Understanding Anesthesiology - The Global Regional Anesthesia ...

tubation, leading to total airway obstruction, particularly
in children and young adults. Extubating the patient
at a deep plane of inhalational anesthesia (when
the reflex is blunted) is one way to avoid laryngospasm
but is an approach that is only safely applied to the pediatric
patient. In adults (and pediatric patients), performing
extubation when the patient is wide awake
(where consciousness abolishes the reflex) will decrease
the risk of post-extubation laryngospasm. Practicing anesthesiologists
understand that extubating the patient
at a light plane of anesthesia (not awake, but not
“asleep” either) increases the risk of post-extubation laryngospasm.
Reversal of Muscle Relaxation
The action of all non-depolarizing muscle relaxants
must be reversed prior to emergence from anesthesia.
The anticholinesterase drugs, sometimes termed “reversal
agents” are edrophonium, neostigmine and
pyridostigmine (Table 16), with neostigmine being
most commonly used.
The anticholinesterases reverse the effects of the
NDMR. However, in order for them to be completely
effective, some degree of spontaneous recovery from
the NDMR block must be present prior to administration
of the anticholinesterase. Adequacy of reversal is
assessed clinically. The peripheral nerve stimulator is
used while the patient is still unconscious. Traditionally,
the anesthesiologist “eyeballs” the number of
twitches and presence of fade although this technique
is known to result in an underestimation of the degree
of residual blockade. Newer anesthetic machines are
equipped to assess the same indices by measuring mechanical
deflection of the thumb. The most important
indicators are clinical and are measured in the awake
patient. A strong hand grip and the ability to lift the
head off the bed for 5 seconds reliably indicate the return
of adequate muscular strength.
Mechanism of action
Anticholinesterases act in the synaptic cleft of the neuromuscular
junction. Here, they inhibit the action of
cholinesterase, thereby decreasing the rate of breakdown
of acetylcholine (Ach). The increased concentration
of Ach in turn displaces the NDMR from the Ach
receptors and thus restores normal neuromuscular
transmission.
Dose, onset, duration and elimination
Relevant pharmacokinetic facts are summarized in Table
16.
Effects
Unfortunately, the anticholinesterase drugs potentiate
the action of Ach at muscarinic receptors as well as at
the nicotinic receptors of the neuromuscular junction.
This can lead to all of the symptoms that are associated
with excessive parasympathetic tone such as bradycardia,
heart block, increased airway secretions, broncho-
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