What is the pathophysiology of malignant hyperthermia?

Malignant hyperthermia (MH) is primarily caused by a defect in ryanodine receptors (RyR) located in the sarcoplasmic reticulum of skeletal muscle cells. In this condition, certain anesthetic agents or stress triggers lead to excessive release of calcium ions from the sarcoplasmic reticulum into the cytosol. This uncontrolled calcium release activates several metabolic pathways, resulting in increased muscle metabolism, rigidity, and hyperthermia.

The excess calcium in the cytoplasm causes sustained muscle contractions and a hypermetabolic state, which leads to a rise in body temperature and an array of metabolic disturbances, including increased carbon dioxide production and lactic acidosis. This cascade of events creates a life-threatening condition if not promptly treated.

While other options address physiological changes that can occur in different contexts, they do not accurately explain the pathophysiology of malignant hyperthermia. Uncontrolled potassium release is more associated with other muscle disorders, while excessive ATP production and increased glucose uptake relate to different metabolic pathways rather than the specific mechanism of malignant hyperthermia.