Mechanism of Action

Magnesium sulfate (MgSO4) is a CNS depressant that reduces neuromuscular excitability by competing with calcium at the neuromuscular junction, decreasing muscle contractility. In preeclampsia/eclampsia it is first-line for seizure prophylaxis — it raises the seizure threshold and stabilizes neuronal membranes; it does NOT lower blood pressure (that needs a separate antihypertensive like labetalol or hydralazine). The therapeutic serum magnesium level for seizure prevention is 4–7 mEq/L (≈4.8–8.4 mg/dL). The window between therapeutic and toxic is narrow, so it must run on an infusion pump.

12 · ~12: respiratory depression

Sub-therapeutic

Therapeutic (seizure prophylaxis)

Toxic

4.8

8.4

mg/dL

Common Medications

magnesium sulfatePrototype

single agent; given IV on a pump, never IV push

Indications

seizure prophylaxis in preeclampsia/eclampsia Hallmark

first-line; protects the brain, not the blood pressure

tocolysis in preterm labor

short-term bridge (24–48 h) to allow antenatal corticosteroids

fetal neuroprotection before 32 weeks

reduces risk of cerebral palsy

Side Effects

flushing

warmth

client may feel 'warm but fine'

lethargy

muscle weakness

feeling heavy / unable to lift arms

slurred speech

Contraindications & Interactions

Contraindications

oliguriaurine output < 30 mL/hr

magnesium is renally excreted; oliguria accelerates accumulation

renal impairment

reduced clearance → toxicity even at unchanged dose

myasthenia gravis

magnesium further impairs neuromuscular transmission

Interactions

concurrent CNS depressants

additive sedation/respiratory depression

concurrent oxytocin

MgSO4 relaxes uterine smooth muscle → may worsen postpartum uterine atony/hemorrhage

Administration & Monitoring

give via IV infusion pump

NEVER IV push — rapid push can cause fatal cardiac arrest

keep calcium gluconate at bedside

the antidote — 1 g IV over ~3 min; must be ready BEFORE the infusion starts

assess deep tendon reflexes q1–2h

patellar reflexes; loss is the earliest toxicity sign

count respirations q1–2h

continuous pulse oximetry

hold infusion for RR < 12/minHoldRR < 12/min

hold infusion for absent DTRsHold

stop and notify provider before respiratory arrest

monitor hourly urine outputHoldurine output < 30 mL/hr

oliguria signals accumulation — report

continuous fetal monitoring

decreased FHR variability may be a drug effect, not distress

Patient Teaching

expect feeling flushed and warm

common and usually benign

report difficulty breathing

report feeling unusually weak or heavy

subjective heaviness can be an early toxicity clue

this drug prevents seizures, not high blood pressure

a separate BP medication may still be needed

you will have frequent reflex and breathing checks

Report Nowescalate immediately

Magnesium toxicity cascade (reflexes → respirations → cardiac)

Loss of deep tendon reflexesfirst warning, ~7–10 mEq/L — STOP the infusion
Respiratory depressionRR < 12/min, ~10–13 mEq/L — first directly lethal sign
Cardiac arrestbradycardia, widened QRS → arrest, > 15 mEq/L

absent deep tendon reflexes Hallmarkserum Mg ~7–10 mEq/L

EARLIEST clinical sign of toxicity; stop the infusion immediately

respiratory depressionRR < 12/min

earliest directly lethal sign; serum Mg ~10–13 mEq/L

hypotension

from marked vasodilation; a late toxicity sign

bradycardia and widened QRS

cardiac conduction failure; serum Mg > 15 mEq/L

cardiac arrest

terminal step of the toxicity cascade

neonatal respiratory depression

magnesium crosses the placenta; alert neonatal team after prolonged infusion

Clinical Pearl

Mag is for the brain, not the blood pressure. Watch reflexes, respirations, renal — in that order. If the knee jerk is gone, the magnesium has gone too far: stop the infusion and have calcium gluconate ready at the bedside before you ever hang the bag.