Depolarizing Neuromuscular Blockade (Phase I and II
Blocks)
Patients with normal plasma cholinesterase activity who are given
a moderate dose of succinylcholine (0.5 to 1.5 mg/kg) undergo a typical depolarizing
neuromuscular block (phase I block) (i.e., the response to TOF or tetanic stimulation
does not fade, and no post-tetanic facilitation
*Results
from a prospective, randomized, and blinded study of postoperative POPC in a total
of 691 adult patients undergoing abdominal, gynecologic, or orthopedic surgery, receiving
either pancuronium, atracurium, or vecuronium.[99]
In 4 of the 46 patients with POPC (1 in the pancuronium group and 3 in the atracurium
and vecuronium groups) the TOF ratio was not available. Because there were no significant
differences in the two groups of patients given the intermediate-acting muscle relaxants,
the data from these groups are pooled.
†P < 0.02
compared with patients in the same group with TOF ratio ≥0.70.
of transmission occurs). In contrast, some patients with genetically determined
abnormal plasma cholinesterase activity who are given the same dose of succinylcholine
undergo a non-depolarizing-like block characterized by fade in the response to TOF
and tetanic stimulation and occurrence of post-tetanic facilitation of transmission
( Fig. 39-19
). This type
of block is called a phase II block (dual, mixed, or desensitizing block). Also,
phase II blocks sometimes occur in genetically normal patients after prolonged infusion
of succinylcholine.
From a therapeutic point of view, a phase II block in normal patients
must be differentiated from a phase II block in patients with abnormal cholinesterase
activity. In normal patients, a phase II block can be antagonized by administering
a cholinesterase inhibitor a few minutes after discontinuation of succinylcholine.
In patients with abnormal genotypes, the effect of intravenous injection of an acetylcholinesterase
inhibitor (e.g., neostigmine) is unpredictable. For example, neostigmine can potentiate
the block dramatically, temporarily improve neuromuscular transmission, and then
potentiate the block or partially reverse the block, all depending on the time elapsed
since administration of succinylcholine and the dose of neostigmine given. Therefore,
unless the cholinesterase genotype is known to be normal, antagonism of a phase II
block with a cholinesterase inhibitor should be undertaken with extreme caution.
Even if the neuromuscular function improves promptly, patient surveillance should
continue for at least 1 hour.
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