Adverse Effects and Contraindications

Succinylcholine produces muscle fasciculation, which may result in myoglobinuria and postoperative muscle pain. The amount produced depends on the level of physical fitness. Succinylcholine causes contractions of extraocular muscles, posing the danger of transient elevated intraocular pressure. Succinylcholine may produce hyperkalemia in patients with large masses of traumatized or denervated muscle (e.g., spinal cord injury). Denervated muscle is especially sensitive to depolarizing drugs because of the increased number of AChRs on the sarcolemma (denervation supersensitiv-ity). Succinylcholine also causes prolonged contraction of the diseased muscles of patients with myotonia or amyotrophic lateral sclerosis.

Succinylcholine-induced hyperkalemia may lead to cardiac arrhythmia and arrest when plasma K+ reaches 7 and 10 mM, respectively. The drug also may precipitate a fulminant attack of malignant hyperthermia in susceptible individuals (not to be confused with neu-roleptic malignant hyperpyrexia, which involves do-pamine and the CNS). Treatment in either case consists of cooling the body and administering oxygen and dantrolene sodium (discussed later).

Nondepolarizing Blockers: d-Tubocurarine, Atracurium, Mivacurium, Pancuronium, Vecuronium, Rocuronium, and Rapacuronium Mechanism of Action

With the exception of succinylcholine, all neuromuscular blocking agents are nondepolarizing. These agents prevent excitation of end plate AChRs by acting as reversible competitive antagonists at the binding sites. The prototype for this group is d-tubocurarine, an alkaloid used as a South American arrow poison. In general, these compounds have two charged heads (e.g., quaternary ammonium) separated by a "thick" organic moiety (e.g., steroid nucleus). These heads enable attachment of the drug to the two AChR binding sites. However, because of the large intervening moiety, the channel is occluded such that the flow of cations is prevented. Because of the competitive nature of this blockade, the effect of nondepolarizing blockers can be reversed by anti-AChE agents and other procedures that increase the synaptic concentration of ACh.

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