Anesthesia1- Muscle Relaxants
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Muscle relaxant drugs do NOT induce...
hypnosis or analgesia
Guaifenesin is commonly used in vetmed for...
large animal anesthesia for muscle relaxation.
Can Guaifenesin be mixed in syringe with other drugs?
What is the duration of action and clinical use of Guaifenesin? (5)
- DOA: 15-20min
- Uses: adjunct to anesthesia, used alone will produce recumbency but not unconsciousness
- Horses: administered prior to ketamine induction, combined with ketamine and xylazine for short-term anesthesia
- Ruminants: combined with ketamine for anesthetic induction
What is Guaifenesin's mechanism of action?
disrupt nerve impulse transmission at the level of internuncial neurons of spinal cord, brain stem, and subcortical areas of the brain--> skeletal muscle relaxation and little to no sedation
What are the cardiac effects of Guaifenesin?
What are the respiratory effects of Guaifenesin?
minimal respiratory depression
Neuromuscular blocking drugs are used to _____________; the prototypical drug in this category is ___________.
skeletal muscle paralysis; curare
Neuromuscular blocking drugs DO NOT produce...
unconsciousness, sedation, or analgesia
Describe the physiology of the neuromuscular junction.
Ach is synthesized from choline and acetate in the presence of Ach transferase--> Ach is released from nerve endings in response to impulse traveling down a motor nerve--> Ca2+ enters the nerve terminal, combines with calmodulin, and facilitates the d/ of Ach--> Ach stimulates nicotinic cholinergic receptors on skeletal muscle membrane to initiation excitation-contraction coupling--> Ach hydrolyzed by acetylcholinesterase
Describe the MOA of depolarizing neuromuscular blocking drugs. (3 principals)
- muscle is initially depolarized, causing contraction then flaccidity
- drug binds to Ach receptors, blocking Ach from binding (refractory to Ach)
- DOA depends on clearance from synaptic cleft
Describe the MOA of non-depolarizing neuromuscular blocking drugs. (3 principals)
- interact with nicotinic Ach receptors but do not trigger it, leading to flaccidity only
- competes with Ach for receptor site
- receptors remain refractory to Ach until drug is removed by metabolism, renal excretion, or chemical breakdown
What clinical difference do you see between depolarizing and non-depolarizing neuromuscular blocking drugs?
- depolarizing causes muscle contraction THEN flaccidity
- non-depolarizing cause ONLY flaccidity
Describe the MOA and DOA of succinylcholine.
- depolarizing neuromuscular blocking drug
- DOA is SHORT (3-5min)
How is succinylcholine eliminated?
action is terminated by hydrolysis with pseudocholinesterase
Describe the MOA and DOA of atracurium.
- non-depolarizing neuromuscular blocking drug
- DOA is 5-20 min (longer than depolarizing)
How is atracurium eliminated?
Hoffmann Elimination: breaks down in plasma at physiologic pH and temperature
What are the clinical uses of neuromuscular blocking drugs? (4)
- aid to intubation
- intraocular surgery
- fracture reduction
- abdominal surgery
What are NM blocking antagonists (3), and what is their MOA?
- Neostigmine, pyridostigmine, edrophonium
- anticholinesterase drugs, which result in increased amounts of Ach available to compete for NM binding sites
NM blocker antagonists are administered with ___________ to...
anticholinergic drugs; block the muscarinic effects of the increased Ach.
Never use neuromuscular blocking drugs without ___________ because...
general anesthesia; they DO NOT produce analgesia or unconsciousness and they DO cause paralysis of all skeletal muscles (including diaphragm--> ventilation must be supported)
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