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21 Cards in this Set

  • Front
  • Back

Apart from NMBs, which agents can produce muscle relaxation?

Volatile anaesthetics


Benzodiazepines


Gueaphenesin


Local anaesthesia

NMBs muscle relaxation

Total - paralysis


(neuromuscular blocking agents)

How does ACh cause muscle contraction?

Crosses nerve terminal and acts at receptors on muscle end plate -> depolarisation and contraction

How do NMBs affect this?

Block these receptors

Depolarising NMB

Activates receptor (muscle fasciculations) before relaxation

Non-depolarising NMB

Occupies receptor site but does not cause activation first

How many of the receptors have to be occupied and blocked to prevent neuromuscular transmission?

70%

Which muscles are affect first and last?

Ocular


Diaphragm

Why use NMBs?

Facilitates endotracheal intubation


Improves surgical access


Still, central eye position for ocular surgery


Facilitates ventilation


Balanced anaesthetic technique

Factors affecting NM blockade

Myasthenia gravis (NM dramatic effect)


Volatiles


Hepatic/renal disease


Acidosis


Electrolyte disturbances


Hypothermia


Aminoglycosides


Other drugs

What do you use to monitor neuromuscular function?

Peripheral nerve stimulator



Electrical stimulation of a nerve - electrodes 1cm apart over required nerve -> muscle twitch (lost if blockade in place)

What doesn't it stimulate?

Muscle directly

What will you see in the train of four if there is a partial non-depolarising NMB?

Fades when it comes to last twitch

Suxamethonium

Depolarising


Short acting: 3-7 mins in cats, 40 mins in dogs


Metabolised by plasma cholinesterases


Inhibited by organophosphates

Atracurium

Non-depolarising


Duration 40 mins


Elimination - Hoffman degradation (hydrolysis) in plasma, no enzymes required

What release might be seen with depolarising agents?

K or IOP

Vecuronium

Non-depolarising


20-25 mins in dogs


Metabolised in liver


Powder -> sterile water solution

What can be administered to antagonise NMBs?

Anticholinesterase - ACh builds up and competes for receptor sites

What should you wait for before administering an antagonist?

Some return of function

What side effect could there be and what could be given to counteract this?

Bradycardia - atropine or glycopyrrolate + neostigmine

Sugammadex

Cyclodextrin - antagonist - any point after NMB administration


Expensive