The adverse reactions seen following administration of
neuromuscular blocking agents are mainly cardiovascular. Due to the lack of specificity for the
nicotinic receptor at the neuromuscular junction, these agents may interact with receptors in autonomic ganglia and
muscarinic receptors in the heart. Furthermore, muscle relaxants may have
histamine-releasing properties. The cardiovascular effects vary with potency and specificity of the
drug, depending mainly on the chemical structure.
Pancuronium,
fazadinium and especially gallamonium block cardiac
muscarinic receptors, and
tachycardia may be seen.
Atracurium,
metocurine and in particular
d-tubocurarine have
histamine-releasing properties and may cause
flushing,
hypotension and
tachycardia.
Vecuronium has no effect on the cardiovascular system. The effect of
succinylcholine on heart rate differs between children, where
bradycardia is seen, and adults in whom
tachycardia may follow. However,
bradycardia may occur in adults following a single dose.
Succinylcholine increases plasma
potassium, especially in patients with nerve damage, and arrhythmias may be observed. The neuromuscular adverse effects of
succinylcholine, such as
fasciculations and increased gastric and intraocular pressure, may be prevented by precurarisation. Many drugs interact with
neuromuscular blocking agents and there is often a potentiation of the
neuromuscular effect. This is of clinical importance in the case of
antibiotics, inhalational anaesthetics,
lithium and
cyclosporin. Difficulty in reversing the block may occur with
calcium channel blockers and
polymyxin. However, some drugs, such as
phenytoin,
carbamazepine and
lithium, may cause resistance to
neuromuscular blocking agents. Furthermore, clinically important interactions exist between individual neuromuscular blocking drugs. Precurarisation with a non-depolarising
drug prolongs the onset of
succinylcholine, and conversely a prolonged effect of non-depolarising drugs is seen following
succinylcholine. The effect of
succinylcholine is markedly prolonged if the
drug is administered during recovery from
pancuronium blockade or following
neostigmine for reversal.
Succinylcholine is hydrolysed by plasma
cholinesterase, and drugs which decrease the activity of this
enzyme may produce a prolonged block, i.e.
contraceptive pills,
cyclophosphamide, echothiopate and
organophosphate.