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15 Cards in this Set
- Front
- Back
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why would we need muscle relaxants? |
to counteract muscle hypertonicity with ketamine / to give a smooth induction of anaesthetics using GGE in horses and cattle/ to improve surgical conditions/ to relieve muscle spasm obv!!/to help intubation/ to relax skletal muscle for easier surgical access/ to control ventilation during anaesthesia/ ophthalmic surgery |
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what other methods cause muscle relaxation and what are we refering to mainly in this lecture. |
deep GAs, local A, central acting muscle relaxants, neuromuscular blocking drug muscle relaxants -either depolarising or non- depolarising which are the main ones used - this lec |
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how do the neuromuscular blocking drugs work and what do they have in common ?
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both interfere with the post synaptic action of AcH....
non- depolarising ( used most ) - competitive antagonist of AcH. Needs to block around 80% of receptor sites. depolarising - agonist of AcH - 1st depolarising phase Eventually, after sufficient depolarization has occurred, phase II (desensitizing phase) sets in and the muscle is no longer responsive to acetylcholine released by the motoneurons. The drug can achieve this because it is metabolised slowly. |
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which type of neuromuscular blocking drugs can be reversed and how. what effect would this have on the other type. What are the side effects and how are these decreased. |
non- depolarising only-by anti-cholinesterases which prevent the break down of the AcH so it can increase its concentrations and overcome the non- depolarising drugs competitive binding. side effects- bradycardia, salivation, bronchoconstriction, urination and defaecation- all muscarinic obv!! Decreased by giving with an anti- cholinergic such as atropine
it would actually enhance the depolarising NMBs |
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can muscles still respond to electrical stimulation and K in animals treated with a non depolarising NMB or a depolarising NMB |
yes to non - depolarising no to depolarising |
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what are the effects ( + and -) , pharmacokinetics and 2 main groups of the non- depolarising NMBs |
+ effects- flacid paralysis, res. muscles are last to be affected and 1st to recover.
-effects- still feels pain./ BP falls, but Tachycardia also.
pharmacokinetics- given IV, variable onset rate and duration, generally met. in the liver or excreated unchanged in the urine, do not cross the bbb.
two main groups : aminosteriods and Benzylisoquinolines |
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the drugs within the group aminosteriods are Vecuronium, rocuronium and pancuronium. What are the characteristics of the 1st 2.
the drug called atracurium is a Ben-zy-lis-o-quin-o-lines describe its character. |
vecuronium- no cardio side effects/ excreated unchanged in the bile/ non cumulative.
rocuronium- fasest onset of any ( <2 mins) / occasional tachycardia in dogs. atracurium- has hofmann elimination ( spontaneous degradation at physiological pH and temp. )/ also uncommonly can release histamine. Just rem. VRA |
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what things have to be considered when using muscle relaxants |
only given IV/ will cause apnoea so must be mechanically ventilated/ only given if already anaesthesised/ no anaesthetic or analgesic effect/ non depolarising ones can be topped up and given by IV infusion for as long as need be/ muscles of the pharynx are very sensitive so it is possible for the animal to start breathing but not be able to maintain a patent airway./ no relaxants are licenced for animal use. |
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how do you choose a muscle relaxant |
usually based on personal preference but could be based on.......
cardiac problems and so would use vecuronium / renal or liver disease and so choose atracurium / rapid onset and so choose rocuronium. |
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what are the effects ( + and - ) of the depolarising neuromuscular blocking agents |
+....
eventally the presence of the agonist will prevent repolarisation so the muscle cant contract, this leads to the 'desensitising' phase 2.
-.......
Initial fasciculations in the 'depolarising' phase 1 / does not respond to K or electrical stimulation./ bradycardia/ potassium release/ increased intra-occular pressure/ prolonged paralysis/ malignant hyperthermia/ cant be topped up/ cant be antagonised |
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describe the phamacology of suxamethonium |
a depolarising neuromuscular blocking agent.
quick onset ( <1 min which is the fastest of any relaxant) and short duration ( 3-6 min in cat and 15-20 mins in dog). only used as a single dose.
metabolised by plasma and liver cholinesterase
rarely used even for its main indication of intubation of a cat. |
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describe the actions of sugammadex |
a new alternative antagonist instead of anti - muscarincs. it surrounds the relaxant making it inactive. expensive. |
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what factors affect a NMB drug |
other drugs ( anaesthetics, antibiotics, anticholinesterases)
disease ( liver or kidney , acid to base balance, electrolite inbalance, myasthenia gravis)
Age
temperature
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what are the centrally acting muscle relaxants |
Diazepam or midazolam Guaifenesin ('GEE-GEE') |
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What is the the MOA, effects and use of 'GEE GEE' aka guaifenesin or glycerol gualacolate |
MOA- blocks impluse transmition in spinal cord and brain stem.
effect- relaxes limb > res. muscles, with mild sedation but no analgesia
uses: to smooth induction of anaesthetic in horses and cattle ( note cattle are sensitive to haemolysis so a homemade 5% solution is made).given IV until ataxic. note it is an irritant so an IV catheter is a must. |
