BNM Flashcards
1
Q
- Describe the physiologic effect of neuromuscular blocking drugs (NMBDs).
A
NMBDs interrupt the transmission of nerve impulses at the neuromuscular junction (NMJ) and produce paresis or paralysis of skeletal muscles. (156)
2
Q
- What are some clinical situations in which NMBDs are used to produce skeletal muscle relaxation?
A
They are used to facilitate tracheal intubation, optimize surgical working conditions, assist in cardiopulmonary resuscitation, and facilitate mechanical ventilation in the emergency department and ICU. (157)
3
Q
- What analgesic effects do NMBDs have?
A
NMBDs have no intrinsic analgesic or anesthetic effects; if used without adequate anesthesia, patients may experience awareness during paralysis. (157)
4
Q
- How does the clinician evaluate the intensity of the neuromuscular blockade?
A
By monitoring the mechanically evoked twitch response using a peripheral nerve stimulator. (157)
5
Q
- What are some characteristics of NMBDs that may influence the choice of which drug is administered to a given patient?
A
They differ in mechanism of action, speed of onset, duration of action, route of elimination, and associated side effects. (157)
6
Q
- What percentage of life-threatening anesthetic-related hypersensitivity reactions are caused by NMBDs?
A
Approximately 11% to 35% of life-threatening anesthetic-related hypersensitivity reactions are attributed to NMBDs. (157)
7
Q
- Which NMBDs are the common offenders to triggering life-threatening anesthetic-related hypersensitivity reactions?
A
Rocuronium and succinylcholine are the most common offenders. (157)
8
Q
- What is an antigenic component that is common to all NMBDs, resulting in possible allergic cross-reactivity of these drugs?
A
The quaternary ammonium group is common to all NMBDs and may cause cross-reactivity. (157)
9
Q
- What is the most common hypersensitivity reaction to sugammadex?
A
Nausea and urticaria are the most common reactions to sugammadex. (157)
10
Q
- What is the neuromuscular junction (NMJ)?
A
The NMJ is the specialized synapse where the motor nerve terminal interfaces with the skeletal muscle fiber’s motor end plate to translate neural signals into muscle contraction. (158)
11
Q
- What events lead to the release of neurotransmitter at the NMJ? What is the neurotransmitter that is released?
A
An action potential arriving at the motor nerve terminal triggers calcium influx, which causes the release of acetylcholine stored in vesicles into the synaptic cleft. (158)
12
Q
- What class of receptors is located at prejunctional and postjunctional sites?
A
Nicotinic acetylcholine receptors are found at both prejunctional and postjunctional sites. (158)
13
Q
- What clinical effect results from the stimulation of postjunctional receptors?
A
Stimulation of postjunctional receptors results in skeletal muscle contraction. (158)
14
Q
- How is the effect of acetylcholine on the postjunctional receptors terminated?
A
Acetylcholine is rapidly hydrolyzed by acetylcholinesterase, which terminates its action and allows repolarization of the muscle membrane. (158)
15
Q
- Where is acetylcholinesterase located in the NMJ?
A
Acetylcholinesterase is located in the folds of the motor end-plate region at the NMJ. (158)
16
Q
- With respect to the NMJ, what are the sites at which nicotinic cholinergic receptors are located?
A
They are located at prejunctional, postjunctional, and extrajunctional sites. (158-159)
17
Q
- What is the role of prejunctional receptors?
A
Prejunctional receptors help facilitate the replenishment and release of acetylcholine in the motor nerve terminal. (159)
18
Q
- What is the structure of nicotinic cholinergic receptors?
A
They are pentameric ion channels composed of five subunits. (159)
19
Q
- Where are the binding sites for acetylcholine on the nicotinic cholinergic receptor?
A
The binding sites are located on the two α-subunits of the receptor. (159)
20
Q
- What effect does acetylcholine binding have on the receptor?
A
Binding of acetylcholine changes the receptor conformation, opening the ion channel to allow sodium and potassium ion flux, which initiates muscle contraction. (159)
21
Q
- What effect does the binding of a nondepolarizing NMBD have on the receptor?
A
Nondepolarizing NMBDs bind to one of the α-subunits, thereby preventing acetylcholine from binding and inhibiting muscle contraction. (159)
22
Q
- What effect does the binding of a depolarizing NMBD have on the receptor?
A
Depolarizing NMBDs (e.g., succinylcholine) bind to both α-subunits, causing initial depolarization followed by sustained depolarization and subsequent neuromuscular blockade. (159)
23
Q
- What is the role of extrajunctional receptors?
A
Extrajunctional receptors are normally suppressed but can proliferate after denervation or trauma, and they are more sensitive to depolarizing agents. (159)
24
Q
- How does the structure of extrajunctional nicotinic cholinergic receptors differ from the postjunctional receptors?
A
Extrajunctional receptors have alterations in their γ and δ subunits compared to postjunctional receptors, while their α-subunits remain identical. (159)
25
25. What is the potential clinical effect of the stimulation of extrajunctional receptors?
Stimulation may lead to an exaggerated hyperkalemic response, particularly in patients with denervation or burn injuries. (159)
26
26. How does the chemical structure of NMBDs relate to their pharmacologic action?
NMBDs share structural similarities with acetylcholine; they are quaternary ammonium compounds with at least one positively charged nitrogen that interacts with the receptor. (159)
27
27. How do the chemical structures of succinylcholine and nondepolarizing NMBDs compare to acetylcholine?
Succinylcholine is essentially two acetylcholine molecules linked by methyl groups, while nondepolarizing NMBDs are bulkier, more rigid molecules that resemble acetylcholine but do not activate the receptor. (161)
28
28. What are some characteristics of succinylcholine that make it unique among the NMBDs?
Succinylcholine is unique for its rapid onset, ultra-short duration, and its depolarizing mechanism of action. (161)
29
29. What is the intubating dose of succinylcholine? What are its approximate time of onset and duration of action when administered at this dose?
An intubating dose of 1.0 to 1.5 mg/kg produces complete paralysis within 30 to 60 seconds and lasts approximately 5 to 10 minutes. (161)
30
30. How should the intubating dose of succinylcholine be altered if a subparalyzing dose of a nondepolarizing NMBD has been administered to blunt fasciculations?
The dose should be increased by approximately 70%. (161)
31
31. What is the mechanism of action of succinylcholine?
Succinylcholine binds to nicotinic receptors causing sustained depolarization of the motor end plate, which prevents repolarization and subsequent muscle contraction. (161)
32
32. What is phase I neuromuscular blockade?
Phase I blockade (depolarizing block) is produced by succinylcholine’s sustained depolarization of the NMJ, with no fade in the train-of-four response. (161)
33
33. What is phase II neuromuscular blockade? What is the mechanism by which it occurs?
Phase II blockade is a desensitization block that occurs after prolonged exposure to succinylcholine, where repolarized membranes become unresponsive to acetylcholine; the exact mechanism is not fully understood. (161)
34
34. When is phase II neuromuscular blockade most likely to occur clinically?
It is most likely with succinylcholine infusions, repeated dosing, or doses exceeding 3 to 5 mg/kg. (161)
35
35. Why do skeletal muscle fasciculations occur with the administration of succinylcholine?
Fasciculations occur due to the initial depolarization and contraction of muscle fibers following succinylcholine administration. (161)
36
36. Why do plasma potassium concentrations increase with the administration of succinylcholine?
Sustained depolarization leads to leakage of potassium from the intracellular compartment into the plasma. (162)
37
37. By how many milliequivalents (mEq) will the plasma potassium concentration increase with the administration of succinylcholine?
Plasma potassium increases by approximately 0.1 to 0.4 mEq/L. (162)
38
38. How is the effect of succinylcholine at the cholinergic receptor terminated?
Its effect is terminated by diffusion away from the NMJ and rapid hydrolysis by plasma (pseudo)cholinesterase. (162)
39
39. How efficiently does plasma cholinesterase hydrolyze succinylcholine?
Plasma cholinesterase hydrolyzes succinylcholine very rapidly and efficiently, so only a small fraction reaches the NMJ. (162)
40
40. How is the duration of action of succinylcholine influenced by plasma cholinesterase?
The duration is directly related to the activity of plasma cholinesterase, which hydrolyzes succinylcholine. (162)
41
41. Where is plasma cholinesterase produced?
Plasma cholinesterase is produced in the liver. (162)
42
42. What are some drugs, chemicals, or clinical diseases that may affect the activity of plasma cholinesterase?
Anticholinesterase agents (e.g., used in insecticides), chemotherapeutic drugs like nitrogen mustard or cyclophosphamide, and severe liver disease can affect its activity. (162)
43
43. What is atypical plasma cholinesterase? What is its clinical significance?
Atypical plasma cholinesterase is a genetic variant that hydrolyzes succinylcholine poorly, leading to prolonged neuromuscular blockade. (162)
44
44. What is dibucaine? What is its clinical use?
Dibucaine is an amide local anesthetic used to inhibit plasma cholinesterase; its inhibition percentage (dibucaine number) is used to assess enzyme quality. (162)
45
45. What is a normal dibucaine number?
A normal dibucaine number is approximately 80. (162)
46
46. In the case of individuals heterozygous for atypical plasma cholinesterase, what is the associated dibucaine number, duration of action of an intubating dose of succinylcholine, and incidence in the population?
Heterozygotes have a dibucaine number between 40 and 60, with neuromuscular blockade lasting about 20 minutes; incidence is roughly 1 in 480. (162)
47
47. In the case of individuals homozygous for atypical plasma cholinesterase, what is the associated dibucaine number, duration of action of an intubating dose of succinylcholine, and incidence in the population?
Homozygotes have a dibucaine number around 20, with blockade lasting 60 to 180 minutes; incidence is about 1 in 3200. (162)
48
48. What is the concern regarding the administration of succinylcholine to children?
The FDA warns against using succinylcholine in children except for emergency airway control, due to risk of acute hyperkalemia in undiagnosed muscular dystrophy. (163)
49
49. What are some adverse cardiac dysrhythmias that may result from the administration of succinylcholine?
Adverse dysrhythmias include sinus bradycardia, junctional rhythms, and even sinus arrest. (163)
50
50. What is the mechanism of cardiac dysrhythmias associated with the administration of succinylcholine?
They likely result from succinylcholine’s stimulation of cardiac postganglionic muscarinic receptors and ganglionic stimulation mimicking acetylcholine. (163)
51
51. When are cardiac dysrhythmias associated with the administration of succinylcholine likely to occur?
They are most likely to occur when a second dose is administered about 5 minutes after the first dose. (163)
52
52. How can the potential risk of adverse cardiac rhythms associated with the administration of succinylcholine be minimized?
Pretreatment with atropine administered 1 to 3 minutes before succinylcholine can minimize the risk. (163)
53
53. What is the mechanism by which massive hyperkalemia may result from the administration of succinylcholine?
Massive hyperkalemia can occur in patients with denervation injury due to proliferation of extrajunctional receptors, leading to an exaggerated potassium efflux. (163)
54
54. Which patients are especially at risk for massive hyperkalemia with the administration of succinylcholine?
Patients with burns, trauma, or spinal cord/neurologic injuries are at high risk. (163)
55
55. Are renal failure patients at increased risk for hyperkalemia in response to the administration of succinylcholine?
No, renal failure patients are not at increased risk unless they have uremic neuropathy. (163)
56
56. What is the mechanism by which succinylcholine administration may cause postoperative myalgia?
Postoperative myalgia is thought to result from unsynchronized, generalized muscle fasciculations during succinylcholine-induced depolarization. (163)
57
57. Which muscles are typically affected by myalgia associated with the administration of succinylcholine?
Myalgia is most often reported in the neck, back, and abdominal muscles. (164)
58
58. Myalgia presenting after the administration of succinylcholine typically manifests in which skeletal muscles?
It often manifests in the neck muscles, which may be mistaken for sore throat pain. (164)
59
59. How might the fasciculations associated with the administration of succinylcholine be prevented?
They may be prevented by pretreatment with a subparalyzing dose of a nondepolarizing NMBD or lidocaine; magnesium can also prevent fasciculations though it does not prevent myalgia. (164)
60
60. What is the treatment for myalgia associated with the administration of succinylcholine?
Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective in treating succinylcholine-induced myalgia. (164)
61
61. What effect does the administration of succinylcholine have on intraocular pressure?
It causes a transient increase in intraocular pressure, peaking 2 to 4 minutes after administration and lasting 5 to 10 minutes. (164)
62
62. What is the clinical significance of the effect of succinylcholine on intraocular pressure?
It may be of concern in patients with open eye injuries, although clinical evidence is limited. (164)
63
63. What effect does the administration of succinylcholine have on intracranial pressure?
Succinylcholine increases intracranial pressure. (164)
64
64. What is the clinical significance of the effect of succinylcholine on intracranial pressure?
The increase in intracranial pressure is generally not of significant clinical concern. (164)
65
65. What effect does the administration of succinylcholine have on intragastric pressure?
It causes unpredictable increases in intragastric pressure, which appear to be related to the intensity of fasciculations. (164)
66
66. What is the clinical significance of the effect of succinylcholine on intragastric pressure?
Increased intragastric pressure may theoretically raise the risk of pulmonary aspiration. (164)
67
67. What effect does the administration of succinylcholine have on masseter muscle tension?
It can cause increased masseter muscle tension, sometimes leading to trismus. (164)
68
68. What is the clinical significance of the effect of succinylcholine on masseter muscle tension?
Severe masseter rigidity may complicate intubation and can be mistaken for malignant hyperthermia, especially in pediatric patients. (164)
69
69. What is the mechanism of action of nondepolarizing NMBDs?
Nondepolarizing NMBDs competitively block acetylcholine from binding to nicotinic receptors at the NMJ, preventing depolarization and muscle contraction. (164)
70
70. How does the limited lipid solubility of nondepolarizing NMBDs affect their clinical effect?
Their limited lipid solubility prevents them from crossing lipid barriers (e.g., the blood-brain barrier), thereby restricting their effects to the NMJ and preventing central effects. (164)
71
71. What are some of the methods by which nondepolarizing NMBDs are cleared? How does this influence their duration of action?
They are cleared via renal filtration and hepatic metabolism; drugs with more efficient clearance have a shorter duration of action. (164)
72
72. What are some drugs and physiologic states that may enhance the neuromuscular blockade produced by nondepolarizing NMBDs?
Enhancement can occur with volatile anesthetics, aminoglycoside antibiotics, local anesthetics, certain antiarrhythmics, dantrolene, magnesium, lithium, tamoxifen, hypothermia, and acidosis. (164)
73
73. What are some drugs and physiologic states that may diminish the neuromuscular blockade produced by nondepolarizing NMBDs?
Calcium, corticosteroids, and anticonvulsants such as phenytoin, as well as conditions like burn injury and cerebrovascular accidents, may diminish the blockade. (165)
74
74. What are some of the methods by which nondepolarizing NMBDs may exert cardiovascular effects?
They may induce histamine release, affect cardiac muscarinic receptors, or act on nicotinic receptors in autonomic ganglia. (165)
75
75. What is the potential adverse effect of the prolonged administration of nondepolarizing NMBDs to patients in the intensive care unit?
Prolonged administration may lead to persistent skeletal muscle weakness or myopathy. (165)
76
76. Which patients are at risk for developing a myopathy in the intensive care unit?
Patients with asthma on corticosteroids and those with multiple organ failure (e.g., sepsis) on prolonged NMBD infusions are at risk. (166)
77
77. What is the recommendation for the administration of nondepolarizing NMBDs to patients in the intensive care unit?
They should be used for as short a duration as possible—ideally no longer than 2 days—and only after optimizing sedation, analgesia, and ventilator settings. (166)
78
78. For pancuronium, what is the ED95, time of onset of action, and duration of action?
For pancuronium, the ED95 is 70 µg/kg, onset is 3 to 5 minutes, and duration is 60 to 90 minutes. (166)
79
79. How is pancuronium cleared from the plasma?
Pancuronium is primarily cleared by glomerular filtration (about 80% unchanged in the urine) and partially by hepatic metabolism. (166)
80
80. How is clearance of pancuronium affected by renal disease?
Renal disease decreases pancuronium clearance by 30% to 50%, leading to prolonged neuromuscular blockade. (166)
81
81. What are the cardiovascular effects of pancuronium? What is the mechanism by which these effects occur?
Pancuronium typically increases heart rate, mean arterial pressure, and cardiac output by 10% to 15%, likely due to selective blockade of cardiac muscarinic receptors. (166)
82
82. Name some intermediate-acting nondepolarizing NMBDs.
Intermediate-acting NMBDs include rocuronium, vecuronium, atracurium, and cisatracurium. (166)
83
83. How do the intermediate-acting nondepolarizing NMBDs compare to pancuronium?
They generally have a similar onset (except rocuronium, which is faster), but their duration of action is about one third that of pancuronium, with a 30% to 50% faster recovery. (166)
84
84. For vecuronium, what is the ED95, time of onset of action, and duration of action?
For vecuronium, the ED95 is 50 µg/kg, with an onset of 3 to 5 minutes and a duration of 20 to 35 minutes. (166)
85
85. How is vecuronium excreted from the body?
Vecuronium is metabolized in the liver and excreted primarily in bile, with partial renal clearance. (166)
86
86. How does renal failure affect the clearance of vecuronium?
Renal failure may impair clearance of vecuronium and its active metabolite, leading to prolonged neuromuscular blockade. (167)
87
87. What are the cardiovascular effects of vecuronium?
Vecuronium has minimal cardiovascular effects. (167)
88
88. For rocuronium, what is the ED95, time of onset of action, and duration of action?
For rocuronium, the ED95 is 0.3 mg/kg, with an onset of 1 to 2 minutes and a duration of 20 to 35 minutes. (167)
89
89. How does the time of onset of rocuronium compare with the time of onset of succinylcholine?
When given at 3 to 4 times its ED95 (approximately 1.2 mg/kg), rocuronium’s onset is similar to succinylcholine’s (around 1–2 minutes). (167)
90
90. How is rocuronium excreted from the body?
Rocuronium is largely excreted unchanged in the bile, with up to 30% excreted renally; its duration may be prolonged in renal failure. (167)
91
91. For atracurium, what is the ED95, time of onset of action, and duration of action?
For atracurium, the ED95 is 0.2 mg/kg, with an onset of 3 to 5 minutes and a duration of 20 to 35 minutes. (167)
92
92. How is atracurium cleared from the plasma?
Atracurium is cleared by nonspecific plasma esterases (ester hydrolysis, about two thirds) and by Hofmann elimination (one third), making its clearance independent of renal or hepatic function. (167)
93
93. What is the major metabolite of atracurium and its potential physiologic effect?
The major metabolite is laudanosine, which can cross the blood-brain barrier and may produce CNS stimulation at high concentrations. (167)
94
94. What are the cardiovascular effects of atracurium?
At larger doses, atracurium may cause hypotension and tachycardia due to histamine release; however, doses less than 2×ED95 rarely produce significant cardiovascular effects. (167)
95
95. For cisatracurium, what is the ED95, time of onset of action, and duration of action?
For cisatracurium, the ED95 is 50 µg/kg, with an onset of 3 to 5 minutes and a duration of 20 to 35 minutes. (167)
96
96. What is the structural relationship between cisatracurium and atracurium?
Cisatracurium is an isolated stereoisomer of atracurium, one of the 10 possible isomers. (167)
97
97. How is cisatracurium cleared from the plasma?
Cisatracurium is primarily eliminated by Hofmann elimination, independent of renal or hepatic function. (167)
98
98. What are the cardiovascular effects of cisatracurium?
Cisatracurium does not cause histamine release and has minimal cardiovascular effects even at high doses. (167)
99
99. For mivacuronium, what is the ED95, time of onset of action, and duration of action?
For mivacuronium, the ED95 is 80 µg/kg, with an onset of 2 to 3 minutes and a duration of 12 to 20 minutes. (167)
100
100. How is mivacuronium cleared from the plasma?
Mivacuronium is metabolized by plasma cholinesterase. (167)
101
101. How is the duration of action of mivacuronium altered in patients with atypical plasma cholinesterase?
In patients with atypical plasma cholinesterase, mivacuronium’s duration of action is prolonged. (168)
102
102. What is the most reliable method for monitoring the effects of NMBDs during general anesthesia?
The use of a peripheral nerve stimulator is the most reliable method to monitor neuromuscular blockade. (168)
103
103. What are some uses of a peripheral nerve stimulator when administering NMBDs during general anesthesia?
It is used to titrate NMBD dosing, assess spontaneous recovery, and evaluate the effectiveness of pharmacologic antagonism. (168)
104
104. Are there advantages to the routine monitoring of the effects of NMBDs during general anesthesia?
Yes; routine monitoring allows for precise titration of NMBDs, reduces the incidence of postoperative residual blockade, and decreases PACU complications. (168)
105
105. Which nerve and muscle are most commonly used to evaluate the neuromuscular blockade produced by NMBDs?
The ulnar nerve and the adductor pollicis muscle are most commonly used. (168)
106
106. Which nerves may be used for the evaluation of the neuromuscular blockade when the arm is not available?
Nerves such as the facial, median, posterior tibial, and common peroneal nerves may be used. (168)
107
107. How do NMBDs vary with regard to their time of onset at the adductor pollicis, orbicularis oculi, laryngeal muscles, and diaphragm?
Nondepolarizing NMBDs generally produce faster blockade of laryngeal and facial muscles than of the adductor pollicis; the diaphragm is more resistant. (168)
108
108. What are some of the mechanical responses evoked by a peripheral nerve stimulator that are used to monitor the effects of NMBDs?
Responses include the single twitch, train-of-four, double burst, tetanus, and post-tetanic stimulation. (168)
109
109. What percentage of depression of a mechanically evoked single twitch response correlates with adequate neuromuscular blockade for intra-abdominal surgery?
A depression of greater than 90% of the twitch response (or loss of two to three twitches in a train-of-four) correlates with adequate blockade. (168)
110
110. What is the train-of-four stimulus delivered by a peripheral nerve stimulator?
It is four electrical stimuli delivered at 2 Hz (one every 0.5 second). (169)
111
111. What is the clinical use of a train-of-four stimulus?
It is used to assess the degree of neuromuscular blockade. (169)
112
112. What is the train-of-four ratio?
The train-of-four ratio is the amplitude of the fourth twitch divided by the first twitch amplitude in the train-of-four sequence. (170)
113
113. What is the clinical use of the train-of-four ratio?
It quantifies the degree of fade in neuromuscular transmission and helps assess recovery from blockade. (170)
114
114. What train-of-four ratio correlates with the complete return to control height of a single twitch response?
A train-of-four ratio of 0.7 or greater is considered to correlate with near-complete recovery; a ratio of 1.0 represents full recovery. (170)
115
115. What train-of-four ratio reflects phase I neuromuscular blockade after the administration of succinylcholine?
Phase I blockade is characterized by a train-of-four ratio of 1.0 (all twitches equally diminished without fade). (170)
116
116. What train-of-four ratio reflects phase II neuromuscular blockade after the administration of succinylcholine?
A train-of-four ratio of less than 0.3, with evident fade, reflects phase II blockade. (170)
117
117. How accurate is the estimation of the train-of-four ratio by clinicians evaluating visually and manually?
Visual or manual estimation of the train-of-four ratio is not reliably accurate. (170)
118
118. What is the double burst stimulus delivered by a peripheral nerve stimulator?
It consists of two bursts of three 50-Hz stimulations separated by 750 ms, perceived as two separate twitches. (170)
119
119. What is the clinical use of the double burst stimulus?
It simplifies the estimation of neuromuscular fade, particularly when the train-of-four response is difficult to assess. (170)
120
120. What is tetanus? How is tetanus mechanically produced by a peripheral nerve stimulator?
Tetanus is a sustained muscle contraction produced by a continuous 50-Hz electrical stimulus for about 5 seconds. (171)
121
121. What is the normal response to tetanus produced by a peripheral nerve stimulator?
A sustained, maximal muscle contraction is the normal response. (171)
122
122. How is the response to tetanus altered by the administration of a depolarizing NMBD?
Under phase I blockade with depolarizing agents like succinylcholine, the tetanic response is markedly reduced without fade. (171)
123
123. How is the response to tetanus altered by the administration of a nondepolarizing NMBD?
Nondepolarizing NMBDs produce a tetanic response that fades over time. (171)
124
124. What is post-tetanic facilitation?
It is the transient increase in acetylcholine availability following a tetanic stimulus that enhances the response to a subsequent train-of-four stimulus. (171)
125
125. What is the clinical use of post-tetanic facilitation?
It is useful for evaluating neuromuscular blockade when no twitches are visible by enhancing the twitch response after a tetanic stimulus. (171)
126
126. Name some anticholinesterase drugs that are used for the antagonism of the effects of NMBDs.
Neostigmine, edrophonium, and, less frequently, pyridostigmine. (171)
127
127. What is the mechanism by which anticholinesterase drugs antagonize the neuromuscular blockade produced by nondepolarizing NMBDs?
They inhibit acetylcholinesterase, increasing acetylcholine concentration at the NMJ, which then outcompetes the NMBD at the receptor. (171)
128
128. How are the cardiac muscarinic effects of anticholinesterases attenuated?
By administering a peripheral-acting anticholinergic such as atropine or glycopyrrolate concurrently. (171)
129
129. If the response to peripheral nerve stimulation is normal, should one still give a small dose of neostigmine or sugammadex?
No; if neuromuscular function has returned to normal, additional antagonist is unnecessary. (172)
130
130. What are some potential complications in the PACU that may be augmented by the presence of postoperative residual neuromuscular blockade?
Complications include airway obstruction, inadequate ventilation, and hypoxia, especially during the first 30 minutes post-extubation. (172)
131
131. Name some factors that influence the success of antagonism of NMBDs.
Factors include the intensity of the blockade at the time of reversal, the choice and dose of antagonist, the rate of spontaneous recovery, and the concentration of inhaled anesthetic. (172)
132
132. How can the adequacy of the recovery from the effects of neuromuscular blockade be evaluated?
By using clinical tests such as sustained head lift, grip strength, and masseter muscle strength, in addition to nerve stimulation measurements. (172)
133
133. When is spontaneous recovery from NMBDs recommended?
Spontaneous recovery without pharmacologic antagonism is not recommended unless there is compelling evidence of full recovery. (172)
134
134. What are some pharmacologic or physiologic factors that may interfere with the antagonism of the neuromuscular blockade produced by NMBDs?
Factors include abnormalities in temperature, acid-base status, electrolyte imbalances, and interactions with other drugs (e.g., aminoglycosides, volatile anesthetics). (172)
135
135. What is sugammadex? What is the mechanism of action of sugammadex?
Sugammadex is an NMBD antagonist that works by encapsulating and inactivating steroidal NMBDs (especially rocuronium and vecuronium). (173)
136
136. What are the major clinical differences between sugammadex and neostigmine?
Sugammadex has no significant cardiovascular effects, can reverse profound neuromuscular blockade rapidly, and works even in deep blockade, unlike neostigmine. (173)
137
137. What are some advantages of sugammadex for the antagonism of neuromuscular blockade?
Advantages include rapid, complete reversal of blockade, reduced risk of residual paralysis, and suitability for rapid sequence induction reversal. (173)
138
138. What is the dose of sugammadex for the reversal of the effects of vecuronium or rocuronium?
For patients with two twitches in the train-of-four, 2 mg/kg; for those with no twitches and 1-2 post-tetanic counts, 4 mg/kg; and for reversal after rocuronium 1.2 mg/kg (rapid sequence induction), 16 mg/kg is used. (173)
