TY - CHAP M1 - Book, Section TI - Cholinesterase Inhibitors & Other Pharmacological Antagonists to Neuromuscular Blocking Agents A1 - Butterworth IV, John F. A1 - Mackey, David C. A1 - Wasnick, John D. Y1 - 2022 N1 - T2 - Morgan & Mikhail’s Clinical Anesthesiology, 7e AB - KEY CONCEPTS The primary clinical use of cholinesterase inhibitors is to reverse nondepolarizing neuromuscular blockers. Acetylcholine is the neurotransmitter for the entire parasympathetic nervous system (parasympathetic ganglions and effector cells), parts of the sympathetic nervous system (sympathetic ganglions, adrenal medulla, and sweat glands), some neurons in the central nervous system, and somatic nerves innervating skeletal muscle. Neuromuscular transmission is blocked when nondepolarizing muscle relaxants compete with acetylcholine to bind to nicotinic cholinergic receptors. The cholinesterase inhibitors indirectly increase the amount of acetylcholine available to compete with the nondepolarizing agent, thereby reestablishing neuromuscular transmission. Acetylcholinesterase inhibitors prolong the depolarization blockade of succinylcholine. Any prolongation of action of a nondepolarizing muscle relaxant from renal or hepatic insufficiency will probably be accompanied by a corresponding increase in the duration of action of a cholinesterase inhibitor. The time required to fully reverse a nondepolarizing block depends on several factors, including the choice and dose of cholinesterase inhibitor administered, the muscle relaxant being antagonized, and the extent of the blockade before reversal. A reversal agent should be routinely given to patients who have received nondepolarizing muscle relaxants unless full reversal can be demonstrated or the postoperative plan includes continued intubation and ventilation. Newer quantitative methods for assessing recovery from neuromuscular blockade, such as acceleromyography, may further reduce the incidence of undetected residual postoperative neuromuscular paralysis. Sugammadex exerts its effects by forming tight complexes in a 1:1 ratio with steroidal neuromuscular blocking agents. Cysteine causes the inactivation of gantacurium via metabolic degradation and adduct formation. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/10/08 UR - accessanesthesiology.mhmedical.com/content.aspx?aid=1190604495 ER -