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Neuromuscular blocking drugs Flashcards

1
Q

Apart from depolarising and non-depolarizing MR, what alternative techniques exist to provide a sufficient degree if muscle relaxation to facilitate intubation and surgery (i.e. in the paediatric population to avoid use of muscle relaxants)

A
  1. High dose induction agent OR high dose volatile agent can provide enough muscle relaxation to facilitate intubation and surgery.
    - Obviously accompanied by increased side effects.
  2. Peripheral nerve blocks will provide muscle relaxation when they are able to block motor nerves.
  3. Neuraxial anaesthesia can also provide substantial motor nerve blockade and adequate muscle relaxation.
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2
Q

How do volatile agents act as muscle relaxants

A

They are calcium channel antagonists

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3
Q

How can indications for neuromuscular blockade be classified?

A
  1. Patient factors
  2. Anaesthetic factors
  3. Surgical factors
  4. Intensive care
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4
Q

What are the patient factors that indicate muscle relaxation?

A

Any patient at risk for gastric contents regurgitation require rapid airway protection of their airway with an endotracheal tube.

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5
Q

Which patients are at risk for regurgitation of gastric contents

A

FULL STOMACH

  1. Patients undergoing emergency surgery
  2. Trauma
  3. Not fasted

GIT PATHOLOGY

  1. Gastroparesis (Diabetic or other)
  2. SBO
  3. Gastric outlet obstruction
  4. Esophageal stricture
  5. GORD

INCREASED INTRA-ABDOMINAL PRESSURE

  1. Morbid Obesity
  2. Ascites

PREGNANCY from 16/40 onwards –> RSI

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6
Q

What are the anaesthetic factors that indicate neuromuscular blockade?

A
  1. Control of patient ventilation
    - respiratory disease
    - abnormal position (prone, lateral, deck chair)
    - Facilitation of endotracheal and airway devices (ETT and rigid bronchoscopes)
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7
Q

What are the surgical factors that indicate muscle relaxation?

A
  1. Microsurgery - any movement or cough would compromise surgical technique: Neurosurgery | ENT |Intra-ocular.
  2. Laparotomy | Laparoscopy –> prevent iatrogenic bowel injury
  3. Orthopedics: Assists with mechanics of relocating joints and fixing fractures
  4. Cardiac and thoracic surgery require paralysis
  5. Psychiatry: ECT –> ECT –> reduction of motor manifestations.
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8
Q

When is muscle relaxation required in intensive care

A

No longer used routinely in ICU but in a few instances prolonged ventilation may require neuromuscular blockade (e.g. tetanus)

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9
Q

What should always be done prior to the administration of a muscle relaxant

A

The airway be assessed and planned for.

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10
Q

What are the 8 P’s for RSI that can be applied to the management of any airway

A 
Plan (DSI/RSI ; Difficult/Not ; LMA/ETT ; Ramping/Not)
Preparation (STOP IC BARS, IMALES, Drugs, Theatre)
Protect C-Spine (if relevant)
Position (flextension)
Preoxygenate
Paralysis and Induction
Placement ETT/LMA
Post intubation care
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11
Q

Define the neuromuscular junction

A

IT is the region where the motor neuron and the muscle cell approximate

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12
Q

What is the distance of the synaptic cleft?

A

20nm

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13
Q

List the sites at which Ach is the neurotransmitter

A
  1. PSNS (entire system)
  2. SNS
    - Sympathetic ganglia
    - Adrenal medulla
    - Sweat Glands
  3. CNS (some neurons)
  4. Somatic nerves ending in skeletal muscle
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14
Q

What is the name of the post synaptic terminal within the neuromuscular junction?

A

Motor end plate - this is the site of Ach receptors

A specialised portion of the muscle membrane

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15
Q

What happens when an action potential arrives at the pre-synaptic terminal

A
  1. Influx of Ca ions via V-gated Ca channels
  2. Ca allows fusion of pre-synaptic Ach vesicles to fuse with the pre-synaptic membrane and exocytose Ach into the synaptic cleft
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16
Q

What happens after the Ach has been released into the synaptic cleft (20nm)

A
  1. Diffuse across the 20nm cleft

2. Bind to nicotinic Ach receptors on a specialised portion of the muscle membrane: the motor end plate

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17
Q

How many nicotinic Ach receptors exist within each neuromuscular junction and activation of how many of these receptors is required for normal muscle contraction.

What is the clinical significance of this

A

5 million Ach receptors per NMJ

Activation of only 500 000 –> normal muscle contraction

Clinical significance - 10 fold safety net is lost in:

  • Eaton Lambert myesthenic syndrome (decrease release Ach)
  • Myesthenia gravis (decreased receptors)
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18
Q

Describe the structure of the Ach receptor

A

5 protein subunits that surround a central transmembrane pore

Protein subunits

  • two alpha
  • epsilon
  • delta
  • beta

Anticlockwise from 12 oclock: alpha, epsilon, alpha, delta, beta.

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19
Q

Which protein subunits on the receptor can Ach bind and when is the central channel opened

A

the alpha subunits

The central ion channel will only open when a molecule of Ach is bound to both subunits

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20
Q

Describe the structure and location of the alternative isoform ‘immature’ Ach receptor

A

Anticlockwise from 12 o’clock: alpha, gamma, alpha, delta, beta

Location:

  • Fetal muscle
  • In the adult: ‘extrajunctional’ –> it may be located anywhere on the muscle membrane: inside or outside the NMJ.
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21
Q

What happens when the conformational change occurs within the Ach receptor

A

The central ion channel opens allowing the brief movement of cations:

Na and Ca –> move in
K –> moves out

This generates an end plate potential

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22
Q

Explain how the postjunctional membrane is depolarized

A

Each Ach vesicle contains a ‘quantum’ (10^4) of Ach molecules. The number quanta released depends on the extracellular Ca concentration (N ± 200 quanta).

When enough nicotinic receptors are occupied by Ach - Voltage gated sodium channels in the perijunctional membrane open and the end plate potential will be sufficiently strong to depolarize the perijunctional membrane.

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23
Q

How is the perijunctional action potential propagated and what is the result of this propagation?

A

Along the T-tubule system, opening Na channels and releasing Calcium from the sarcoplasmic reticulum –> Increasing intracellular calciumallows contractile proteins actin and myosin to interact, bringing about muscle contraction.

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24
Q

How is Ach removed from the cleft

A

Acetylcholinesterase hydrolyzes Ach into acetate and choline.

Achase is embedded in the motor end plate membrane immediately adjacent to the Ach receptors. Choline is taken up by the pre-synaptic membrane where it is re-cycled and a=combined with acetyl Co A to form acetylcholine

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25
Q

What happens after Ach unbinds

A

The ion channel closes. The end plate repolarizes. Calcium is resequestered back in the SR. The muscle cell relaxes.

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26
Q

List three ways that muscles can be relaxed

A

Block the:

  1. Nerve: Local anaesthetics and botox
  2. NMJ: NMBs
  3. Muscle: Dantrolene (Rx malignant hyperthermia)
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27
Q

Differentiate the mechanism of action of depolarizing and non-depolarizing muscle relaxants

A

DEPOLARIZING
- 2 Ach molecules bound –> binds to Ach receptor –> depolarization –> occupies the Ach receptor until metabolized by pseudocholinesterase (takes ± 5 mins) (not acetylcholinesterase)

NON-DEPOLARIZING

  • Bind Ach receptor - do not cause depolarization - prevent Ach from binding (competitive antagonists)
  • In the early stages the bond is very strong and cannot be displaced by increasing Ach (Neostigmine)
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28
Q

List 5 factors that potentiate and prolong the action of muscle relaxants

A
  1. Drugs:
    - Volatile agents
    - Aminoglycosides (gentamicin)
  2. Electrolytes
    - Increase Mg
    - Decrease Ca
    - Increase/Decrease K
  3. Acidosis
  4. Temperature
    - Hypothermia potentiates SUX
    - Hyperthermia potentiates non-depolarizers
  5. Myaesthenia gravis and other inherited muscle abnormalities: e.g dystrophies/dystonias
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29
Q

Classify the muscle relaxants (NMJ)

A

DEPOLARISING (4 - 10 minutes)
- Succinylcholine/Scoline (1 - 1.5 mg/kg)

NON-DEPOLARISING
Short acting (12 - 18 mins)
- Mivacurium (0.15 mg/kg) (not in RSA)

Intermediate acting

  • Rocuronium (0.6 - 1.2 mg/kg) High dose for RSI
  • Vecuronium (0.1 mg/kg)
  • Cisatracurium (0.1 mg/kg) Good for renal/liver failure
  • Atracurium (0.5 mg/kg) Good for renal/liver failure

Long acting
- Pancuronium (0.1 mg/kg) (being phased out)

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30
Q

Describe the chemical structure of succinylcholine

A

Consists of two molecules of acetylcholine liked together by two quaternary amine groups

31
Q

Describe the presentation of succinylcholine

A

Glass ampoule stored in the fridge

2ml: 50mg/ml

32
Q

How long does it take sux to cause flaccid paralysis

A

30 - 60 seconds (after fasciculations)

33
Q

How long does flaccid paralysis last after sux

A

Depends on Age/Dose/Route

IV: 4 - 10 mins
IM: 10 - 30 mins

34
Q

How long can muscle pain last after sux

A

up to 3 days
Can be very severe
More common in fit and active individuals

35
Q

By how much does a single does of sux increase plasma potassium concentration and why does this occur. Which patient’s are at risk from this sudden rise in potassium

A

0.5 mmol/L. Ubiquitous muscle depolarization and contraction leads to release of K from the muscle into the plasma.

Patient’s at risk:

  1. Renal failure with K > 5 mmol/L
  2. Massive tissue injury (burns/crush)
  3. Disuse of muscle for weeks to months (paraplegia/stroke/end stage disease)
36
Q

Summarise the adverse effects of succinylcholine

A
  1. Fasciculations and muscle pain for 3 days
  2. Raised IOP, ICP, IGP
  3. Tachycardia (usually adults 1st dose)
  4. Bradycardia (children and adults 2nd dose)
  5. Rise in K by 0.5 mmol/L relevant in
    - Renal failure with K > 5.0 mmol/L
    - Massive tissue injury: crush/burns
    - Prolonged tissue disuse: Stroke/Paraplegia/End stage
    - –> dysrhythmias
  6. Trigger of Malignant hyperthermia
37
Q

Describe the metabolism of succinylcholine and factors that affect the break down of succinylcholine and hence potentiate the action of sux.

A

Broken down by plasma cholinesterase (also called pseudocholinesterase or butyrylcholinesterase)
–> Synthesised in the liver and present in the plasma

The action of plasma cholinesterase and hence SUX metabolism can be affected by the following factors:

  1. Hypothermia/Acidosis/Electrolytes/Drugs
  2. Liver disease
  3. Pregnancy
  4. Drug interaction
    - Acetylcholinesterase inhibitors (neostigmine)
    - Aminoglycosides
    - Lithium
    - Loop diuretics
38
Q

What is scoline apnoea and what is the treatment of scoline apnoea

A 
Inherited disorder (homo/heterozygous)
- Abnormal pseudocholinesterase --> varying degrees of activity and prolonged paralysis

Treatment:

  1. Supportive: Sedate, ventilate and wait.
  2. Administer FFPs –> contains normal plasma cholinesterase
39
Q

How does succinylcholine bring about muscle relaxation if it depolarizes the motor end plate, perijunctional membrane, T-tubules and the muscle tissue?

A

Succinylcholine binds to the alpha subunit of the nicotinic Ach receptor BUT is not quickly metabolised by acetylcholinesterase and hence remains bound. Continuous end-plate depolarization causes muscle relaxation because opening of perijunctional sodium channels is TIME limited –> sodium channels rapidly ‘deactivate’ (Two gate theory). The sodium channels cannot reopen until the end plate repolarizes. This is called phase 1 block. After a period of time, prolonged end plate depolarization can cause poorly understood changes in the ACh receptor that result in a phase 2 block, which clinically resembles that of nondepolarizing muscle relaxants

40
Q

What is phase 2 block

A

Prolonged motor end plate depolarization leads to poorly understood changes in the ACh receptor that result in a phase 2 block, which clinically resembles that of nondepolarizing muscle relaxants.

41
Q

How do non-depolarizing muscle relaxants cause muscle relaxation

A

Competitive antagonists of postsynaptic ACh receptors
- Upon binding the Ach receptor, no conformational change occurs for ion channel opening but Ach is prevented from binding to its receptors. Neuromuscular blockade occurs even if only one alpha subunit is blocked.

42
Q

Describe how the presence of prolonged muscle disuse would affect the actions of depolarising and non-depolarising muscle relaxants

A

Chronic disuse –> Upregulation of mature nicotinic Ach receptors within the neuromuscular junction and promoted expression of immature isoform extrajunctional Ach receptors.

For depolarising MR
–> An exaggerated response is observed with compounding of side effects

For non-depolarizing MR
–> Resistance (more receptors must be blocked)

43
Q

Describe the impact of myasthenia gravis on depolarising and non-depolarising muscle relaxants

A

Myesthenia gravis is the autoimmune destruction of nicotinic Ach receptors in the neuromuscular junction.

This leads to lower numbers (less expression/down regulation) of these receptors.

This leads to a resistance to depolarizing agents and increased sensitivity to non-depolarizing agents.

44
Q

Do acetylcholinesterase inhibitors (neostigmine/pyridostigmine) reverse muscle relaxation brought about by succinylcholine?

A

Phase 1 block

  • no reversal
  • possible potentiation and prolongation of block by inhibiting pseudocholinesterase

Phase 2 block
- Possibly assists with reversal of a phase 2 block (altered Ach receptors by prolonged depolarization) when TOF fade is present and sufficient time has past for circulating sux to be negligible.

45
Q

What is suggamadex and how does it work

A
  1. Modified gamma-cyclodextrin
  2. Rapidly encapsulates aminosteroid NDMR (1:1)
    - -> this promotes their dissociation from Ach receptors and terminating their action.
  3. Rapid onset
  4. Reverses profound block without evidence of reversibility
  5. CVS stable
  6. Excretion: Renal
  7. Very expensive - not available in all scenarios
  8. Used in CICO scenarios

Works for Aminosteroids = Roc | Vec | Pan

Does not work for benylisoquinoliniums (Cis | Atra | Miv)

46
Q

Does suggamadex reverse Atracurium/Cisatracurium/Mivacurium

A

No. It does not reverse benzylisoquinoline compounds. It only binds and reverses steroid NDMR (Vecuronium/Rocuronium/Pancuronium)

47
Q

What is the name of the first NDMR and where does it come from

A

Curare. South American vine. Used by hunters on the tips of arrows. Chemically curare is a benxylisoquinoline. the muscle relaxants atracurium, cisatracurium and mivacurium are based on this chemical structure

48
Q

Name the aminosteroid NDMR

A

Vecuronium
Rocuronium
Pancuronium (no longer in general use due to its long elimination and context-sensitive half time and predominantly renal clearance)

49
Q

Do NDMR cross the BBB/Placenta

A

No. They are large, highly ionized, water soluble and have virtually no penetration of lipid barriers such as the placenta and BBB

50
Q

How long can the following agents be stored outside the refrigerator in theatre (±25 deg C)

Vecuronium
Cisatracurium
Atracurium
Rocuronium

Succinylcholine

A

Vecuronium - 1 week
Cisatracurium - 3 weeks
Atracurium - 1 month
Rocuronium - 3 months

Succinylcholine - 1 month

VCARS 13131

51
Q

Describe the presentation of the muscle relaxants

A

SUX - Liquid. Brown glass. Fridge (2 - 8 deg C). 100mg/2ml

ROC - Clear liquid in clear glass. Fridge. 50mg/5ml

CIS - Clear liquid in clear glass. Fridge. 10mg/5ml

ATRA - Clear liquid in clear glass. Fridge .50mg/5ml

VEC - White Powder. Clear glass. Reconstitute to 2mg/ml.

52
Q

Which 2 muscle relaxants do not cause histamine release

A

No Histamine release
CIS
VEC

53
Q

How are atracurium and cisatracurium metabolized and why is this relevant

A

Metabolism is via nonspecific esterases occurring at physiological pH and temperature.

Both agents are safe in Liver and Renal disease

VEC and ROC have renal and hepatic metabolism

54
Q

Summarise the duration of action (time to 25% recovery) of the muscle relaxants

A

DEPOLARISING
- Succinylcholine/Scoline: 5 - 10 mins

NON-DEPOLARISING
Short acting
- Mivacurium: ± 15 mins

Intermediate acting

  • Rocuronium ± 30 mins
  • Vecuronium ± 30 mins
  • Atracurium ± 30 mins
  • Cisatracurium ± 45 mins

Long acting
- Pancuronium ± 90 mins

55
Q

Historically, why were muscarinic and nicotinic receptors distinguised

A

Muscarine - poison from the mushroom amanita muscaria - binds muscarinic receptors –> hypercholinergic state: bradycardia and increased secretions.

MUSCARINIC receptors
- End organ effector cells
--> Heart (SA and AV)
--> Smooth Muscle (bronchi and GIT)
--> Glands (salivary and lacrimal)
BLOCKED by anticholinergics like atropine and glycopyrrolate

Nicotine - Nicotiana tabacum –> binds nicotine receptors

NICOTINIC receptors
- autonomic ganglia
- skeletal muscle
BLOCKED by non-depolarizing muscle relaxants

56
Q

How long does Acetylcholinesterase usually take to work and why is this relevant to NDMR

A

Milliseconds
if AChase is inhibited by neostigmine there is significantly more Ach available to compete with the NDMR at the end-plate nicotinic receptors and hence reversal is possible using AChase inhibitors

57
Q

What are the unwanted PSNS effects that will result from the administration of neostigmine and what is given to prevent this

A 
Bradycardia
Bronchospasm
Secretions
Increased bowel motility
Pupillary constriction

Muscarinic blocking agents are given: Atropine or Glycopyrrolate

58
Q

Where does atropine come from and what does intoxication cause

A

Plant: Deadly night shade (Belladonna)
Anticholinergic syndrome:

Hot as a hare - no sweating –> heat retained
Red as a beet - no sweating –> VD to try remove heat
Dry as a bone - dried secretions and no sweating
Blind as a bat - pupillary dilatation + ineffective accommodation
Mad as a hatter - CNS muscarinic receptors blocked

59
Q

What are the doses for the reversal agents

A

0.2 mg/kg Pyridostigmine (10 - 15 mg)

  1. 04 mg/kg - Neostigmine (2.5mg)
  2. 02 mg/kg - Atropine (1 mg)
  3. 01 mg/kg - Glycopyrrolate (0.4 - 0.6 mg)
60
Q

How long does it take neostigmine | Glycopyrrolate | Atropine take to work and what is their duration of action

A

Neostigmine IV
TTPE: 5 mins
Duration: 90 mins

Glycopyrrolate IV
TTPE: 3 mins
Duration: 120 mins hours

Atropine IV
TTPE: 2 mins
Duration: 60 mins

61
Q

When is it safe to administer the reversal agent and what happens if this is administered too early?

A

When is it safe to administer reversal

  1. Clinical signs (unreliable)
    - Gag reflex | breathing | coughing | eye opening
    - Head lift 5 - 10s | hand squeeze | Jaw grip tongue depressor
  2. Peripheral nerve stimulator
    “Evidence of reversibility”
    - > 30 minutes since administration of last dose AND 3 or more twitches present

Early reversal leads to residual neuromuscular blockade and postoperative pulmonary complications (POPCs)

62
Q

What is a “supramaximal stimulus”

A

Supramaximal stimulation is stimulation having current significantly above that required to activate all the muscle fibers. …

63
Q

Which nerves can be used for monitoring and why

A

Ulnar nerve - adductor pollicis brevis
Posterior tibial nerve - ankle plantar flexion
Facial nerve - orbicularis occuli
Common peroneal nerve (neck of fibula)

These are all superficial nerves

64
Q

What current is usual entered into the PNS and what is the usual duration of each stimulus

A

Current: 15 - 40 mA
Duration: 2 ms

65
Q

What are the common types of stimulation used and what is the specific benefit of each

A
  1. Twitch (1 Hz every 10 seconds) - immediately after administration MR to ensure patient is paralyzed before intubation
  2. Train-of-four (TOF) (2 Hz = 4 twitches over 2 seconds)
    - Fade present (1st twitch bigger than 4th twitch with NDMR)
    - May be less than 4 twitches if PNS used soon after administration NDMR.
    - No fade with SUX - all twitches have lower amplitude
  3. Tetany (50 - 100 Hz) used to detect any residual block
  4. Double-Burst Stimulation (DBS) - two bursts of 50 Hz - easier to see if fade is present when TOF is difficult to distinguish
  5. Post-tetanic facilitation or potentiation
    –> Used to assess more profound degrees of NMB
    50 Hz for 5 seconds (5 second tetanus)
    then 3 second pause and 20 twitches at 1Hz
    The number of contractions visible post tetany will predict the time required before reversal feasible.
66
Q

List 8 signs of inadequate reversal

A

A

B - Abnormal breathing x 4

  1. Tracheal tug
  2. Jerky respiration
  3. Poor chest expansion
  4. Poor ability to cough

C

D - Abnormal Neuro x 4

  1. Weak hand grip
  2. Inability to raise head from pillow > 5 s
  3. Restlessness
  4. Ptosis
67
Q

Explain the clinical use of post-tetanic facilitation

A

It is a method for monitoring intense neuromuscular blockade.

50-Hz tetanic stimulus to the ulnar nerve for 5 s,

3 second break

followed by single twitch stimulation at 1 Hz.

The number of twitches observed in the period of
post-tetanic facilitation, the post-tetanic count,
correlates inversely with the degree of neuromuscular blockade.

Post-tetanic counts of 6-7 indicate that the return of the first TOF twitch is imminent.

68
Q

What are the physiological implications of residual neuromuscular blockade?

A

A - Aspiration (impaired cough, impaired phonation), obstruction
B - Aspiration, ventilation, oxygenation
C
D + E: impaired muscle tone and co-ordination

69
Q

What are the signs and symptoms of residual muscle paralysis

A

“Fish out of water”

  • Difficulty: breathing, speaking, seeing
  • Uncoordinated weakness
  • Significant patient distress
70
Q

What are the clinical implications of residual muscle paralysis

A

Airway - obstruction/aspiration

Breathing - POPC, prolonged ventilator weaning, postoperative hypoxia

71
Q

How man receptors are blocked with TOFC 0, 1, 2, 3, 4

A 
TOFC 4: 0 - 75%
TOFC 3: 75%
TOFC 2: 80%
TOFC 1: 90%
TOFC 0: 100%
72
Q

Describe how the TOF and PTP is administered including current, frequency, duration

A

TOF

  • Current: Supramaximal > 60 mA
  • Frequency: 2 Hz (2 stimuli/second) (each twitch 0.5s)
  • Duration: 2 seconds (4 twitches)

PTP

  • Current: supramaximal > 60 mA
  • Frequency: 50 Hz (50 stimuli/second) for 5 seconds followed by 1 Hz for prn seconds
  • Duration: variable - count the 1 Hz twitches and interpret
73
Q

How is post tetanic stimulation interpreted

A

Count of 1 twitch post tetany - First TOF twitch should appear in about 30 minutes

Count of 7 twitches post tetany - First TOF twitch should appear imminently

74
Q

What is the physiology behind the ‘fade’ phenomenon?

A

Fade may be due to prejunctional effect of non-depolarising muscle relaxants that reduces the amount of Ach in the nerve terminal available for release during stimulation

DA (50 decks)

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