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Malignant Hyperthermia

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Malignant Hyperthermia

Malignant Hyperthermia is primarily thought to be an autosomal dominant genetic disorder that causes a hypermetabolic state after administration of volatile anesthetics. When a patient is under anesthesia, the muscles are usually relaxed, but when a patient is experiencing Malignant Hyperthermia crisis, certain IV anesthesia causes the opposite effect. Most inhaled anesthetics other than nitrous oxide, cause or trigger Malignant Hyperthermia. More specifically, the anesthetic agents: Halothane, Chloroform, and Succinylcholine. The genic condition of Malignant Hyperthermia only becomes apparent when a patient is exposed to certain anesthetics such as halothane, which causes muscle rigidity.

During the relaxed phase of muscle contraction, adenosine triphosphate and phosphate (ADP and Pi) are bound to the myosin S1 fragment, which is in a strained vertical position. Depolarization to the sarcoplasmic reticulum occurs followed by the depolarization of the triad region which initiates the release of calcium into the cytosol. This calcium then binds to troponin. A conformational change in the actin-tropomyosin interaction is induced by the troponin-calcium complex, which allows myosin to bind to actin. The binding allows the S1 to move to the unstrained position, causing muscle contraction. During this process, ADP and Pi are released. The muscle contraction results from the shortening of every sarcomere in every muscle fiber of the motor units that is recruited. ATP, if available, then binds to the S1. The ATP is then broken down to ADP and Pi. This result causes the S1 to move to the strained position. ADP and Pi remain attached to the S1. Halothane induces muscle stiffness or rigidity in by an excessive amount of calcium prolonging muscle contraction. The excess calcium released by the muscle cell causes the calcium...

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