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.
Keywordscardiac arrhythmia, eclampsia, hypermagnesemia, hypomagnesemia, magnesium, renal dysfunction
A 23-year-old pregnant woman at 34 weeks and 3 days’ gestation with severe preeclampsia is brought emergently to the operating room for cesarean delivery under general anesthesia. She is currently receiving a magnesium infusion for treatment of her preeclampsia. Forty-five minutes after uneventful rapid-sequence induction with propofol and rocuronium, followed by an uneventful delivery, the patient has continued profound neuromuscular blockade (train of four 0/4 with no posttetanic facilitation). After waiting 30 minutes in the operating room with no improvement, she is brought intubated to the intensive care unit; she is extubated 6 hours later.
Magnesium is the fourth most abundant cation in the body, with total body stores of about 2000 mEq. Normal serum magnesium (Mg 2+ ) concentrations are between 1.4 and 2.1 mEq/L, equivalent to 1.7 and 2.5 mg/dL, respectively (see Table 90.1 for unit conversions); however, serum Mg 2+ concentrations correlate poorly with total body stores, reflecting less than 1% of the total. Gastrointestinal absorption in the duodenum and jejunum represents the principal source of Mg 2+ (8 to 9 mEq/day). The amount of Mg 2+ lost from the body via gastrointestinal secretions is relatively constant (2 mEq/day). In contrast, the kidney can dramatically affect losses in response to lowered serum Mg 2+ concentrations due to reabsorption of Mg 2+ in the proximal renal tubules and the loop of Henle.
|Magnesium sulfate (MgSO 4 )||1 g = 8.13 mEq of Mg 2+|
|Magnesium oxide (MgO)||1 g = 46 mEq of Mg 2+|
|Magnesium acetate (MgC 4 H 6 O 4 )||1 g = 9.35 mEq of Mg 2+|
|Magnesium chloride (MgCl 2 )||1 g = 9.75 mEq of Mg 2+|
|Serum concentrations (all compounds)||1 mg/dL = 0.83 mEq/L = 0.415 mmol/L|
Role in Cellular Function
Magnesium serves as an essential cofactor for many important cellular enzymes (e.g., adenylyl cyclase, Na + ,K + -ATPase). In addition, the magnesium complex, with adenosine triphosphate, serves as a substrate for the enzymatic reaction mediating muscle contraction and relaxation. Magnesium also regulates cellular function by antagonizing the effects of calcium and modulating several potassium currents ( Box 90.1 ).
Ca 2+ Antagonism
Modulates handling of Ca 2+ by sarcoplasmic reticulum
Inhibits Ca 2+ influx into myocyte through sarcolemmal channels
Modulates second messenger system (i.e., adenyl cyclase–adenosine monophosphate)
Competes with Ca 2+ for high affinity site on actin
K + Current
Enhances function of Na + ,K + -ATPase
Blocks outward K + current to result in an increase in inward rectifying K + current
Mediates inwardly rectifying properties