Neuromuscular Blocking Agents Flashcards

1
Q

What are the clinical indications for use of a neuromuscular blockade?

A

Relax skeletal muscles for surgical access
Facilitate control of ventilation
Facilitate tracheal intubation in cats/pigs
Ophthalmic surgery
Assist reduction of fresh dislocations and fractures?
Reduce amount of anaesthetic required?

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2
Q

Describe the physiology of the neuromuscular junction.

A

Motor neurone and muscle cell separated by synaptic cleft
Acetylcholine (ACh) released from nerve ending
Binds to post-synaptic nicotinic receptor
Two subunits must be bound
Results in muscle contraction
ACh rapidly hydrolysed by acetylcholinesterase within synaptic cleft

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3
Q

What must be available if neuromuscular blockades are used in a patient?

A

Facilities for ET intubation and IPPV!

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4
Q

What analgesic and anaesthetic effects do NMBs have?

A

None!

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5
Q

Describe onset/duration of the depolarising muscle relaxant Suxamethonium.

A

Fast onset
Duration 3-5 mins in cats, 20 mins in dogs

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6
Q

How is Suxamethonium broken down?

A

By pseudocholinesterase/plasma cholinesterase

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7
Q

What are the possible side effects of the depolarising muscle relaxant Suxamethonium?

A

Initial muscle fasciculation
Malignant hyperthermia
Increase serum potassium levels (care with urinary issues/burns)

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8
Q

Describe non-depolarising (competitive) muscle relaxants.

A

Compete with ACh for post-junctional binding sites
No initial muscle fasciculation
Relatively slow onset
Can be antagonised

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9
Q

Describe the non-depolarising muscle relaxant Atracurium.

A

Bis-isoquinolinium compound, mixture of 10 isomers
Not wholly hepatically metabolised (choice for renal/hepatic compromise)
Histamine release - give via slow IV
Stored in the fridge

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10
Q

What important isomers are associated with Atracurium?

A

Cisatracurium - only active isomer in Atracurium (more expensive to buy isolated)
Laudanosine - compound produced by metabolism

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11
Q

Describe the non-depolarising muscle relaxant Vecuronium.

A

Steroid compound
No histamine release
40-50% undergoes hepatic biotransformation
Powder - stable for 24hrs once reconstituted

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12
Q

What should we monitor when using NMBs?

A

IPPV resulting in effective ventilation
ET tube not kinked/dislodged
Breathing system connected to animal
Movement of thoracic wall
ETCO2 and SpO2

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13
Q

What are the signs of inadequate depth of anaesthesia?

A

Increase in pulse rate/BP/ETCO2
Salivation/lacrimation
Vasovagal response (bradycardia/hypotension/pallor)
Slight muscle twitching
Pupillary dilation

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14
Q

How can we monitor the efficacy of an NMB?

A

Peripheral nerve stimulator
Ulnar/peroneal/facial nerve
Train of four (4 electrical impulses applied to nerve over 2 second period - twitch strength should decrease/disappear)
Only monitors degree of NMB not depth of anaesthesia!

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15
Q

What factors can influence duration of an NMB?

A

Volatile agent
Hypothermia - prolong
Hepatic/renal insufficiency - prolong
Electrolyte/acid-base abnormalities
Muscle diseases e.g. myasthenia gravis - smaller doses required
Aminoglycoside antibiotics - prolong
Dose administered

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16
Q

When can we antagonise a non-depolarising NMB?

A

Once 1 or 2 twitches return (train of four)

17
Q

How do we antagonise an NMB?

A

Anticholinesterases (neostigmine and edrophonium)
ACh conc. increases, competes with NMB

18
Q

What are possible side effects of antagonising NMBs and how do we minimise these?

A

Bradycardia, salivation, bronchospasm, diarrhoea

Anticholinergic drugs administered with anticholinesterase (atropine or glycopyrrolate)

19
Q

When can we stop manual ventilation for patients who have received NMBs?

A

Ventilation must be supported until spontaneous ventilation commences
Risk of residual URT weakness (noise, cyanosis, paradoxical ventilation post-extubation)