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Anaesthesia > Day 4: Neuromuscular blocking agents > Flashcards

Day 4: Neuromuscular blocking agents Flashcards

1
Q

What is the role of the Neuromuscular Junction (NMJ) in skeletal muscle?

A

The NMJ converts nervous impulses into skeletal muscle contractions.

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2
Q

What neurotransmitter is key at the NMJ?

A

Acetylcholine (Ach) is the key neurotransmitter at the NMJ.

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3
Q

How is acetylcholine broken down at the NMJ?

A

Acetylcholine is broken down by Acetylcholinesterase (AChE) at the NMJ.

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4
Q

Excitation-contraction coupling

A

Nervous impulse is converted into a skeletal muscle contraction at the NMJ

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5
Q

formation of Acetylcholine

A

Formed from ACETYL CoA + CHOLINE

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6
Q

storage of acetylcholine

A

Stored in pre-synaptic vesicles

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7
Q

What type of receptors does acetylcholine bind to on the post-junctional membrane at the NMJ?

A

Acetylcholine binds to NICOTINIC cholinergic receptors on the post-junctional membrane at the NMJ.

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8
Q

what blocks the release of Ach

A

magnesium
aminoglycosides
botox

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9
Q

how to achieve muscle relaxations

A

blockade of
- motor nerves (local anaesthetics)
-the NMJ (intravenous muscle relaxants)
- receptors inside the muscle cells (dantrolene)

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10
Q

What historical event is associated with the discovery of NMJ blockers in the 16th century?

A

Explorers encountering the Amazonians in South America observed the use of poison arrows that caused death by skeletal muscle paralysis. This poison, known as curare, contained tubocurarine, which was later discovered to block the NMJ at the nicotinic acetylcholine receptor.

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11
Q

What was the active ingredient in curare, the poison used by Amazonians?

A

The active ingredient in curare was tubocurarine, which was later found to block the NMJ at the nicotinic acetylcholine receptor.

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12
Q

What specific receptor does tubocurarine block at the neuromuscular junction (NMJ)?

A

Tubocurarine blocks the nicotinic acetylcholine receptors on the post-junctional membrane at the NMJ.

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13
Q

classification of neuromuscular blockers

A

depolarising agents
non- depolarising agents

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14
Q

depolarising agents

A

suxamethonium

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15
Q

non- depolarisng agents

A

all other muscle relaxants in common use

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16
Q

mechanism of depolarising agents

A

Non-competitive action

Cannot be reversed… wear off / are metabolised over time

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17
Q

mechanism of action of non- depolarising agents

A

-Competitive inhibition
-Compete with Ach for nicotinic receptors
-Require reversal

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18
Q

ED95

A

“Effective Dose”
Dose of muscle relaxant that will paralyse 95% of normal people

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19
Q

Usual intubating does

A

2 x ED95

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20
Q

Adequate does of muscle relaxant will result in:

A

Inability to breathe
Inability to maintain an airway
Loss of protective reflexes

Consciousness is completely unimpaired

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21
Q

factors that potentiate muscle relaxants

A

drugs
electrolytes
pH
Temperature
Diseases

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22
Q

drugs

A

-Inhalational agents (up to 15%)
-Aminoglycoside antibiotics (e.g. gentamicin)

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23
Q

electrolytes

A

↓ Calcium
↑ Magnesium
↓ Potassium

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24
Q

pH

A

acidosis

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25
Q

temperature

A

Cold
Warm – non-depolarisers
(potential problem post-op ‘recurarisation’)

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26
Q

diseases

A

Myasthenia gravis (non-depolarisers)
Muscular dystrophies, dystonias, myopathies
Renal failure

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27
Q

surgical indications for muscle relaxation

A

facilitate surgical access
immobile filed required

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28
Q

anaesthetic indications for muscle relaxation

A

-intubation/ protection of airway required
-controlled ventilation required
-prone/ abnormal positioning

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29
Q

patient indications for muscle relaxation

A

various/ critical illness

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30
Q

examples of muscle relaxation cases

A

-Improved surgical access (abdominal surgery)
-Facilitate intubation or bronchoscopy
-Prevention of movement in microsurgery
*Unconscious patients can still move!
-Manipulation of fractures
-Preventing / mitigating physical effects of convulsions
-ICU
*Tetanus
*Respiratory failure
*Severe ↑ ICP

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31
Q

How is suxamethonium typically supplied in ampoules?

A

Suxamethonium is typically supplied in 100mg ampoules, equivalent to 2mls.

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31
Q

Before administering muscle relaxant it is essential to:

A

-Assess the airway
-Be competent in airway management
-Have necessary equipment

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32
Q

What is the chemical structure of suxamethonium?

A

Suxamethonium consists of two acetylcholine molecules.

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33
Q

What is the recommended dose of suxamethonium, and how should it be stored?

A

The recommended dose of suxamethonium is 1-2mg per kilogram of body weight. It should be stored in the fridge.

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34
Q

What are the effects of suxamethonium?

A

Suxamethonium induces profound paralysis within 60 seconds of administration. It is ultra-short-acting and causes fasciculations. Its effects last approximately 5 minutes.

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35
Q

What enzyme is responsible for metabolizing suxamethonium?

A

Suxamethonium is metabolized by pseudocholinesterase, also known as plasma cholinesterase.

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36
Q

Where is pseudocholinesterase synthesized?

A

Pseudocholinesterase is synthesized in the liver.

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37
Q

How is pseudocholinesterase distributed in the body?

A

Pseudocholinesterase is found freely in the plasma.

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38
Q

What condition is associated with markedly decreased levels of pseudocholinesterase?

A

Scoline apnoea, inherited either homozygous or heterozygous, leads to markedly decreased levels of pseudocholinesterase.

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39
Q

What are the consequences of prolonged paralysis due to reduced pseudocholinesterase activity?

A

Prolonged paralysis due to reduced pseudocholinesterase activity requires supportive treatment with ventilation, sedation, and may necessitate the administration of fresh frozen plasma (FFPs).

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40
Q

side effects of suxamethonium

A

-Muscle pains (myalgia)
-Bradycardia
-Hyperkalaemia and arrhythmias, even cardiac arrest
-Triggers Malignant Hyperthermia
-Scoline Apnoea
-Histamine release
-Anaphylaxis

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41
Q

contraindications of suxamethonium

A

Drug allergy
Scoline apnoea
MH
Unknown myopathies
Risk of hyperkalaemia
–Renal failure
–Paralysis
–Crush / Burn injury

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42
Q

What are the two main types of non-depolarizing neuromuscular blocking agents?

A

Benzylisoquinolines and Aminosteroids.

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43
Q

Name two examples of Benzylisoquinoline-based neuromuscular blocking agents

A

Atracurium and cisatracurium.

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44
Q

What are the three examples of Aminosteroid-based neuromuscular blocking agents?

A

What are the three examples of Aminosteroid-based neuromuscular blocking agents?

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45
Q

How are the doses of non-depolarizing agents typically calculated?

A

Doses are typically based on lean body mass.

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46
Q

What are the physical properties of non-depolarizing agents in terms of ampoule size and storage?

A

They are usually available in 2-5ml ampoules and may require refrigeration for storage.

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47
Q

What is the typical onset time for non-depolarizing neuromuscular blocking agents?

A

The onset time is typically 1-5 minutes, but they may take longer to act compared to depolarizing agents.

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48
Q

Do non-depolarizing agents cause fasciculations?

A

No, non-depolarizing agents do not typically cause fasciculations.

49
Q

How would you describe the duration of action of non-depolarizing agents?

A

The duration of action is variable and depends on whether the agent is short-acting, intermediate-acting, or long-acting.

50
Q

What is the primary metabolic pathway for non-depolarizing agents?

A

Non-depolarizing agents are primarily metabolized hepatically, often through Hoffman degradation.

51
Q

excretion of non- depolarisers

A

renal
hepatobiliary

52
Q

specific non- depolarising drugs

A

Pancuronium (rarely used)
Rocuronium (commonest)
Vecuronium
Atracurium
Cisatracurium

53
Q

What form does vecuronium typically come in?

A

Vecuronium usually comes in powder form that must be mixed with water before administration.

54
Q

How would you describe the cardiovascular effects of vecuronium?

A

Vecuronium is cardiovascularly stable and does not typically cause histamine release.

55
Q

What is the duration of action of vecuronium?

A

Vecuronium is classified as an intermediate-acting neuromuscular blocking agent.

56
Q

What is the primary route of excretion for vecuronium?

A

Vecuronium is largely excreted through hepato-biliary pathways, making it safe in renal failure but should be avoided in hepatic disease.

57
Q

What is the typical storage condition for rocuronium?

A

Rocuronium solution is usually kept in the fridge, with a typical concentration of 50mg in 5mL.

58
Q

How would you describe the cardiovascular stability of rocuronium?

A

Rocuronium is known for its cardiovascular stability, making it suitable for various patient populations.

59
Q

At what dose can rocuronium provide intubating conditions within 1 minute?

A

A high dose of rocuronium, around 1mg/kg, can rapidly induce paralysis and facilitate intubation.

60
Q

What is the duration of action of rocuronium?

A

Rocuronium is classified as having an intermediate duration of action, with the duration of paralysis increasing with higher doses.

61
Q

drug for modified RSI

A

rocuronium

62
Q

higher doses of rocuronium

A

the longer the paralysis

63
Q

What is the storage recommendation for Atracurium?

A

Atracurium should be kept in the fridge.

64
Q

What is the mechanism of histamine release associated with Atracurium?

A

Atracurium is known for histamine releasing properties.

65
Q

What is the increased risk associated with Atracurium use?

A

There is an increased risk of anaphylaxis with Atracurium administration.

66
Q

What is the degradation process termed as for Atracurium?

A

The degradation process is known as Hoffman degradation.

67
Q

How does Atracurium degrade spontaneously?

A

Atracurium spontaneously degrades, breaking up into inactive molecules.

68
Q

What factors influence the degradation of Atracurium?

A

Degradation of Atracurium is dependent on pH and temperature.

69
Q

What potentially toxic metabolite is associated with Atracurium?

A

Atracurium may produce the potentially toxic metabolite, laudanosine.

70
Q

Is Atracurium safe to use in patients with renal and liver failure?

A

Yes, Atracurium is safe in patients with renal and liver failure.

71
Q

What is the duration of action for Atracurium?

A

Atracurium has an intermediate duration of action.

72
Q

What is the storage recommendation for Cisatracurium?

A

Cisatracurium should be kept in the fridge.

73
Q

Cisatacurium vs Atracurium

A

An isomer of atracurium

74
Q

How does Cisatracurium compare to Atracurium in terms of histamine release?

A

Cisatracurium does not cause histamine release.

75
Q

Is Cisatracurium safe to use in renal failure?

A

Yes, Cisatracurium is safe in renal failure due to the presence of Hoffman Degradation.

76
Q

Does Cisatracurium produce any toxic metabolites?

A

No, Cisatracurium does not produce toxic metabolites.

77
Q

What is the duration of action for Cisatracurium?

A

Cisatracurium has an intermediate duration of action.

78
Q

How does the onset of action of Cisatracurium compare to Atracurium?

A

Cisatracurium has a slower onset of action compared to Atracurium.

79
Q

Why is it important to reverse NDMRs even after they have clinically worn off?

A

NDMRs may still be present in the body and could bind to receptors again, necessitating reversal to prevent prolonged muscle relaxation.

80
Q

What is the purpose of reversal when it comes to NDMRs?

A

Reversal of NDMRs does not mean waking the patient up; it aims to counteract their effects and restore normal neuromuscular function.

81
Q

How can NDMRs be reversed pharmacologically?

A

NDMRs can be reversed by creating enough acetylcholine (Ach) to displace the NMDR from the nicotinic receptor.

82
Q

What is one method to increase Ach levels for reversal of NDMRs?

A

Inhibiting the enzyme acetylcholinesterase, which normally breaks down Ach, can increase Ach levels and facilitate NDMR reversal.

83
Q

drugs use in NDMR reversal

A

neostigmine
anticholinergic agent

84
Q

What is the primary pharmacological action of Neostigmine?

A

Neostigmine is an acetylcholinesterase inhibitor, increasing the concentration of acetylcholine (Ach) in the synaptic cleft.

85
Q

How does Neostigmine aid in NDMR reversal?

A

Neostigmine increases Ach levels, allowing Ach to compete with NDMRs at the nicotinic receptors, facilitating reversal.

86
Q

What potential side effects can arise from increased Ach levels due to Neostigmine administration?

A

Elevated Ach levels can stimulate both nicotinic and muscarinic receptors, leading to side effects such as bronchial secretions, bronchospasm, bradycardia, and increased peristalsis.

87
Q

anticholinergic agents

A

atropine
glycopyrrolate

88
Q

What is the primary function of anticholinergic agents in the context of NDMR reversal?

A

Anticholinergic agents, specifically anti-muscarinic agents like Atropine or Glycopyrrolate, are given to counteract muscarinic effects induced by increased Ach levels.

89
Q

What are the muscarinic effects that anticholinergic agents aim to prevent?

A

Anticholinergic agents are administered to prevent muscarinic effects, often remembered by the “B’s”: bronchial secretions, bronchospasm, bradycardia, and increased peristalsis.

90
Q

typical adult reversal doses

A

Neostigmine 2.5 mg + Glycopyrrolate 0.4–0.6 mg

Neostigmine 2.5 mg + Atropine 1 mg

91
Q

Why is Glycopyrrolate chosen as an adjunct to Neostigmine in this combination?

A

Glycopyrrolate is preferred because it does not cross the blood-brain barrier, thus avoiding central nervous system side effects.

92
Q

What is the rationale behind using Atropine alongside Neostigmine?

A

Atropine is utilized to counteract potential muscarinic side effects induced by increased acetylcholine levels.

93
Q

Why is reversal with suxamethonium not recommended?

A

Reversal with suxamethonium is not effective and could potentially prolong its action, thus it is not recommended.

94
Q

What is the potential risk associated with using suxamethonium for reversal?

A

Reversal with suxamethonium may not effectively reverse the effects of NDMRs and could lead to prolonged neuromuscular blockade, posing risks for the patient.

95
Q

What risk is associated with administering reversal too early after the administration of a muscle relaxant?

A

Early reversal can lead to inadequate displacement of the muscle relaxant from the nicotinic receptor by acetylcholine, resulting in ineffective reversal.

96
Q

How can inadequate reversal be avoided?

A

To prevent inadequate reversal, readiness for reversal is assessed using a peripheral nerve stimulator.

97
Q

What criteria are typically used to assess readiness for NDMR reversal?

A

Readiness for reversal is determined by observing at least 3 twitches present when using a peripheral nerve stimulator.

98
Q

What is the significance of observing at least 3 twitches during readiness assessment?

A

The presence of at least 3 twitches indicates sufficient recovery of neuromuscular function, suggesting readiness for reversal.

99
Q

When is it generally considered safe to administer a muscle relaxant to a patient already breathing adequately?

A

If a patient is already breathing adequately, it is generally considered safe to administer a muscle relaxant, as there is no immediate risk of respiratory compromise.

100
Q

What is the purpose of using a peripheral nerve stimulator in anesthesia practice?

A

A peripheral nerve stimulator is used to assess the level of neuromuscular blockade and readiness for reversal.

101
Q

What specific technique is commonly used with a peripheral nerve stimulator to assess neuromuscular function?

A

The Train-of-Four (TOF) technique is frequently employed with a peripheral nerve stimulator.

102
Q

What does it indicate if four twitches are observed during Train-of-Four monitoring?

A

If four twitches are present, it suggests that approximately 75% of neuromuscular junctions (NMJs) are still blocked.

103
Q

Why is it important to monitor neuromuscular function during anesthesia?

A

Monitoring neuromuscular function ensures appropriate dosing and timing of muscle relaxants, preventing complications such as inadequate paralysis or residual blockade.

104
Q

Why should caution be exercised when using neuromuscular blocking agents in patients with compromised liver or kidney function?

A

Patients with compromised liver or kidney function may experience altered metabolism or elimination of neuromuscular blocking agents, potentially leading to prolonged effects or increased sensitivity to these medications.

105
Q

How does impaired liver or kidney function affect the pharmacokinetics of neuromuscular blocking agents?

A

Impaired liver or kidney function can result in decreased metabolism or clearance of neuromuscular blocking agents, prolonging their effects and increasing the risk of residual blockade.

106
Q

signs of inadequate reversal

A

“fish out of water”

Jerky respiration
Reduced VT
Tracheal tug
Restlessness, may be worsened by hypoxia
Inability to raise head from pillow
Weak hand grip
Poor ability to cough
ptosis

107
Q

Why is it important to exclude other potential causes of residual neuromuscular blockade?

A

Residual neuromuscular blockade can mimic symptoms of various conditions, such as anesthesia-related factors, analgesia, hypo or hypercarbia, and cerebrovascular accidents (CVA). Excluding these causes ensures accurate diagnosis and appropriate management.

108
Q

What is a crucial step in managing residual neuromuscular blockade?

A

Maintaining adequate ventilation is essential to prevent respiratory compromise associated with residual blockade.

109
Q

How can potentiators of neuromuscular blockade be managed to reduce the risk of residual paralysis?

A

Reversing any potentiators of neuromuscular blockade helps mitigate the effects contributing to residual paralysis.

110
Q

Why is it important to keep the patient warm in the management of residual neuromuscular blockade?

A

Maintaining the patient’s body temperature helps optimize neuromuscular function and metabolism, potentially reducing the duration of residual blockade.

111
Q

Why is it necessary to check magnesium (Mg), potassium (K), and calcium (Ca) levels in the management of residual neuromuscular blockade?

A

Imbalances in Mg, K, and Ca levels can affect neuromuscular function and contribute to residual blockade. Monitoring and correcting these electrolyte imbalances are crucial in management.

112
Q

What role does the peripheral nerve stimulator (PNS) play in managing residual neuromuscular blockade?

A

PNS helps assess the degree of neuromuscular blockade and guides the decision-making process regarding the need for further intervention.

113
Q

What intervention can be considered if residual blockade persists despite initial reversal?

A

If residual blockade persists, a repeat dose of neostigmine can be administered, with a maximum dose of 5 mg. However, caution is warranted as larger doses of neostigmine may induce weakness.

114
Q

management of inadequate reversal

A

Exclude another cause
Maintain ventilation
Reverse any potentiators
Warm patient
Check Mg, K, Ca
Use PNS
Repeat dose neostigmine (max: 5mg)

115
Q

What is the primary function of Sugammadex in anesthesia practice?

A

Sugammadex is primarily used to reverse the effects of rocuronium, and it also works on vecuronium.

116
Q

How does Sugammadex work as a selective relaxant-binding agent (SRBA)?

A

Sugammadex acts as a modified sugar that encapsulates rocuronium molecules, effectively binding and neutralizing them. This complex is then excreted renally.

117
Q

How does the timing of Sugammadex administration differ from traditional reversal agents like neostigmine?

A

Sugammadex can be administered at any time without the need to wait for spontaneous recovery, unlike neostigmine.

118
Q

What distinguishes Sugammadex from neostigmine in terms of side effects?

A

Sugammadex does not induce muscarinic side effects, which are commonly associated with neostigmine.

119
Q

What is a notable limitation of Sugammadex in clinical practice?

A

What is a notable limitation of Sugammadex in clinical practice?

120
Q

Is Sugammadex readily available in all states?

A

Sugammadex may not be available in every state due to its high cost and specialized nature.

Anaesthesia (14 decks)

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