Magnesium is a divalent cation that competes with calcium and inhibits many calcium-dependent processes. With regard to muscle relaxation, it is known to:
(1) antagonize calcium either at the motor end plate or cell membrane, reducing calcium influx into the myocyte
(2) Compete with calcium for low-affinity calcium binding sites on the outside of the SR membrane and prevent the rise in free intracellular calcium concentration
(3) Attenuate the: release of Ach at NMJ, sensitivity of the motor endplate to Ach, and excitability of the muscle membrane.
Implications for and potential interactions with anesthesia care are many.
Magnesium may increase the likelihood of hypotension with epidural use (studies with gravid ewes demonstrated reduced maternal MAP, but not uterine blood flow or fetal oxygenation during epidural).
Magnesium can potentiate the effects of both depolarizing and non-depolarizing muscle relaxants (probably not as much with depolarizing) increasing potency and duration (clinically it is still advised to use the same intubating dose as potentiation can be variable; and smaller maintenance doses).
Magnesium can trigger hypotension, especially with concurrent use calcium entry-blocking agents (nifedipine).
Sedation is very commonplace with therapeutic levels of serum magnesium; a 20% decrease in MAC can be seen with serum magnesium levels 7-11 mg/dL.
Magnesium can hypothetically affect any calcium-dependent process, but inhibition of coagulation due specifically to isolated magnesium use is not thought to be clinically significant.
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