Skeletal Muscle Relaxants Flashcards
(36 cards)
Types of Skeletal Muscle Relaxants
Neuromuscular blockers
- Antagonists/ Non-depolarizing blockers
- Agonists/ Depolarizing blockers
Spasmolytics
- Chronic spasm agents
- Acute spasm agents
Non-depolarizing blockers (types & names)
- Benzylisoquinolines
- Tubocurarine
- Atracurium
- Cisatracurium
- Mivacurium - Ammonio Steroids
- Pancuronium
- Rocuronium
- Vecuronium
MOA of Non-depolarizing Blockers
Competitive antagonists
- causes motor weakness –>
- skeletal muscles become totally flaccid & inexcitable to stimulation
Reversal of Non-depolarizing antagonists actions
Inc conc. of ACh in synapse
- Neostigmine
- Edrophonium
Classification of Non-depolarizing Muscle relaxants based on Duration of Action
Short-acting
- Mivacurium
Intermediate-acting
- Atracurium
- Cisatracurium
- Rocuronium
- Vecuronium
Long-acting
- Tubocurarine
- Pancuronium
Excretion of Non-depolarizing blockers
- Kidney – Long Half-life – Long Duration of Action
2. Liver – Short Half life – Short Duration of Action
Elimination mechanism & DOA of Benzylisoquinolones
- Mivacurium - Plasma pseudocholinesterase - 15 mins
- Atracurium - Enzymatic & Non-enzymatic ester hydrolysis - 45 mins
- Cisatracurium - Spontaneous (80%) & renal - 45 mins
- Tubocurarine - Renal & hepatic - 80 mins
Elimination mechanism & DOA of Ammonio steroids
- Rocuronium - Hepatic (80%) & Renal - 30 mins
- Vecuronium - Hepatic (80%) & Renal - 45 mins
- Pancuronium - Renal (80%) & Hepatic - 90 mins
Metabolism & AEs of Atracurium
Metabolite - Laudanosine
- Hypotension
- Seizures
Metabolism & AEs of Cisatracurium (Stereoisomer of Atracurium)
Metabolite = Laudanosine (much less than Atracurium)
- less histamine release
Replaced Atracurium in clinical practice
Metabolism of Mivacurium
Hydrolysis (inactivation) by Butyrylcholinesterase
- not dependent on kidney or liver
Metabolism & uses of Rocuronium
- Most rapid onset non-depolarizing blockers
- Used as an alternative to Succinylcholine for rapid sequence intubation
Depolarizing blockers (names)
-Succinylcholine (2 ACh molecules linked end-to-end)
MOA of Succinylcholine
Activates Nicotinic receptors –> depolarization of junction –> Unresponsiveness to additional impulses
- Fasciculations
- Flaccid paralysis
Time of onset & Duration of action of Succinylcholine
Time of onset = < 1 min
Duration of action = 5-10 mins (bc of rapid hydrolysis)
Metabolism/ Hydrolysis of Succinylcholine
Rapid hydrolysis by plasma Pseudocholinesterase
- not effectively metabolized by Acetylcholinesterase
Polymorphisms of Butyrylcholinesterase
Muscle blockade may be prolonged in pts. w/ abnormal variant of Butyrylcholineserase that uses Succinylcholine or Mivacurium.
Treatment of pts. w/ Abnormal Butyrylcholinesterase & Succinylcholine or Mivacurium use
Mechanical ventilation until normal muscle function returns
Pharmacokinetics of Neuromuscular blockers
- Highly polar & poorly soluble in lipids
- IV or IM use always (inactive if given by mouth)
- Poor membrane penetration
- Do not enter cells or cross the BBB
AEs of Benzylisoquinolines
Hypotension
- Histamine release & ganglion blockade
AEs of Ammonio steroids
Tachycardia –> Arrhythmias
- Muscarinic blockade (cardiac M2 receptors)
Pancuronium - Moderate tachycardia
- usually not a problem
Drugs that causes Histamine release
Tubocurarine
Lesser extent
- Mivacurium
- Atracurium
Drugs that cause Ganglion blockade
Tubocurarine
-block nicotinic receptors of Autonomic ganglia & adrenal medulla –>
- Hypotension
- Tachycardia
AEs of Tubocurarine
- Hypotension
- Tachycardia
