EVENTS TRIGGERED BY MH
The primary MH defect resides in the skeletal muscle at the level of calcium release from the sarcoplastic reticulum of the muscle cell. The resulting hypercalcemia leads to hypermetabolism, which in turn results in increased sympathetic activity, increased carbon dioxide production, increased oxygen consumption, and disruption of the cell membranes. Muscle tissue is unable to return to a resting state in the susceptible patient, and because of this the primary signs of MH begin to appear (AORN 2012, p. 623-625).