Introduction
- Pharmacology
- Magnesium is the second most abundant intracellular cation (after potassium) and an essential enzymatic cofactor in a number of vital biochemical pathways.
- Magnesium has a direct effect on the Na+/K+-ATPase pump in cardiac and nerve tissues. It may facilitate the influx of K+ and stabilize myocardial membrane potentials. Further, magnesium has some calcium-blocking activity and may indirectly antagonize digoxin at the myocardial Na+/K+-ATPase pump.
- Magnesium modifies skeletal and smooth-muscle contractility. Rapid infusions can cause vasodilation, hypotension, and bronchodilation. It can reduce or abolish seizures associated with eclampsia.
- Magnesium is primarily an intracellular ion, and only 1% is in the extracellular fluid. A low serum Mg level (<1.2 mg/dL) may indicate a net body deficit of 5,000 mg or more.
- Hypomagnesemia can be associated with a number of acute or chronic disease processes, diuretic use, cisplatin administration, or alcoholism. It is a potentially serious, life-threatening consequence of hydrofluoric acid and ammonium bifluoride poisoning.
- Indications and Uses
- Treatment of hypomagnesemia.
- Prevention and treatment of torsade de pointes ventricular tachycardia.
- Solublebarium salt ingestions.
- Eclampsia and severe pre-eclampsia.
- Acute severe exacerbations of asthma.
- Other arrhythmias suspected to be related to hypomagnesemia. Magnesium repletion may be helpful in selected patients with cardiac glycoside toxicity but it is not a substitute for digoxin-specific Fab fragments.
- Magnesium may have a role in the treatment of cardiac arrhythmias associated with aluminum and zinc phosphide intoxications.
- Contraindications
- Magnesium should be administered cautiously in patients with renal impairment to avoid the potential for serious hypermagnesemia.
- Magnesium inhibits acetylcholine release and can cause acute muscle weakness and respiratory failure in patients with myasthenia gravis.
- Heart block and bradycardia.
- Adverse effects
- Flushing, sweating, hypothermia.
- Depression of deep tendon reflexes, flaccid paralysis, respiratory paralysis.
- Hypotension, bradycardia, and circulatory collapse with rapid administration.
- Gastrointestinal upset and diarrhea with oral administration.
- Use in pregnancy. FDA Category A. Magnesium sulfate is used commonly as an agent for premature labor (Introduction).
- Drug or laboratory interactions
- Additive effects may occur when CNS depressants are combined with magnesium infusions.
- Concomitant administration of magnesium with neuromuscular blocking agents may enhance and prolong their effect.
- Dosage and method of administration. Magnesium can be given orally, IV, or by IM injection. When it is given parenterally, the IV route is preferred and the sulfate salt generally is used. Dosing is empiric and guided by serum levels, estimated total body magnesium deficit, and clinical response.
- Adults: Give 1 g (8.12 mEq) every 6 hours IV for four doses. For severe hypomagnesemia, doses as high as 8-12 g/d in divided doses have been used. Magnesium sulfate is usually diluted in 50-100 mL of D5W or NS and infused over 60 minutes.
- Children: 25-50 mg/kg/dose IV for three to four doses. Maximum single dose should not exceed 2,000 mg.
- For treatment of life-threatening arrhythmias (ventricular tachycardia or fibrillation associated with hypomagnesemia), give 1-2 g (children, 25-50 mg/kg/dose up to 2 g) IV or IO over 1-2 minutes (if pulseless) or over 5-60 minutes (in a patient with a pulse), diluted in 50-100 mL of D5W or NS. A second dose can be given if the ventricular arrhythmia recurs. A common regimen for adults is 2 g IV over 20 minutes.
- For soluble barium ingestions, magnesium sulfate can be given orally to form insoluble, poorly absorbed barium sulfate in the GI tract. Adults should receive 30 g orally or by lavage, and children 250 mg/kg. Magnesium sulfate should not be given IV in these cases as it may lead to precipitation in renal tubules and acute kidney injury.