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AAA-ANESTHESIOLOGY > Neuromuscular Blocking Agents > Flashcards

Neuromuscular Blocking Agents Flashcards

1
Q

Does muscle relaxation ensure unconsciousness, amnesia, or analgesia?

A

No, muscle relaxation does not ensure unconsciousness, amnesia, or analgesia.

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2
Q

How do depolarizing muscle relaxants differ from nondepolarizing muscle relaxants?

A

Depolarizing muscle relaxants act as acetylcholine (ACh) receptor agonists, while nondepolarizing muscle relaxants function as competitive antagonists.

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3
Q

How are depolarizing muscle relaxants metabolized?

A

Depolarizing muscle relaxants are not metabolized by acetylcholinesterase, they are hydrolyzed in the plasma and liver by pseudocholinesterase.

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4
Q

How are nondepolarizing muscle relaxants metabolized?

A

Nondepolarizing muscle relaxants are not significantly metabolized by acetylcholinesterase or pseudocholinesterase. Their blockade is reversed by redistribution, metabolism, and excretion or by cholinesterase inhibitors.

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5
Q

Why do muscle relaxants have paralytic properties?

A

Muscle relaxants mimic acetylcholine (ACh). For example, succinylcholine consists of two joined ACh molecules.

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6
Q

What happens in patients with homozygous atypical enzyme after succinylcholine administration?

A

Patients with homozygous atypical enzyme will have a prolonged blockade, lasting 4–8 hours, following succinylcholine administration.

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7
Q

Why is succinylcholine contraindicated in children and adolescents?

A

Succinylcholine is contraindicated due to the risk of hyperkalemia, rhabdomyolysis, and cardiac arrest in children with undiagnosed myopathies.

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8
Q

What conditions increase the risk of hyperkalemia with succinylcholine?

A

Conditions like burn injury, massive trauma, neurological disorders, and several others can cause life-threatening potassium elevation with succinylcholine administration.

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9
Q

How does renal failure affect the action of muscle relaxants?

A

Doxacurium, pancuronium, vecuronium, and pipecuronium are partially excreted by the kidneys, and their action is prolonged in renal failure.

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10
Q

How do liver and kidney diseases affect the pharmacokinetics of muscle relaxants?

A

Liver cirrhosis and chronic renal failure may result in a greater initial dose but smaller maintenance doses for muscle relaxants, depending on the drug.

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11
Q

How do atracurium and cisatracurium degrade?

A

Atracurium and cisatracurium undergo degradation in plasma at physiological pH and temperature through Hofmann elimination, independent of organ function.

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12
Q

What cardiovascular effects are associated with pancuronium?

A

Pancuronium may cause hypertension and tachycardia due to vagal blockade and catecholamine release from adrenergic nerve endings.

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13
Q

What is a possible complication of long-term vecuronium administration?

A

Long-term vecuronium use can result in prolonged neuromuscular blockade, possibly from accumulation of its active metabolite or development of polyneuropathy.

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14
Q

What is the onset and duration of rocuronium?

A

Rocuronium has an onset of action that approaches succinylcholine (60–90 s), making it suitable for rapid-sequence induction, but with a much longer duration of action.

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15
Q

How do depolarizing and nondepolarizing muscle relaxants differ in their blockade mechanism?

A

Depolarizing muscle relaxants act as ACh receptor agonists, while nondepolarizing relaxants are competitive antagonists that prevent ACh binding.

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16
Q

How do chronic conditions affect the response to depolarizing and nondepolarizing muscle relaxants?

A

Chronic conditions like muscle denervation injuries lead to upregulation of ACh receptors, causing exaggerated responses to depolarizing relaxants but resistance to nondepolarizing ones.

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17
Q

What is the effect of nondepolarizing muscle relaxants in conditions with fewer ACh receptors (e.g., myasthenia gravis)?

A

Conditions like myasthenia gravis show resistance to depolarizing relaxants and increased sensitivity to nondepolarizing relaxants.

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18
Q

How does neostigmine reverse neuromuscular blockade?

A

Neostigmine reverses nondepolarizing neuromuscular blockade by inhibiting acetylcholinesterase, which increases ACh concentration at the neuromuscular junction.

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19
Q

How does succinylcholine differ from nondepolarizing relaxants in terms of reversal?

A

Succinylcholine is not metabolized by acetylcholinesterase and requires pseudocholinesterase for metabolism, with no specific reversal agent for its blockade, unlike nondepolarizing relaxants.

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20
Q

What is sugammadex and how does it reverse neuromuscular blockade?

A

Sugammadex is a selective relaxant-binding agent that forms tight complexes with steroidal nondepolarizing agents (e.g., vecuronium, rocuronium) to reverse their blockade.

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21
Q

How do drugs that interfere with ACh receptor function cause neuromuscular blockade?

A

Drugs may interfere with ACh receptor function by causing either closed or open channel blockade, affecting ACh binding or channel function.

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22
Q

How does tetanic stimulation help assess neuromuscular recovery?

A

Tetanic stimulation (50–100 Hz) helps assess neuromuscular recovery, with the presence of fade indicating a nondepolarizing blockade or phase II block after succinylcholine.

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23
Q

What is posttetanic potentiation?

A

Posttetanic potentiation is the transient increase in ACh mobilization after tetanic stimulation during a partial nondepolarizing block, leading to a greater response to subsequent twitches.

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24
Q

What is phase II blockade in depolarizing muscle relaxants?

A

Phase II blockade in depolarizing muscle relaxants resembles nondepolarizing blockade and may occur after prolonged succinylcholine administration.

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25
Q

How is neuromuscular blockade assessed using acceleromyography?

A

Acceleromyography is a newer method to quantitatively assess neuromuscular blockade by measuring exact train-of-four ratios, reducing subjective interpretation.

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26
Q

What is the structure of succinylcholine?

A

Succinylcholine consists of two joined ACh molecules, which underlie its mechanism of action, side effects, and metabolism.

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27
Q

How is succinylcholine metabolized?

A

Succinylcholine is metabolized rapidly by pseudocholinesterase into succinylmonocholine, limiting its duration of action.

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28
Q

What factors can prolong the action of succinylcholine?

A

Prolonged action of succinylcholine can occur due to high doses, infusion, hypothermia, reduced pseudocholinesterase levels, or genetically aberrant enzymes.

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29
Q

How is pseudocholinesterase activity tested?

A

Pseudocholinesterase activity is tested by the dibucaine number, which measures the percentage of inhibition of pseudocholinesterase by dibucaine.

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30
Q

What drug interactions affect succinylcholine?

A

Cholinesterase inhibitors and organophosphate pesticides can prolong succinylcholine’s action by inhibiting acetylcholinesterase and reducing pseudocholinesterase activity.

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31
Q

What is the usual dose of succinylcholine for intubation?

A

The usual adult dose of succinylcholine for intubation is 1–1.5 mg/kg intravenously.

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32
Q

What side effects are associated with succinylcholine?

A

Side effects include hyperkalemia, bradycardia, fasciculations, muscle pain, and malignant hyperthermia.

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33
Q

How does succinylcholine affect the cardiovascular system?

A

Succinylcholine can cause bradycardia or tachycardia depending on dose, with children particularly susceptible to profound bradycardia.

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34
Q

What is the relationship between succinylcholine and hyperkalemia?

A

Succinylcholine can increase serum potassium, which can be life-threatening in patients with preexisting hyperkalemia, such as those with burns, trauma, or neurological disorders.

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35
Q

How can fasciculations caused by succinylcholine be prevented?

A

Fasciculations can be prevented by pretreatment with a small dose of nondepolarizing muscle relaxant.

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36
Q

How does succinylcholine affect intraocular pressure?

A

Succinylcholine can raise intraocular pressure temporarily due to contraction of extraocular muscles.

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37
Q

How does succinylcholine affect masseter muscle rigidity?

A

Succinylcholine can transiently increase masseter muscle tone, which may cause difficulty in mouth opening or laryngoscopy.

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38
Q

What is malignant hyperthermia and its relationship to succinylcholine?

A

Malignant hyperthermia is a hypermetabolic disorder triggered by succinylcholine in susceptible individuals, causing severe muscle rigidity and hyperthermia.

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39
Q

What is the general difference between depolarizing and nondepolarizing muscle relaxants?

A

Depolarizing muscle relaxants act as acetylcholine (ACh) receptor agonists, whereas nondepolarizing muscle relaxants function as competitive antagonists.

40
Q

What factors determine the choice of a particular nondepolarizing muscle relaxant?

A

The choice depends on the drug’s unique pharmacological characteristics, often related to its structure, but differences among intermediate-acting relaxants are usually inconsequential for most patients.

41
Q

Why are benzylisoquinolines more likely to release histamine compared to steroidal muscle relaxants?

A

Benzylisoquinolines tend to release histamine, whereas steroidal compounds have fewer histamine-releasing properties.

42
Q

What is the effect of a priming dose for nondepolarizing muscle relaxants?

A

A priming dose (10% to 15% of the intubating dose) can speed up the onset of action of nondepolarizing muscle relaxants, allowing paralysis to follow quickly after the full dose is administered.

43
Q

What is the typical dose for nondepolarizing muscle relaxants to produce intubating conditions?

A

The usual dose is one to two times the ED95 (effective dose for 95% twitch depression), typically used to achieve intubation conditions.

44
Q

How can nondepolarizing muscle relaxants be used to prevent fasciculations from succinylcholine?

A

A 10% to 15% dose of a nondepolarizing muscle relaxant can be administered 5 minutes before succinylcholine to prevent fasciculations and myalgias.

45
Q

How does maintenance relaxation with nondepolarizing muscle relaxants work?

A

Maintenance is achieved by intermittent boluses or continuous infusion, with monitoring of neuromuscular function to prevent over- or underdosing.

46
Q

How do volatile anesthetics affect the dosage of nondepolarizing muscle relaxants?

A

Volatile anesthetics reduce the dosage requirements of nondepolarizing relaxants by at least 15%.

47
Q

How can the combination of nondepolarizing relaxants produce potentiation?

A

Some combinations of nondepolarizing relaxants produce synergistic effects, leading to greater than additive neuromuscular blockade.

48
Q

What autonomic effects are associated with older nondepolarizing relaxants like tubocurarine?

A

Older agents like tubocurarine block autonomic ganglia, reducing sympathetic responses to hypotension and stress, whereas newer nondepolarizers generally lack these effects.

49
Q

Which nondepolarizing relaxants are known for causing histamine release?

A

Atracurium and mivacurium are known to cause histamine release, especially at higher doses.

50
Q

How do nondepolarizing muscle relaxants behave in liver failure?

A

Pancuronium and vecuronium are metabolized by the liver, so liver failure may prolong their action, whereas atracurium and cisatracurium are less affected by liver dysfunction.

51
Q

How do nondepolarizing muscle relaxants behave in renal failure?

A

Doxacurium, pancuronium, vecuronium, and pipecuronium are excreted by the kidneys, and their action is prolonged in renal failure.

52
Q

What is the effect of temperature on nondepolarizing muscle relaxants?

A

Hypothermia prolongs the blockade by decreasing metabolism (e.g., mivacurium, atracurium) and delaying excretion (e.g., pancuronium, vecuronium).

53
Q

How does respiratory acidosis affect nondepolarizing muscle relaxants?

A

Respiratory acidosis potentiates the blockade of most nondepolarizing relaxants and can antagonize its reversal, potentially hindering neuromuscular recovery.

54
Q

Which electrolyte abnormalities affect nondepolarizing muscle relaxants?

A

Hypokalemia and hypocalcemia augment nondepolarizing block, while hypermagnesemia potentiates the blockade by competing with calcium.

55
Q

What is the effect of nondepolarizing muscle relaxants on muscle groups?

A

The diaphragm, jaw, larynx, and facial muscles respond and recover from muscle relaxation more quickly than the adductor pollicis.

56
Q

What is the dose and duration of atracurium for intubation?

A

The dose for intubation is 0.5 mg/kg intravenously, with 0.25 mg/kg administered for intraoperative relaxation, followed by incremental doses of 0.1 mg/kg every 10–20 minutes.

57
Q

How is atracurium metabolized?

A

Atracurium is metabolized by ester hydrolysis and Hofmann elimination, independent of renal and hepatic function.

58
Q

What is a significant side effect of atracurium?

A

Atracurium can trigger dose-dependent histamine release, leading to bronchospasm, hypotension, or skin flushing.

59
Q

Why should atracurium be avoided in asthmatic patients?

A

Atracurium can cause severe bronchospasm, even in patients without a history of asthma.

60
Q

What is laudanosine and its relevance to atracurium?

A

Laudanosine is a breakdown product of atracurium that may cause central nervous system excitation and even seizures in large doses or in patients with hepatic failure.

61
Q

What temperature sensitivity is associated with atracurium?

A

Atracurium’s duration of action is prolonged by hypothermia and to a lesser extent by acidosis due to its unique metabolism.

62
Q

How should atracurium be stored to maintain potency?

A

Atracurium should be stored at 2–8°C and used within 14 days after exposure to room temperature.

63
Q

What is the dosage for cisatracurium?

A

Cisatracurium is dosed at 0.1–0.15 mg/kg for intubation, with a maintenance infusion of 1.0–2.0 mcg/kg/min.

64
Q

How does cisatracurium differ from atracurium?

A

Cisatracurium is four times more potent than atracurium and does not produce a dose-dependent increase in histamine levels.

65
Q

What is the metabolism of cisatracurium?

A

Like atracurium, cisatracurium undergoes Hofmann elimination but does not involve nonspecific esterases. Its metabolism is independent of renal or hepatic function.

66
Q

What side effects are associated with cisatracurium?

A

Cisatracurium may cause the production of laudanosine, and it shares atracurium’s temperature and pH sensitivity and chemical incompatibility.

67
Q

What is the structure of pancuronium?

A

Pancuronium consists of a steroid ring with two modified ACh molecules positioned on it, making it a bisquaternary relaxant.

68
Q

How is pancuronium metabolized and excreted?

A

Pancuronium is metabolized by the liver and excreted primarily through the kidneys, with some excretion through bile.

69
Q

How do renal and hepatic failures affect pancuronium?

A

Renal failure prolongs pancuronium’s blockade, and liver disease requires a larger initial dose but reduces maintenance requirements.

70
Q

What side effects are associated with pancuronium?

A

Pancuronium can cause hypertension, tachycardia, arrhythmias, and allergic reactions, especially in those sensitive to bromides.

71
Q

What structural difference does vecuronium have compared to pancuronium?

A

Vecuronium is pancuronium minus a quaternary methyl group, a minor change that alters side effects without affecting potency.

72
Q

How is vecuronium metabolized and excreted?

A

Vecuronium is metabolized to a small extent by the liver and primarily excreted via biliary routes, with 25% excreted by the kidneys.

73
Q

What happens with prolonged administration of vecuronium in ICU patients?

A

Prolonged use of vecuronium in ICU patients may lead to prolonged neuromuscular blockade, potentially lasting several days, especially in patients with risk factors like renal failure or corticosteroid therapy.

74
Q

What is the typical dosing for vecuronium during intubation?

A

The intubating dose of vecuronium is 0.08–0.12 mg/kg.

75
Q

What are the risks of vecuronium use in female patients?

A

Women may be approximately 30% more sensitive to vecuronium, requiring smaller doses, as evidenced by a greater degree of blockade and longer duration of action.

76
Q

How does vecuronium affect cardiovascular function?

A

At doses up to 0.28 mg/kg, vecuronium has no significant cardiovascular effects, but it may potentiate opioid-induced bradycardia in some patients.

77
Q

How is vecuronium affected by liver failure?

A

In liver failure, vecuronium’s duration of action is not significantly prolonged unless doses exceed 0.15 mg/kg.

78
Q

What is the physical structure of rocuronium?

A

Rocuronium is a monoquaternary steroid analogue of vecuronium designed for a rapid onset of action.

79
Q

How is rocuronium metabolized and excreted?

A

Rocuronium undergoes no metabolism and is primarily eliminated by the liver with minimal renal excretion.

80
Q

What is the usual dose of rocuronium for intubation?

A

Rocuronium requires 0.45–0.9 mg/kg intravenously for intubation.

81
Q

How does rocuronium compare to vecuronium for rapid-sequence inductions?

A

Rocuronium has a rapid onset (60–90 s), making it a suitable alternative to succinylcholine for rapid-sequence inductions, but with a much longer duration.

82
Q

What is the potential side effect of rocuronium at doses of 0.1 mg/kg?

A

Rocuronium at 0.1 mg/kg has been shown to decrease fasciculations and postoperative myalgias when used as precurarization before succinylcholine.

83
Q

What older muscle relaxants are no longer in use?

A

Muscle relaxants like tubocurarine, metocurine, gallamine, alcuronium, rapacuronium, and decamethonium are no longer used or manufactured.

84
Q

What is a key issue with tubocurarine?

A

Tubocurarine often produced hypotension and tachycardia due to histamine release and could exacerbate bronchospasm.

85
Q

How is mivacurium metabolized?

A

Mivacurium is metabolized by pseudocholinesterase, and its duration of action may be prolonged in patients with low pseudocholinesterase levels.

86
Q

What are the cardiovascular effects of mivacurium?

A

Mivacurium releases histamine to a degree similar to atracurium, which can cause cardiovascular effects such as hypotension.

87
Q

How is doxacurium eliminated?

A

Doxacurium is primarily eliminated by renal excretion and is essentially devoid of cardiovascular and histamine-releasing side effects.

88
Q

What are the key characteristics of gantacurium?

A

Gantacurium is a chlorofumarate class nondepolarizing neuromuscular blocker with ultrashort duration of action, similar to succinylcholine.

89
Q

What is the onset and duration of gantacurium?

A

Gantacurium has an onset of 1-2 minutes and a duration of 5-10 minutes, similar to succinylcholine.

90
Q

How does gantacurium degrade?

A

Gantacurium undergoes nonenzymatic degradation through cysteine adduction and ester hydrolysis.

91
Q

What is AV002 (CW002)?

A

AV002 (CW002) is an investigational benzylisoquinolinium fumarate ester-based muscle relaxant with intermediate duration of action.

92
Q

How does AV002 compare to gantacurium?

A

AV002 is similar to gantacurium in its metabolism and elimination but is an intermediate-duration muscle relaxant.

93
Q

How does the presence of liver disease affect rocuronium?

A

Liver disease modestly prolongs the duration of action of rocuronium, while renal function has minimal effect.

94
Q

How does pregnancy affect rocuronium?

A

Pregnancy may modestly prolong the duration of action of rocuronium due to changes in hepatic metabolism.

95
Q

Why might elderly patients experience prolonged effects from rocuronium?

A

Elderly patients may have decreased liver mass, which can result in prolonged duration of action for rocuronium.

AAA-ANESTHESIOLOGY (9 decks)

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