Magnesium Sulfate

Magnesium sulfate prevents convulsions in preeclamp-sia and directly uncouples excitation-contraction in myometrial cells through inhibition of cellular action potentials. Furthermore, magnesium sulfate decreases calcium uptake by competing for its binding sites, activating adenylyl cyclase (thereby reducing intracellular calcium), and stimulating calcium-dependent adenosine triphosphatase (ATPase), which promotes calcium uptake by the sarcoplasmic reticulum. Magnesium is filtered by the glomerulus, so patients with low glomeru-lar filtration will have low magnesium clearance. Although the compound does have some cardiac side effects, magnesium sulfate may be preferred over ß-adrenergic agents in patients with heart disease, diabetes, hypertension, or hyperthyroidism.

There is much debate as to the efficacy of magnesium sulfate. For effective inhibition of uterine activity, enough must be given to maintain a blood plasma level of at least 5.5 mEq/L. Even at this level, tocolysis may be hard to achieve.

Magnesium toxicity can be life threatening. Patients given magnesium lose patellar reflexes at plasma levels greater than 8 to 10 mEq/L. Respiratory depression can occur at levels greater than 10 to 12 mEq/L, with respiratory paralysis and arrest soon after (e.g., at levels greater than 12-15 mEq/L). Higher levels cause cardiac arrest. Toxicity can be avoided by following urine output and checking patellar reflexes in patients receiving magnesium. Other side effects include sweating, warmth, flushing, dry mouth, nausea, vomiting, dizziness, nystagmus, headache, palpitations, pulmonary edema, maternal tetany, profound muscular paralysis, profound hypotension, and neonatal depression.

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