Inhaled Anesthetics
Deep anesthesia with potent volatile anesthetics (in the absence
of neuromuscular blockade) may cause a slight reduction in neuromuscular transmission,
as measured by depression of sensitive indicators of clinical neuromuscular function
such as tetanus and TOF responses.[446]
Inhaled
anesthetics also potentiate the neuromuscular blocking effect of nondepolarizing
neuromuscular blockers. This potentiation results mainly in a decrease in the dosage
requirement of the neuromuscular blocker and prolongation of both the duration of
action of the relaxant and recovery from neuromuscular blockade.[447]
[448]
The magnitude of potentiation depends on
several
factors, including the duration of anesthesia,[446]
[449]
[450]
[451]
[452]
the specific inhaled anesthetic,[196]
[453]
and the concentration used.[454]
The rank of order of potentiation is desflurane > sevoflurane > isoflurane
> halothane > nitrous oxide-barbiturate-opioid or propofol anesthesia ( Fig.
13-26
).[455]
[456]
[457]
[458]
Figure 13-26
Cumulative dose-response curves for rocuronium-induced
neuromuscular block during 1.5 MAC anesthesia with desflurane, sevoflurane, isoflurane,
and total intravenous anesthesia. (Redrawn from Wulf H, Ledowski T, Linstedt
U, et al: Neuromuscular blocking effects of rocuronium during desflurane, isoflurane,
and sevoflurane anesthesia. Can J Anaesth 45:526–532, 1998.)
The more intense clinical muscle-relaxing effect produced by less
potent anesthetics is mainly caused by their larger aqueous concentrations.[459]
Desflurane and sevoflurane have low blood/gas and tissue/gas solubility, so equilibration
between the end-tidal concentration and the neuromuscular junction is reached more
rapidly with these agents than with other inhaled anesthetics.[460]
[461]
The interaction between volatile anesthetics and neuromuscular
blockers is a pharmacodynamic (and not a pharmacokinetic) interaction.[247]
[448]
Proposed mechanisms include (1) a central
effect on α-motor neurons and interneuron synapses,[462]
(2) inhibition of the postsynaptic nAChR,[463]
[464]
[465]
and (3) augmentation of the antagonist affinity
at the receptor site.[459]
