-3g

Intubation pre-treatment: 1–2 g, 2–3 min before laryngoscopy blunts sympathetic response comparably to lidocaine.

Antiarrhythmic: 1-2 g over 5-60 min. For torsades de pointes: 1-2 g over 5-20 min.

Pediatric Dose: 25–50 mg/kg IV over 10–20 min; max single dose 2 g

Seizure/Eclampsia prophylaxis: 4-6g loading dose over 15-20 min, 1-2g/hr thereafter.

Tocolysis: 4-6g over 20-30 min, 1-4 g/hr thereafter.

Perioperative Adjunct: 0.5 - 1g/hr; Monitor serum levels if prolonged.

Rapid infusion of any loading dose can result in hypotension, flushing, and cardiac depression

4–5 g deep IM (each buttock); used when IV access unavailable — painful and rarely used

Blocks NMDA receptor channels, inhibiting calcium influx and excitatory neurotransmission. Reduces presynaptic acetylcholine release at the neuromuscular junction. Competes with calcium to stabilize cell membranes and inhibit smooth muscle contraction. Additionally, magnesium decreases catecholamine release, reduces peripheral vascular resistance, inhibits platelet aggregation, and provides neuroprotection in preterm neonates via NMDA blockade.

Not metabolized; magnesium is an endogenous ion

Renal filtration and reabsorption by the kidney; excreted almost entirely in urine

Calcium Gluconate (preferred): 1 g (10 mL of 10% solution) IV over 3–5 min; may repeat as needed

Calcium Chloride: 500 mg–1 g IV over 3–5 min; 3× more elemental calcium than gluconate — use cautiously via central line if possible.

Onset of the above is around 1-3 min and lasts 15-30 min, so repeated dosing or infusion may be needed.

Calcium reversal is temporizing — definitive management requires enhanced renal elimination or dialysis if toxicity is severe.

Do NOT administer calcium in same line as magnesium sulfate.