NEUROMUSCULAR BLOCKING DRUGS Flashcards
1
Q
- Describe the physiologic effect of neuromuscular blocking drugs.
A
- Neuromuscular blocking drugs interrupt transmission of nerve impulses at the
neuromuscular junction and thereby produce paresis or paralysis of skeletal
muscles. (
2
Q
- What are some clinical situations in which skeletal muscle relaxation is desired?
A
Skeletal muscle relaxation (i.e., paralysis) is desired most frequently to facilitate
intubation of the trachea and provide excellent surgical conditions. Other clinical
situations in which skeletal muscle relaxation is desired include to facilitamechanical ventilation of the lungs either intraoperatively, in the intensive care
unit, or during cardiopulmonary resuscitation.
3
Q
- What are some methods by which skeletal muscle relaxation can be achieved
without the administration of neuromuscular blocking drugs?
A
- Skeletal muscle relaxation can be achieved without the administration of
neuromuscular blocking drugs by the administration of high concentrations
of volatile anesthetics, regional anesthesia, and by proper patient positioning on the
operating table.
4
Q
- What analgesic effects do neuromuscular blocking drugs have?
A
Neuromuscular blocking drugs do not have any anesthetic or analgesic effects.
The potential therefore exists for the patient to be rendered paralyzed without adequate
anesthesia and subsequent unrecognized awareness during anesthesia
5
Q
- What are some characteristics of neuromuscular blocking drugs that may influence
the choice of which drug is administered for clinical use for a given patient?
A
- Neuromuscular blocking drugs vary in their mechanism of action, speed of onset,
duration of action, route of elimination, and associated side effects. These
characteristics of a neuromuscular blocking drug may influence whether a specific
neuromuscular blocking drug is chosen for administration to a given patient
6
Q
- What is the neuromuscular junction?
A
The neuromuscular junction is the location where the transmission of neural
impulses at the nerve terminal becomes translated into skeletal muscle contraction
at the motor endplate. The highly specialized neuromuscular junction consists of the
prejunctional motor nerve ending, a highly folded postjunctional skeletal muscle
membrane, and the synaptic cleft in betwe
7
Q
- What events lead to the release of neurotransmitter at the neuromuscular junction?
What is the neurotransmitter that is released?
A
- A nerve impulse conducted down the motor nerve fiber, or axon, ends in the
prejunctional motor nerve ending. The resulting stimulation of the motor nerve
terminal causes an influx of calcium into the nerve terminal. The influx of calcium
results in a release of the neurotransmitter acetylcholine into the synaptic cleft. This
is why administration of calcium briefly improves neuromuscular function. The
nerve synthesizes and stores acetylcholine in vesicles in the motor nerve terminals,
which is available for release with the influx of calcium. Acetylcholine released into
the synaptic cleft binds to receptors in the postjunctional skeletal muscle membrane,
leading to skeletal muscle contraction
8
Q
- What class of receptors is located on postjunctional membranes? What clinical
effect results from the stimulation of these receptors?
A
Nicotinic cholinergic receptors are located on the skeletal muscle membrane, or
postjunctional membrane. When acetylcholine binds to the nicotinic cholinergic
receptor, there is a change in the permeability of the skeletal muscle membrane to
sodium and potassium ions. The resultant movement of these ions down their
concentration gradients causes a decrease in the membrane potential of the skeletal
muscle cell from the resting membrane potential to the threshold potential. The
resting membrane potential is the electrical potential of the skeletal muscle cell at
rest, usually about 90 mV. The threshold potential is about 45 mV. When the
threshold potential is reached, an action potential becomes propagated over the
surfaces of skeletal muscle fibers. This leads to the contraction of these skeletal
muscle fiber
9
Q
- How, and in what time course, is the action of acetylcholine terminated in the
synaptic cleft? What is the clinical relevance of this?
A
- Acetylcholine is hydrolyzed in the synaptic cleft by the enzyme
acetylcholinesterase, or true cholinesterase. This occurs rapidly, within 15 ms.
Clinically, this allows for the restoration of the membrane to its resting membrane
potential. The metabolism of acetylcholine also prevents sustained depolarization of
the skeletal muscle cells, and thus prevents tetany from occurring
10
Q
- With respect to the neuromuscular junction, what are the three sites at which
nicotinic cholinergic receptors are located?
A
Nicotinic cholinergic receptors are located in three separate sites relative to the
neuromuscular junction and are referred to by their varied locations. Each of these
receptors also has a different functional capacity with regard to its role in
skeletal muscle contraction. The three types of nicotinic cholinergic receptors are
prejunctional, postjunctional, and extrajunctional. Prejunctional receptors are
located at the motor nerve terminal. Postjunctional receptors are located just
opposite the prejunctional receptors in the endplate and are the most important
receptors for the action of neuromuscular blocking drugs. Extrajunctional receptors
are immature in form and are located throughout the skeletal muscle membrane.
They are located in areas other than the endplate region of the muscle membrane as
well as at the motor endplate region.
11
Q
- What is the role of prejunctional receptors?
A
- Prejunctional receptors are located on the motor nerve terminal and influence
the release and replenishment of acetylcholine from the nerve terminal.
12
Q
- What is the role of extrajunctional receptors? What is their effect when stimulated?
A
13
Q
- What is the structure of nicotinic cholinergic receptors? How is the junction of the
cholinergic receptor related to its structure?
A
14
Q
- What is the binding site for an agonist at the nicotinic cholinergic receptor?
A
15
Q
- How does the chemical structure of neuromuscular blocking drugs relate to their
pharmacologic action?
A
16
Q
- What is the intubating dose of succinylcholine? What are its approximate time of
onset and duration of action when administered at this dose?
A
17
Q
- What is the mechanism of action of succinylcholine?
A
18
Q
- What is phase I neuromuscular blockade?
A
19
Q
- What is phase II neuromuscular blockade? What is the mechanism by which it
occurs? When is phase II neuromuscular blockade most likely to occur clinically?
A
20
Q
- What occurs clinically as a result of the opening of the nicotinic cholinergic receptor
ion channel that occurs with the administration of succinylcholine?
A
21
Q
- How efficiently does plasma cholinesterase hydrolyze succinylcholine? Where is
plasma cholinesterase produced?
A
22
Q
- How is the effect of succinylcholine at the cholinergic receptor terminated?
A
23
Q
- How is the duration of action of succinylcholine influenced by plasma
cholinesterase?
A
24
Q
- What are some drugs, chemicals, or clinical diseases that may affect the activity
of plasma cholinesterase?
A
25
Q
- What is atypical plasma cholinesterase? What is its clinical significance?
A
26
Q
- What is dibucaine? What is its clinical use?
A
27
Q
- What is the normal dibucaine number? For heterozygous and homozygous
atypical cholinesterase patients, what is their associated dibucaine number,
duration of action of an intubating dose of succinylcholine, and incidence
in the population?
A
28
Q
- Why is succinylcholine usually not administered to children under nonemergent
conditions?
A
29
Q
- What are some adverse cardiac rhythms that may result from the administration
of succinylcholine? When and why are they likely to occur?
A
30
Q
- How can the potential risk of adverse cardiac rhythms associated with the
administration of succinylcholine be minimized?
A
31
Q
- What is the mechanism by which succinylcholine may induce a hyperkalemic
response with its administration? Which patients are especially at risk for this effect
of succinylcholine?
A
32
Q
- Are renal failure patients at greater risk for a hyperkalemic response to the
administration of succinylcholine?
A
33
Q
- What is the mechanism by which succinylcholine may induce postoperative
myalgias with its administration? Which muscles are typically affected? Which
patients are especially at risk for this effect of succinylcholine?
A
34
Q
- How might the fasciculations associated with the administration of succinylcholine
be blunted?
A
35
Q
- What effect does the administration of succinylcholine have on intraocular
pressure? What is the clinical significance of this?
A
36
Q
- What effect does the administration of succinylcholine have on intragastric
pressure? What is the clinical significance of this?
A
37
Q
- What effect does the administration of succinylcholine have on masseter
muscle tension? What is the clinical significance of this?
A
38
Q
- What is the mechanism of action of nondepolarizing neuromuscular blocking
drugs?
A
39
Q
- Describe the lipid solubility of nondepolarizing neuromuscular blocking drugs.
How does this influence its volume of distribution and clinical effect?
A
40
Q
- What are some of the methods by which nondepolarizing neuromuscular blocking
drugs are cleared? How does this influence its duration of action?
A
41
Q
- What are some drugs and physiologic states that may enhance the
neuromuscular blockade produced by nondepolarizing neuromuscular blocking
drugs?
A
42
Q
- What is the mechanism by which volatile anesthetics are believed to enhance the
neuromuscular blockade produced by nondepolarizing neuromuscular blocking
drugs?
A
43
Q
- What are some of the methods by which nondepolarizing neuromuscular blocking
drugs are able to exert cardiovascular effects?
A
44
Q
- What is a concern regarding patients receiving long-term nondepolarizing
neuromuscular blocking drugs in the intensive care unit?
A
45
Q
- Which patients are at risk for developing a myopathy after the administration
of nondepolarizing neuromuscular blocking drugs in the intensive care unit?
How might they present clinically?
A
46
Q
- How is the clearance of pancuronium affected by renal or liver disease?
A
47
Q
- What are the cardiovascular effects associated with the administration of
pancuronium? What is the mechanism by which these effects occur?
A
48
Q
- Name some intermediate-acting nondepolarizing neuromuscular blocking drugs.
What is their approximate time of onset and duration of action?
A
49
Q
- How is vecuronium excreted from the body? How does renal failure affect the
clearance of vecuronium?
A
50
Q
- How does the time of onset of rocuronium compare with the time of onset of
succinylcholine?
A
51
Q
- How is rocuronium excreted from the body? How does renal failure affect the
clearance of rocuronium?
A
52
Q
- How are cisatracurium and atracurium structurally related?
A
53
Q
- How are atracurium and cisatracurium cleared from the plasma? How does renal
failure affect the clearance of these drugs?
A
54
Q
- What is the principal metabolite of atracurium and its potential adverse physiologic
effect? Which patients are especially at risk for this adverse effect?
A
55
Q
- What are some of the cardiovascular effects of atracurium?
A
56
Q
- What are some differences between cisatracurium and atracurium that make
cisatracurium more desirable for clinical use?
A
57
Q
- Name a short-acting nondepolarizing neuromuscular blocking drug. What is its
approximate time of onset and duration of action?
A
58
Q
- How is mivacurium cleared from the plasma? How is the duration of action of
mivacurium altered in patients who have deficiencies in plasma cholinesterase
enzyme, liver disease, or renal disease?
A
59
Q
- Does the administration of neostigmine reverse the neuromuscular blockade
produced by mivacurium?
A
60
Q
- What are some of the cardiovascular effects of mivacurium?
A
61
Q
- What is the most common method for monitoring the effects of neuromuscular
blocking drugs during general anesthesia?
A
62
Q
- What are two ways in which a peripheral nerve stimulator may be useful during the
administration of neuromuscular blocking drugs during general anesthesia?
A
63
Q
- Which nerve and muscle are most commonly used to evaluate the neuromuscular
blockade produced by neuromuscular blocking drugs?
A
64
Q
- Which nerves may be used for the evaluation of the neuromuscular blockade
produced by neuromuscular blocking drugs through the use of a peripheral nerve
stimulator when the arm is not available to the anesthesiologist?
A
65
Q
- How do the neuromuscular blocking drugs vary with regard to their time of onset at the
adductor pollicis muscle, orbicularis oculi muscle, laryngeal muscles, and diaphragm?
A
66
Q
- How do the neuromuscular blocking drugs vary with regard to their time of onset at the
adductor pollicis muscle, orbicularis oculi muscle, laryngeal muscles, and diaphragm?
A
67
Q
- What percent of depression of a mechanically evoked single twitch response from
its control height correlates with adequate neuromuscular blockade for
intubation of the trachea or for the performance of intraabdominal surgery?
What approximate percent of nicotinic cholinergic receptors must be occupied by
a nondepolarizing neuromuscular blocking drug to achieve this effect?
A
68
Q
- What is the train-of-four stimulus delivered by a peripheral nerve stimulator? What
is its clinical use?
A
69
Q
- What is the train-of-four ratio? What is its clinical use?
A
70
Q
- What train-of-four ratio correlates with the complete return to control height of
a single twitch response?
A
71
Q
- What is the train-of-four ratio during phase I neuromuscular blockade resulting
from the administration of a depolarizing neuromuscular blocking drug such
as succinylcholine?
A
72
Q
- How accurate is the estimation of the train-of-four ratio by clinicians evaluating the
response visually and manually? What percent of the first twitch control height
must be present before the fourth twitch is detectable?
A
73
Q
- What is the double burst suppression stimulus delivered by a peripheral nerve
stimulator? What is its clinical use?
A
74
Q
- What is tetany? How might it be mechanically produced by a peripheral nerve
stimulator?
A
75
Q
- How is the normal response to tetany altered by the administration of depolarizing
and nondepolarizing neuromuscular blocking drugs?
A
76
Q
- What is posttetanic stimulation? What is its clinical use?
A
77
Q
- What is the mechanism by which the neuromuscular blockade produced by
nondepolarizing neuromuscular blocking drugs is antagonized?
A
78
Q
- How are the cardiac muscarinic effects of anticholinesterases attenuated?
A
79
Q
- Name two factors that influence the choice of anticholinesterase drug to be
administered to antagonize the neuromuscular blockade produced by
nondepolarizing neuromuscular blocking drugs.
A
80
Q
- When might neostigmine or edrophonium be an appropriate choice of
anticholinesterase drug to administer to antagonize neuromuscular blockade?
What anticholinergic drug is often paired with each?
A
81
Q
- What are some tests that can be done to evaluate the adequacy of the recovery from
the effects of neuromuscular blockade?
A
82
Q
- How might the residual effects of neuromuscular blockers be manifest clinically
in the awake patient?
A
83
Q
- What are some pharmacologic or physiologic factors that may interfere with the
antagonism of the neuromuscular blockade produced byneuromuscular blocking drugs?
A
84
Q
- What risk factors contribute to adverse respiratory events in the first hour
postoperative in the postanesthetic care unit (PACU)?
A
85
Q
- In addition to induction of anesthesia, what is the most dangerous time for
anesthetic complications in the postoperative period?
A
86
Q
- What is sugammadex? What is the mechanism of action of sugammadex?
A
87
Q
- What are the major clinical differences between sugammadex and neostigmine?
A
88
Q
- What are some advantages of sugammadex for the antagonism of neuromuscular
blockade?
A
