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Anaesthesia- MBChB Year 4 > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

1
Q

How do volatile anaesthetics affect calcium channels?

A

They are calcium channel antagonists.

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2
Q

Which patient factors are included under risk factors for aspiration of gastric contents and would thus require rapid protection of their airways?

A

Emergency surgery in patients who have not been fasted
• Trauma patients (trauma results in gastric stasis)
• Comatose patients with a Glasgow Coma Scale (GCS) of less than 8
• Bowel obstruction
• Any suggestion of delayed gastric emptying
• Pregnant women after 12 weeks’ gestation
• History of reflux or hiatus hernia
• Morbid obesity

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3
Q

List surgical factors that would where a muscle relaxant would be required.

A

Microsurgery where any movement or cough would compromise on surgical
technique and outcome, e.g. neurosurgery, ENT, or intra-ocular procedures.
• Laparotomies and laparoscopic surgery require good abdominal muscle relaxation.
• Orthopaedic surgery: Muscle relaxation may help to reduce dislocated joints or
fractured long bones.
• Cardiac and thoracic surgery generally require an immobile, paralysed patient.
• General anaesthesia is provided for psychiatric patients undergoing electroconvulsive
therapy (ECT). Suxamethonium is administered to reduce the motor manifestations
and potential harm that may occur from the induced seizure.

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4
Q

Are muscle relaxants used routinely in ventilated patients in ICU?

A

No, but in a few
instances prolonged ventilation may require neuromuscular blockade (tetanus is a
famous example)

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5
Q

What must always be done BEFORE you administer a muscle relaxant?

A

You must first assess the patient’s airway. Includes opening the mouth opening, neck movement, upper airway/ neck anatomy.
[Done in all anaesthetic cases nonetheless]

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6
Q

Where is Ach formed and stored?

A

Acetylcholine (ACh) is formed and stored in the terminal axon of the motor nerve, in pre-synaptic
vesicles

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7
Q

List the various receptor sites of acetylcholine.

A

The entire
parasympathetic nervous system (PNS); parts of the sympathetic nervous system (SNS) -
63
sympathetic ganglia, adrenal medulla and sweat glands; some neurons in the central nervous
system; and somatic nerves innervating skeletal muscle.

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8
Q

Ach diffuses across the cleft and binds with the receptor. Then, a second Ach binds causing a conformation change.
What happens following this conformation change in the receptor?

A

The central pore opens which results in an influx of sodium.
Threshold potential reached–> depolarisation of the muscle membrane.
Propagation of AP–> increase in intracellular calcium which causes muscle contraction (interaction of actin and myosin)

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9
Q

What are the 3 ways in which muscle relaxation may be achieved?

A

a) Nerve, e.g. local anaesthetics and Botox
b) Neuromuscular junction (this is the site of action of neuromuscular blockers or NMBs)
c) Muscle itself, e.g. dantrolene (treatment for malignant hyperthermia)

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10
Q

The 2 classifications of neuromuscular blockers.

A

Depolarising and non-depolarising agents.

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11
Q

what is the mechanism of action for Depolarising NMBs?

A

chemical similarities to ACh and bind to ACh receptors generating an
action potential. They act as ACh receptor agonists and have a non-competitive mechanism of
action.

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12
Q

what is the mechanism of action for Non-depolarising NMBs?

A

Non-depolarising NMBs also bind to ACh receptors but they do not induce the required receptor
changes for depolarization to occur. They simply prevent ACh from binding. No threshold
potential develops. They therefore function as competitive antagonists. They compete with ACh
for receptors on the post-junctional membrane and can be reversed by increasing the
concentration of ACh. In the early stages the bond is very strong and they cannot be displaced
by high concentrations of Ach.

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13
Q

Which reflexes/functions will be lost due to administration of neuromuscular blockers?

A

Inability to maintain an airway (loss of muscle tone)
• Inability to breathe and cough
• Loss of laryngeal reflex

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14
Q

Why is it important to call the depolarising and non-depolarising agents “neuromuscular blockers” and not muscle relaxants?

A

Specificity. Muscle relaxants is a broad term which can also refer to benzodiazepines such as midazolam/diazepam. Neuromuscular blockers is a more accurate term and narrows down that which you are referring to.
They ARE muscle relaxants, but has a specific mode of action, one that is different to the mechanism of action of the benzodiazepines.

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15
Q

What drug factors can potentiate/prolong the action of muscle relaxants?

A

Inhalational anaesthetic agents

Aminoglycoside antibiotics, e.g. gentamycin

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16
Q

What electrolyte factors can potentiate/prolong the action of muscle relaxants?

A

↓ calcium
↑ magnesium
↑ or ↓ potassium

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17
Q

How can temperature affect the action of muscle relaxants?

A

Hypothermia potentiates suxamethonium

Hyperthermia potentiates the non-depolarisers

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18
Q

Which pH imbalance potentiates/ prolongs the action of muscle relaxants?

A

Acidosis

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19
Q

Depolarising Agent?

A

Suxamethonium (Scoline®, succinylcholine) is the only depolarizing agent in current
use and is short acting with a very rapid onset. It is the classic relaxant for a rapid
sequence induction.

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20
Q

Short acting non-depolarising agent.

A

Mivacurium (Mivacron ®) – not routinely used or available in South Africa

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21
Q

Intermediate acting non-DA

A

Vecuronium (Norcuron®)
• Rocuronium (Esmeron®) – in high dose, can be used for rapid sequence induction
• Atracurium (Tracrium®) — useful for patients in renal failure
• Cisatracurium (Nimbex®) — an isomer of atracurium also used for patients in renal
failure

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22
Q

Long acting non-DA

A

Pancuronium (Pavulon®) (no longer in widespread use, being phased out)

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23
Q

Chemical structure of Suxamethonium chloride

A

Consists of two molecules of ACh linked together with two quaternary amine groups

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24
Q

What is the dose for sux and how quickly does it cause paralysis?

A

A dose of 1 mg/kg

profound paralysis in 60 seconds

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25
Q

What is paralysis preceded by when administering sux? Why does this happen?

A

Paralysis is preceded by fasciculations as a result of random depolarization of
myofibrils, causing uncoordinated contractions

26
Q

Who is at risk when given sux?

A

Renal failure patients with K+ > 5,0
mmol/L; patients who have had massive tissue injury, e.g. burns and crush injury; and those who
have disuse of their muscles over weeks to months, e.g. patients living with paraplegia, stroke
patients, and end-stage disease

27
Q

Why are hyperkalaemic states relevant when administering sux?

A

Depolarisation results in the release of K+ from the muscle into the plasma. A single dose of suxamethonium
increases plasma K+ by 0,5 mmol/L. Can worsen condition and cause dysrhythmias and asystole.

28
Q

Side effects of sux.

A

Hyperkalaemia
Hyperkalaemia leads to dysrhythmias and asystole
bradycardia which may lead to cardiac arrest
malignant hyperthermia

29
Q

Upon receiving repeated doses of suxamethonium, a patient enters a state of bradycardia. What should be administered?

A

a vagolytic drug, e.g.atropine

30
Q

What enzyme breaks sux down?

A 
plasma cholinesterase (also called pseudocholinesterase or
butyrylcholinesterase)
31
Q

In which patients is the action of pseudocholinesterase reduced in?

A

reduced in patients with hypothermia, liver disease, pregnant women and if
the patient is taking another drug that requires this enzyme for its breakdown.

32
Q

an inherited disorder of pseudocholinesterase where the enzyme produced is chemically different to
the normal enzyme with resultant varying degrees of activity and prolonged paralysis.

A

Scoline Apnoea

33
Q

How to treat a patient if discovered to have scoline apnoea?

A

Ensure adequate sedation whilst continuing mechanical ventilation until muscle
power returns as the suxamethonium is metabolised. Alternatively, fresh frozen plasma (FFP)
may be transfused to accelerate suxamethonium degradation, as plasma contains the necessary
enzyme, plasma cholinesterase.

34
Q

Irrelevant question?

What was the first NMB agent?

A

Curare. obtained from a South American vine, the curare plant

35
Q

Which ND NMB’s are benzylissoquinolones?

A

atracurium, cisatracurium and mivacurium

36
Q

Which ND NMB’s are aminosteroids?

A

Vecuronium, rocuronium and pancuronium

37
Q

Vecuronium

A

Dose: 0,1 mg kg-1
Presentation: White powder in ampoule contains 4 mg.
Usually dilute to 2 mg ml-1 with sterile water.
Features:
• Cardiovascularly stable; occasional bradycardia especially when given with
etomidate and / or fentanyl.
• No histamine release.
66
• Relies on hepato-biliary excretion and therefore safe in renal failure
patients (only 15 % renally excreted)

38
Q

Rocuronium

A

Dose: 0.45 – 1.2 mg kg-1 (depending on the clinical situation, patient and surgical
factors)
Presentation: 5 ml ampoules containing 50 mg (10 mg ml-1)
Features:
• The “ROC” in Rocuronium stands for “Rapid Onset Curare”
• A low dose results in a slow onset of action—3-5 minutes before patient
can be intubated, with a subsequently short duration of action
• A high dose (0.9–1.2 mg kg-1) facilitates intubation within 60 - 90 s,
however it then has a long duration of action (up to an hour) as opposed to
suxamethonium
• Cardiovascularly stable; mild ↑ in BP and HR

39
Q

Atracurium

A

Dose: 0.5 mg kg-1
Presentation: 10 mg ml-1 solution
Features:
• Cardiovascularly stable but it can release histamine and cause
hypotension
• Metabolism via nonspecific esterases and non-enzymatic chemical
breakdown occurring at physiologic pH and temperature
• Safe in renal failure

40
Q

Cisatracurium

A 
Dose: 0,15 mg kg-1
Presentation: Ampoules containing either 5 mg or 10 mg with a concentration of 2 mg ml-1
Features:
• Useful in liver and renal failure
• NO histamine release
41
Q

Difference in location of muscarinic vs nicotinic receptors.

A

Nicotinic receptors are located on the autonomic ganglia and in skeletal muscle (blocked by the
non-depolarising muscle relaxants).
Muscarinic receptors are located on end-organ effector cells in the heart (sinoatrial and
atrioventricular nodes); smooth muscle (bronchi and GIT) and glands (salivary and lacrimal).
They are blocked by anticholinergic drugs such as atropine and glycopyrrolate.

42
Q

What is the name of the NDA reversal agent

A

Neostigmine

43
Q

Mechanism of action of neostigmine? How does reversal work, w.r.t. Ach

A

AchE is inhibited by neostigmine. Normally ACh is rapidly degraded by acetyl cholinesterase (AChE) within milliseconds. By
inhibiting this enzyme with Neostigmine, there will be more ACh available to compete with the
NMBs and displace them and reverse their effect.

44
Q

What is a side effect of administering neostigmine

A

If an AChE inhibitor is administered ; Ach concentration will increase at all cholinergic receptors.
The unwanted parasympathetic manifestations of this are bradycardia, bronchospasm and
bronchosecretion, increased bowel motility and pupillary constriction

45
Q

How are the side effects of neostigmine treated?

A

acetylcholinesterase inhibitor
neostigmine is always given with an anticholinergic blocking the muscarine receptors. The two
antimuscarinic (or anticholinergic) drugs in common use are atropine and glycopyrrolate

46
Q

Dose of neostigmine

A

0,04 - 0,05 mg kg-1 Adults, ( 2,5 mg)

47
Q

Dose of glycopyrrolate

A

0,01 - 0,015 mg kg-1 ( 0,4 - 0,6 mg )

48
Q

Dose of atropine

A

0,02 mg kg-1 (1 - 1,2 mg)

49
Q

When is it safe to administer a reversal agent, clinically?

Is this way reliable?

A

exhibiting signs of
spontaneous recovery from the neuromuscular blockade are a gag reflex, breathing, coughing,
and eye opening.
Sustained head lift for 5 - 10 seconds; sustained hand squeeze; and sustained jaw grip of tongue
depressor
Nope, not reliable.

50
Q

Best way to determine patient readiness for reversal?

A

Peripheral nerve stimulation, aka Train of Four.

51
Q

How does the train of four work?

A

If ≥ 3 twitches
are present, and ≥ 30 minutes since the last dose of muscle relaxant has been administered, then
the reversal can safely be given

52
Q

Which nerves can be used for train of four?

A

Ulnar at the wrist; facial nerve; common peroneal at neck of the fibula; and the
posterior tibial at the ankle

53
Q

What is a twitch and when are twitches useful?

A

1 short duration 0,1-1 Hz
stimulus.
Useful immediately after administering a muscle relaxant when you want to be sure that the patient is paralysed before intubation.

54
Q

Define train of four, including the frequency required.

A

used to monitor the degree of
neuromuscular block and assess for
reversibility; 4 twitches of 2 Hz each
applied over 2 seconds.

55
Q

How does suxamethonium differ from rocuronium, for example, with regards to train of four twitches.

A

For sux, there is no fade, the twitches are all the same height, simply reduced in size.
Rocuronium exhibits fade, (1st twitch is bigger than the 4th
twitch

56
Q

Signs of inadequate reversal.

A
  1. Jerky respiration
  2. Poor chest expansion with ↓ tidal volume
  3. Tracheal tug
  4. Restlessness, which may be aggravated by hypoxia
  5. Inability to raise the head from the pillow
  6. Weak hand grip
  7. Poor ability to cough
  8. Ptosis
57
Q

Name of the medication with the brand name Bridion.

A

Sugammadex.

58
Q

What is the mechanism of action and chemical structure of sugammadex?

A

Has the ability to rapidly encapsulate
amino-steroid neuromuscular blocking agents, promoting their dissociation from nicotinic receptors at the neuromuscular junction and terminating their action.
It is a modified gammacyclodextrin, a cyclic oligosaccharide carbohydrate

59
Q

What is Sugammadex mainly used for and what other NMBA’s can it also be used for?

A

rocuronium, but is also effective against

vecuronium and pancuronium (i.e. the amino-steroids)

60
Q

True or false: Sugammadex can’t be used for benzylisoquinolones.

A

Trueness!

Anaesthesia- MBChB Year 4 (5 decks)

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