Mechanism of Action
Magnesium Metabolism
To fully understand how magnesium sulfate works clinically, a basic understanding of how magnesium works intracellularly is helpful. Magnesium is a positively charged divalent cation that is absorbed in the gastrointestinal tract from our diets. Regulation of magnesium concentration in the serum occurs mostly through renal reabsorption and excretion. Parathyroid hormone causes magnesium reabsorption in the cortical thick ascending limb, but hypercalcemia and hypermagnesemia will cause magnesium excretion. Serum magnesium levels should remain within a range of 0.7 to 1 mmol/L (1.4 to 2.0 meq/L) concentration, but almost half of the total body magnesium is taken up by the bone.[5]
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Physiological Role of Magnesium
One role that magnesium plays is helping ion transport and maintain balance across the cellular membrane. Magnesium also acts as a cofactor for enzymatic activation in multiple biochemical pathways, such as glycolysis and the Krebs cycle. Intracellular magnesium is vital for neurochemical transmission and muscular contractions by working indirectly at the neuromuscular junction. More specifically, Mg2+ ions compete on voltage-gated calcium channels, affecting the distribution of calcium uptake and release. Magnesium also affects calcium metabolism by the stimulation or suppression of parathyroid hormone (PTH).
Hypermagnesemia
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Hypermagnesemia is a state of elevated magnesium levels with serum concentrations higher than 2 mmol/L. It rarely presents unless renal insufficiency is present or the patient is exposed to high levels of exogenous magnesium. Clinical signs of hypermagnesemia result in neuromuscular blockade or vasodilation—high levels of circulating magnesium lead to inhibition of calcium influx through the voltage-gated channels. Without calcium influx into the cell at the neuromuscular junction, no acetylcholine is released, leading to muscle contraction slowing. Clinical symptoms of hypermagnesemia include, but are not limited to, weakness, decreased respiratory drive, hyporeflexia, hypotension, or electrocardiogram (ECG) changes. The most notable ECG changes are P-R interval prolongation, an increase in the Q-T interval, or an increase in QRS duration leading to heart block.
Hypomagnesemia
It is usually defined as the depletion of magnesium and is seen when serum concentrations are less than 0.7 mmol/L, typically due to intestinal malabsorption or renal disease leading to failed reabsorption. Low levels of magnesium can result in the loss of competitive inhibition at the neuromuscular junction, allowing for increased acetylcholine release, resulting in neuromuscular irritability. Without competitive inhibition, the threshold of motor nerve excitation diminished, leading to enhanced myofiber contraction. Clinical symptoms of hypomagnesemia include but are not limited to, muscle spasms, hyperreflexia, or ECG changes. The most notable changes seen on ECG include the widening of the P-R interval, widening of the QRS complex, and peaking of the T waves.[6]
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