MAGNESIUM PHYSIOLOGY

Magnesium sulfate has been used for many years on an empirical basis to control convulsions in patients with preeclamptic toxemia. Magnesium ions are essential for many biochemical reactions, and a deficiency may produce clinically important consequences. Many of the pharmacologic properties have only recently been appreciated. Magnesium is excreted through the gastrointestinal tract and kidneys.

Total-body magnesium is approximately 2000 mEq. Magnesium is the fourth most important cation in the body and the second most important intracellular cation. Magnesium activates approximately 300 enzyme systems, including many involved in energy metabolism.^[54] It is essential for the production and functioning of adenosine triphosphate, which is fully functional only when chelated to magnesium. Other processes dependent on magnesium include the production of DNA, RNA, and protein synthesis.^[54]

Magnesium is an essential regulator of calcium access into the cell and of the actions of calcium within the cell. Magnesium plays an essential role in the regulation of most cellular functions and may be regarded as a natural physiologic calcium antagonist.^[54]

Hypomagnesemia

With an absence of magnesium in the diet, the kidneys are able to significantly decrease excretion; however, hypomagnesemia is common in hospitalized patients, especially those in critical care areas, and it manifests with findings similar to hypocalcemia. Slight hypomagnesemia occurs in athletes, in hypermetabolic states such as pregnancy, and during cold acclimatization. Magnesium stores can become depleted in patients undergoing prolonged diuretic therapy or patients with chronic diarrhea. Chronic alcohol ingestion leads to significant loss of magnesium, and most hospitalized alcoholics have low magnesium levels. Magnesium deficiency alone or in combination with diuretic-induced hypokalemia and digitalis-induced arrhythmia can respond to magnesium therapy.^[52]

It is likely that anesthetizing patients with magnesium deficiency increases the risk of perioperative arrhythmias. Respiratory muscle power is impaired by hypomagnesemia, which may have important clinical consequences for anesthesia and critical care. Additional manifestations include central nervous system irritability with seizures and hyperreflexia and skeletal muscle spasm (i.e., positive Trousseau and Chvostek signs). Treatment includes magnesium sulfate (1 to 2 mEq/kg), which should be administered over 8 to 12 hours with careful measurement and assessment of electrolyte levels.^[53] For acute arrhythmias, magnesium can be administrated in a dose of 8 to 12 mmol/L (200 to 300 mg) intravenously over 1 to 5 minutes with close monitoring of blood pressure and heart rate. Arterial pressure, deep tendon reflexes, and magnesium concentration should be monitored during asymptomatic or life-threatening replacement. In asymptomatic patients with mild hypomagnesemia, oral replacement is preferred. Beyond the theoretical risks of magnesium deficiency and neuromuscular blockade, the critical clinical importance of hypomagnesemia is related to the conditions and pathophysiologic processes associated with management of these conditions ( Table 46-13 ).