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CEACCP > Neuromuscular blocking agents > Flashcards

Neuromuscular blocking agents Flashcards

1
Q

What CVS effects can sux have?

A

Suxamethonium can cause bradycardia, especially if second or further doses are given. This can be prevented by the prior administration of atropine. Children develop this complication more commonly than adults.

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2
Q

What metabolic effects can sux have?

A

The potassium level in the serum will rise by about 0.2-0.4 mmol/L in normal patients and by much more in patients with recent burns, paraplegias or severe muscle trauma

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3
Q

What effects on the brain/eyes can sux have?

A

Raised intracranial and intraocular pressure

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4
Q

List the adverse effects of sux

A 
Bradycardia (especially if >1 dose given)
Hyperkalaemia (burns/paraplegia)
Raised ICP
Raise IOP
Malignant hyperthermia
Sux apnoea
Anaphylaxis
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5
Q

What is sux apnoea?

A

Suxamethonium is metabolised by the enzyme plasma cholinesterase. Some patients lack this enzyme or have an altered enzyme that does not metabolise the suxamethonium as rapidly. These patients may remain paralysed for many hours after a standard dose of suxamethonium, and must be kept anaesthetised and ventilated until the suxamethonium has been eliminated by other, slower methods.

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6
Q

What effects can sux have on the MSK system?

A

Myalgia

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7
Q

What effects can sux have on the GI system?

A

Increased intragastric pressure. This is offset by an increase in oesophageal barrier pressure.

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8
Q

What are the CVS effects of atracurium?

A

Minimal unless histamine release pronounced

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9
Q

What are the RS effects of atracurium?

A

Apnoea. Can cause bronchospasm and histamine release

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10
Q

What are the CNS effects of atracurium?

A

None

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11
Q

What are the GI effects of atracurium?

A

LOS pressure is unaffected

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12
Q

What are the CVS effects of mivacurium?

A

Small (<7%) increase in HR and decrease in BP

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13
Q

What are the RS effects of mivacurium?

A

Apnoea. Bronchospasm with histamine release

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14
Q

What are the CNS effects of mivacurium?

A

No ganglion blockade

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15
Q

What are the effects of liver or kidney disease on atracurium?

A

Unaffected - degraded by ester hydrolysis and Hofmann degradation

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16
Q

What are the effects of liver or kidney disease on mivacurium?

A

Renal and liver failure increase duration of action

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17
Q

What are the CVS side effects of pancuronium?

A

Increased HR/BP/cardiac output, no effect on SVR
Causes noradrenaline release
Vagal blockade effect - can cause tachyarrhythmias, especially in those taking tricyclic antidepressants

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18
Q

What are the RS side effects of pancuronium?

A

Apnoea, histamine release unlikely

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19
Q

What are the coagulation effects of pancuronium?

A

Reduced APTT and PT

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20
Q

What are the CVS SEs of vecuronium?

A

Only large doses produce increased cardiac output and decrease SVR.

Can potentiate opioid-induced bradycardia

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21
Q

What are the RS SEs of vecuronium?

A

Apnoea, histamine release unlikely

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22
Q

What are the coagulation effects of vecuronium?

A

Reduced APTT and PT

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23
Q

What are the CVS SEs of rocuronium?

A

Large doses produce a mild vagolytic effect (increased HR and MAP)

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24
Q

What are the RS SEs of rocuronium?

A

Apnoea, histamine release unlikely

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25
Q

What effects does renal/hepatic failure have on rocuronium action?

A

Renal failure doesn’t effect duration
Hepatic failure does affect it - most of the drug is taken up by the liver and eliminated via the bile. The only metabolite detected in plasma (17-desacetylrocuronium) is 20 times less potent than the parent drug and not likely to contribute to neuromuscular block

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26
Q

What effect does renal/hepatic failure have on pancuronium?

A

Both prolong it’s action

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27
Q

What effect does hypothermia have on non-depolarising neuromuscular blockers?

A

Prolongs blockade by decreasing metabolism and elimination

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28
Q

What effect does respiratory acidosis have on non-depolarising neuromuscular blockers?

A

Potentiates neuromuscular blockade and antagonizes reversal

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29
Q

What effect do electrolyte abnormalities have on non-depolarising neuromuscular blockers?

A

Hypokalemia and hypocalcemia potentiate blockade; in preeclamptic patients who are taking magnesium sulfate can present with hypermagnesemia which also potentiates blockades

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30
Q

What effect does hepatic failure/disease have on non-depolarising neuromuscular blockers?

A

Decreases clearance and increase volume of distribution

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31
Q

What effect does renal failure have on non-depolarising neuromuscular blockers?

A

Decreases clearance, though prolongation of blockade varies

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32
Q

What type of binding do non-depolarising neuromuscular blockers exhibit at the nicotinic receptors?

A

nNMBs are competitive acetylcholine (ACh) antagonists which directly bind to the alpha subunits of nicotinic receptors on the postsynaptic membrane

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33
Q

What would normally happen when ACh binds to the nicotinic receptors on the motor endplate?

A

Binding of the receptor activates its sodium (Na+) channel domain allowing the influx of Na+ and depolarizing the motor endplate from a resting membrane potential of -100 mV to +40 mV depolarized potential.

The depolarizing signal would reach the sarcoplasmic membrane which would signal a release of calcium ions (Ca2+) that facilitates muscular contraction

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34
Q

What are the doses of rocuronium for intubation and maintentance?

A
  1. 5 - 1 mg/kg for intubation

0. 15 mg/kg for maintenance

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35
Q

What are the doses of atracurium and cisatracurium for intubation and maintentance?

A

Atracurium: 0.5 mg/kg given for intubation in 2 mins, 0.1 mg/kg for maintenance every 10-20mins

Cisatracurium: 0.1 to 0.15 mg/kg for intubating conditions within 2mins

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36
Q

What are the doses of pancuronium for intubation and maintentance?

A
  1. 1 mg/kg used for intubation within 2 to 3 minutes

0. 01 mg/kg every 20 to 40 minutes maintenance

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37
Q

What are the doses of vecuronium for intubation and maintentance?

A
  1. 08 to 0.12 mg/kg used for intubation

0. 01 mg/kg every 15 to 20 minutes for maintenance

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38
Q

What are the doses of mivacurium for intubation?

A

0.2 mg/kg for intubation in about 2.5mins

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39
Q

What is the effect of lidocaine on nNMBs?

A

Lidocaine by an open-channel block mechanism

40
Q

How does succinylcholine affect BP?

A

In contrast to its action at cardiac muscarinic receptors, the effect of succinylcholine at ganglionic nicotinic receptors may produce increases in heart rate and blood pressure

41
Q

How does succinylcholine affect BP?

A

In contrast to its action at cardiac muscarinic receptors, the effect of succinylcholine at ganglionic nicotinic receptors may produce increases in heart rate and blood pressure

42
Q

How does succinylcholine affect the ACh receptor permeability to sodium?

A

During depolarization, the acetylcholine receptor permeability to sodium is increased.

43
Q

How fast is mivacurium metabolised compared to succinylcholine?

A

It’s metabolised at 88% of the rate of succinylcholine

44
Q

What are the active metabolites of mivacurium metabolism?

A

There are none

45
Q

Which isomer of mivacurium is least potent?

A

The cis-cis isomer

46
Q

What % of cisatracurium is excreted in the urine?

A

About 15% of cisatracurium is excreted in the urine

47
Q

What % of cisatracurium undergoes Hofmann degradation?

A

77% of cisatracurium undergoes Hofmann degradation

48
Q

What is cisatracurium?

A

Cisatracurium is a bisquaternary benzylisoquinoline

49
Q

Why is cisatracurium slower onset that atracurium?

A

All the isomers of atracurium obey the rule that, within a series of compounds, the more potent the non-depolarizing neuromuscular blocking drug, the slower the onset of action

50
Q

If you give an equipotent dose of cisatracurium and atracurium, which will produce more laudanosine?

A

An equipotent dose of cisatracurium is four times smaller than that of atracurium, and therefore the amount of laudanosine produced is less

51
Q

What is rocuronium?

A

Rocuronium is a monoquaternary aminosteroid

52
Q

What is the ED95 dose of rocuronium?

A

0.3 mg/kg

53
Q

Which is more lipid-soluble, vecuronium or rocuronium?

A

Rocuronium

54
Q

What is rocuronium mainly excreted as?

A

Rocuronium is excreted mainly into the bile and urine as the parent drug.

55
Q

Why is rocuronium faster acting than vecuronium?

A

Rocuronium is less potent than vecuronium and is therefore given in a larger dose, which allows more molecules to reach the neuromuscular junction within fewer circulations.

56
Q

Why is rocuronium faster acting than vecuronium?

A

Rocuronium is less potent than vecuronium and is therefore given in a larger dose, which allows more molecules to reach the neuromuscular junction within fewer circulations.

57
Q

What are the bisquaternary amines?

A

succinylcholine, pancuronium and atracurium contain two quaternary ammonium cations

58
Q

What are the monoquaternary amines?

A

rocuronium, tubocurarine and
vecuronium which have only one permanent
quaternary cation and one tertiary amine

59
Q

Why is NMBs action prolonged in acidosis?

A

at physiological pH, and especially
in acidotic conditions, the tertiary amine can
become protonated and therefore positively
charged, increasing the potency of monoquaternary NMBDs

60
Q

Why is NMBs action prolonged in acidosis?

A

at physiological pH, and especially
in acidotic conditions, the tertiary amine can
become protonated and therefore positively
charged, increasing the potency of monoquaternary NMBDs

61
Q

What is desensitization block?

A

Desensitization occurs when ACh receptors are
insensitive to the channel-opening effects of
agonists, including ACh itself

62
Q

What is a phase 2 block?

A

It occurs after repeated boluses or a prolonged infusion of succinylcholine.

The block is characterized by fade of the train-of-four (TOF) twitch response, tetanic fad and post-tetanic potentiation, which are all features of competitive block. After the initial depolarization, the membrane potential gradually returns towards the resting state, even though the neuromuscular junction is still exposed to the drug. Neurotransmission remains blocked throughout because ACh will not be able to depolarise

63
Q

What is the dose of succinylcholine for intubation?

A

1 - 1.5 mg/kg which will allow intubating conditions in 60s

64
Q

How quickly does sux wear off?

A

Neuromuscular block starts to recover within 3 mins and is completely recovered within 12-15 minutes

65
Q

Why is laudanosine build up in hepatic failure a problem?

A

It can cause seizures due to it’s CNS excitation

66
Q

What is the ED95 of sux?

A

0.3 mg/kg

67
Q

What is the ED95?

A

The dose that depresses the twitch height by 95%

68
Q

What % of hypersensitivity reactions to NMBs are caused by sux?

A

50%

Estimated to be in 1:4000

69
Q

What type of hypersensitivity reaction does sux tend to cause?

A

Type 1 hypersensitivity anaphylaxis (IgE-antibody mediated)

70
Q

What would happen if you gave neostigmine without glycopyrolate?

A

Neostigmine is an acetylcholinesterase inhibitors, causes increased parasympathetic effects; the most worrisome of these effects being bronchospasm and laryngeal collapse.

71
Q

What gene determines the structure of plasma cholinesterase?

A

By a single gene that is located on chromosome 3 (3q26)

72
Q

What is normal plasma cholinesterase?

A

The gene of which is designated E1u
It’s a tetrameric glycoprotein consisting of four identical subunits.
Each subunit consists of 574 amino acids

73
Q

What is the atypical gene for plasma cholinesterase?

A

The atypical gene, E1a produces the most
common variant, where Asp-70 to Gly-70 substitution significantly reduces the binding capacity of the enzyme for succinylcholine

74
Q

What % of receptors must be occupied to produce a complete block?

A

92%

75
Q

What is an open ion-channel block?

A

In open-channel block, the molecules enter the open ion channel and occlude it. It is use-dependent, which means that the molecules can enter the channel only when it is opened by an agonist. With the channels blocked, influx of sodium ions is obstructed. This prevents depolarization, and weaker or complete block of neurotransmission results

76
Q

What is a closed ion-channel block?

A

In closed-channel block, the drug molecules occupy the mouth of the receptors. By their presence, ions are prevented from passing through the channel to depolarize the end-plate. It has been proposed as the mechanism of action of tricyclic antidepressants, naltrexone and naloxone in potentiating neuromuscular block.

77
Q

What is the structure of the benzylisoquinolinium compounds?

A

They consist of two quaternary ammonium groups
joined by a thin chain of methyl groups. The methyl chain contains one or more chiral atoms, which leads to
the existence of several stereoisomers of these drugs

78
Q

What is atracurium presented as?

A

A racemic mixture of 10 stereoisomers and geometric isomers

79
Q

What is the duration of atracurium?

A

45mins (cisatracurium same duration)

80
Q

What is the duration of pancuronium?

A

75 mins

81
Q

What is the duration of vecuronium?

A

33 minutes

82
Q

What is the duration of rocuronium?

A

33 mins

83
Q

What is the duration of mivacurium?

A

16 mins

84
Q

What % of atracurium is metabolised by Hoffman degradation?

A

45%

85
Q

What % of atracurium is excreted in the urine?

A

10%

86
Q

What is laudanosine?

A

A tertiary amine

87
Q

What is mivacurium made of?

A

A racemic mixture of three isomers. The more
potent cis-trans and trans-trans isomers form 95% of the drug; they are rapidly hydrolysed by plasma cholinesterase.

The cis-cis isomer, which has 10–15 times less neuromuscular blocking activity than the other two, is slowly hydrolysed, mainly excreted in the urine and not likely to contribute to neuromuscular block.

88
Q

WHat is doxacurium?

A

It’s the most potent non-depolarizing NMBD; the
intubating dose is 0.05 mg/kg. It produces no histamine release or cardiovascular effects over the clinical dose range. It has a long onset of action and a prolonged duration of effect. It is excreted mainly
in the urine and the bile.

89
Q

What is cisatracurium?

A

It is the 1R-cis 10 R-cis isomer of atracurium. It constitutes 15% of the mixture of atracurium. It is four times more
potent than atracurium and has a slightly longer onset and duration of action

90
Q

What unwanted effects does cisatracurium produce?

A

It does not release histamine and has no

direct cardiovascular effect

91
Q

What is the structure of the aminosteroid compounds?

A

Aminosteroid compounds contain an androstane skeleton to which ACh-like moieties are introduced at the A ring and ring. Most depend on organ function for their excretion. Some undergo deacetylation in
the liver, and the deacetylated metabolites may possess neuromuscular blocking properties.

92
Q

What is the metabolism of pancuronium?

A

60% of the drug is excreted unchanged through the

kidney. A small amount undergoes deacetylation in the liver.

93
Q

What is vecuronium supplied as?

A

Vecuronium is unstable in solution, so it is supplied as lyophilized powder

94
Q

What is more lipid soluble, vecuronium or pancuronium?

A

Compared with pancuronium, it is more lipid-soluble; this promotes significant hepatic uptake and biliary excretion

95
Q

What is the metabolism of vecuronium?

A

About 30–40% of the drug undergoes deacetylation in the liver, and one of the metabolites (3-desacetylvecuronium) is nearly as potent (80%) as the parent drug. This can accumulate in renal failure and prolong the block.

96
Q

What is pipecuronium?

A

A more potent version of pancuronium with no vagolytic or sympathomimetic effects

97
Q

What is more potent, rocuronium or vecuronium?

A

Rocuronium is 6-8 times less potent than vecuronium

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