Clinical Uses
In spite of its many adverse effects, succinylcholine is still
commonly used. Its popularity is probably due to its rapid onset of effect, the
profound depth of neuromuscular blockade that it produces, and its short duration
of action. Although it may be less commonly used than in the past for routine endotracheal
intubation, it is the neuromuscular blocker of choice for rapid-sequence induction
of anesthesia. In a study[147]
comparing intubating
conditions after 1 mg/kg succinylcholine with those after 0.1 mg/kg vecuronium or
0.1 mg/kg pancuronium at 30 seconds after the administration of a relaxant and at
30-second intervals after that for up to 120 seconds, intubation could be accomplished
in all patients receiving succinylcholine at 30 seconds, in contrast to the other
neuromuscular blockers studied. Furthermore, at all time points studied, up to 90
seconds, intubating conditions were better after the administration of succinylcholine
than after either of the other two neuromuscular blockers. Although 1.0 mg/kg succinylcholine
has long been recommended to facilitate endotracheal intubation at 60 seconds, recovery
of neuromuscular function may not occur quickly enough to prevent hemoglobin desaturation
in an apneic patient.[148]
[149]
Recent studies have indicated that 0.5 to 0.6 mg/kg succinylcholine should allow
for adequate intubating conditions 60 seconds after administration for nonrapid sequence
intubation.[150]
[151]
A small dose of nondepolarizing neuromuscular blocker is commonly
given 2 minutes before administering the intubating dose of succinylcholine. This
defasciculating dose of nondepolarizing neuromuscular blocker will attenuate increases
in intragastric and intracranial pressure, as well as minimize the incidence of fasciculations
in response to succinylcholine. The previous administration of a nondepolarizing
agent will render the muscle relatively resistant to succinylcholine, and the succinylcholine
dose should therefore be increased by 50%.[152]
The use of a defasciculating dose of a nondepolarizing neuromuscular blocker may
also slow the onset of succinylcholine and produce less favorable conditions for
tracheal intubation.[136]
[137]
Typically after administering succinylcholine for intubation,
a nondepolarizing neuromuscular blocker is given to maintain neuromuscular blockade.
Succinylcholine given first may enhance the depth of block induced by a subsequent
dose of nondepolarizing neuromuscular blocker.[153]
[154]
[155]
However,
the effect on duration of action is variable. Succinylcholine has no effect on pancuronium,
pipecuronium, or mivacurium,[155]
[156]
but it increases the duration of atracurium and rocuronium.[153]
[154]
The reasons for these differences are not
clear.
The changing characteristics of succinylcholine neuromuscular
blockade over the course of prolonged administration have been reviewed by Lee and
Katz[157]
and are summarized in Table
13-3
. TOF stimulation is a very safe and useful guide in detecting the
transition from a phase 1 to a phase 2 block. A phase 1 block has all the characteristics
of a depolarizing block as described previously in the section on monitoring. A
phase 2 block has the characteristics of a nondepolarizing block. With the administration
of large doses of succinylcholine, the nature of the block, as determined by a neuromuscular
blockade
*Cumulative
dosage of succinylcholine by infusion under nitrous oxide anesthesia supplemented
with intravenous agents. The dosage requirement to cause a phase 2 block is less
in the presence of potent volatile anesthetics (e.g., isoflurane). Adapted
from Lee C, Katz RL: Neuromuscular pharmacology. A clinical update and commentary.
Br J Anaesth 52:173–188, 1980.
monitor, changes from that of a depolarizing agent to that of a nondepolarizing agent.
Clearly, both the dose and the duration of administration of succinylcholine are
important variables, although the relative contribution of each has not been established.
Practically, if administration of the drug is terminated shortly after TOF fade
is clearly evident, rapid return of normal neuromuscular function should ensue.
In addition, the decision of whether to attempt antagonism of a phase 2 block has
always been controversial. However, if the TOF ratio is less than 0.4, administration
of edrophonium or neostigmine should result in prompt antagonism. Ramsey and colleagues
[158]
recommended that antagonism of a succinylcholine-induced
phase 2 block with edrophonium or neostigmine be attempted after spontaneous recovery
of the twitch response has been observed for 20 to 30 minutes and has reached a plateau
phase with further recovery proceeding slowly. These researchers state that in this
situation, edrophonium and neostigmine invariably produce "dramatic" acceleration
of the return of the TOF ratio toward normal. Monitoring neuromuscular function
with TOF stimuli will help avoid succinylcholine overdose, detect the development
of a phase 2 block, observe the rate of recovery of neuromuscular function and assess
the effect of edrophonium or neostigmine on recovery.
