What is the pathophysiology of MH?
An uncontrolled increase in intracellular
calcium, usu-ally due to an abnormal ryanodine receptor, results in sus-tained
and forceful muscle contracture. This culminates in massive increases in both
aerobic and anaerobic muscle metabolism, with subsequent production of heat,
carbon dioxide (CO2), and lactate. Eventually, muscle cell mem-brane
integrity is lost, and spillage of intracellular contents into the circulation
occurs. While the precise cellular events causing MH are not known, triggering
agents cause an imbalance of calcium release and reuptake from sites of the
sarcoplasmic reticulum. The resulting increase in intra-cellular calcium favors
contraction and limits relaxation.
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