Adverse Effects of Depolarising Neuromuscular Blocking Agents

Abstract

Muscle relaxants block neuromuscular transmission, acting at nicotinic acetylcholine receptors of the neuromuscular junction. Suxamethonium (succinylcholine) is a depolarising agent, whereas all other relaxants in clinical use are nondepolarising. The desired neuromuscular block results from the structural similarity of muscle relaxants to acetylcholine, enabling the interaction with receptors at the neuromuscular junction. Adverse effects of suxamethonium are generally related to its agonist mode of action. Autonomic cardiovascular effects may result. Other adverse effects include anaphylactic or anaphylactoid reactions, and histamine release. Various disease states may present specific considerations in the use of muscle relaxants. Although many complications of muscle relaxants (such as prolonged block or resistance) are easily treated, others may require immediate intervention and vigorous therapy. Careful selection of appropriate relaxants for particular patients will usually prevent the occurrence of complications.

Airway Management of the Critically Ill Patient*

“…Aspiration usually does not occur by way of this effect because of a coincident increase in tone of the esophageal sphincter. 104,105 Succinylcholine increases both intraocular and intracranial pressure, but these effects are transient and clinically unimportant. 106,107 Patients should receive succinylcholine only if adequate face-mask ventilation can be achieved if intubation fails.…”

Adverse reactions to neuromuscular blocking agents

“…Myoglobinemia and increased serum creatinine kinase have been reported following succinylcholine administration, particularly in children [59,62]. The etiology could be the shearing forces set up by asynchronous contractions of adjacent muscle cells following their activation by succinylcholine.…”

Myocardial Muscarinic Receptor Upregulation and Normal Response to Isoproterenol in Denervated Hearts by Familial Amyloid Polyneuropathy

“…Denervation increases myocardial MR density, but without change in cardiac ␤-receptor responsiveness to catecholamines. This probably explains the depression of cardiac automaticity and conductivity during anesthesia with agents such as suxamethonium (succinylcholine) with structural similarity to acetylcholine, 33 and the prompt response to therapeutic infusion of isoproterenol. 11 Whether heterogeneous cardiac autonomic denervation, sympathetic and parasympathetic imbalance, and the loss of the HR circadian rhythmicity could be responsible for an excess of sudden death, even in patients with a pacemaker, is to be determined by further study.…”