Abstract

Magnesium is the fourth most abundant cation in the body and plays a significant role in the homeostasis of multiple body systems. Magnesium levels are regulated through gastrointestinal absorption and secretion, as well as renal excretion and reabsorption. Magnesium plays a significant role in smooth muscle relaxation, both vascular and uterine, and functions to inhibit skeletal muscle contraction at the motor endplate. Magnesium also suppresses cardiac automaticity and decreases atrioventricular conduction. In addition, magnesium can function as an anticonvulsant by antagonizing the N-methyl-D-aspartate receptor. The multiple significant roles of magnesium allow it great leeway as a therapeutic, and it has use as an antiarrhythmic, antihypertensive, and anticonvulsant in multiple venues. Hypomagnesemia is often unrecognized, as it typically occurs with alteration in other serum electrolytes. It occurs only rarely without associated conditions and is usually identified by these conditions. It is treated by mitigation of causes and enteral or parenteral replacement. Hypermagnesemia is typically identified by its adverse symptoms, ranging from generalized vasodilatation and lethargy to respiratory failure and asystole. Because magnesium homeostasis is most commonly managed by the kidney, renal dysfunction can rapidly lead to hypermagnesemia. Hypermagnesemia can also interfere with certain medications, specifically nondepolarizing muscle relaxants, leading to prolonged muscle relaxation. It is treated by primary prevention, supportive care if necessary, administration of furosemide, calcium chloride, and dialysis.