Without competitive inhibition, the threshold of motor nerve excitation diminished, leading to enhanced myofiber contraction. 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. Typically due to intestinal malabsorption or renal disease leading to failed reabsorption. Usually defined as depletion of magnesium and is seen when serum concentrations are less than 0.7 mmol/L. 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. Clinical symptoms of hypermagnesemia include, but are not limited to, weakness, decreased respiratory drive, hyporeflexia, hypotension, or electrocardiogram (ECG) changes. Without calcium influx into the cell at the neuromuscular junction, no acetylcholine is released, leading to muscle contraction slowing. 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. It rarely presents unless renal insufficiency is present or the patient is exposed to high levels of exogenous magnesium. Hypermagnesemia is a state of elevated magnesium levels with serum concentrations higher than 2 mmol/L. Magnesium also affects calcium metabolism by stimulation or suppression of Parathyroid Hormone (PTH). More specifically, Mg2+ ions compete on voltage-gated calcium channels, affecting the distribution of calcium uptake and release. Intracellular magnesium is vital for neurochemical transmission and muscular contractions by working indirectly at the neuromuscular junction. Magnesium also acts as cofactors for enzymatic activation in multiple biochemical pathways such as glycolysis and the Krebs cycle.

One role that magnesium plays is helping ion transport and maintain balance across the cellular membrane. 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.

Parathyroid hormone causes magnesium reabsorption in the cortical thick ascending limb, but hypercalcemia and hypermagnesemia will cause magnesium excretion.

Regulation of magnesium concentration in the serum occurs mostly through renal reabsorption and excretion. Magnesium is a positively charged divalent cation that is absorbed in the gastrointestinal tract from our diets. To fully understand how magnesium sulfate works clinically, a basic understanding of how magnesium works intracellularly is helpful.

Mag sulfate antidote