Neuromuscular Blockers Flashcards

1
Q

Tubocurarine

A

Isoquinoline class non-depolarizing neuromuscular blocker

  • competitive antagonists of nicotinic acetylcholine receptor at the NMJ- bind to same site as acetylcholine, prevents ACh from binding, non-depolarizing because prevents channels from opening
  • Onset 4-6 minutes; duration 45-60 minutes
  • Termination of action by kidney
  • Weak block on autonomic ganglia; no effect on muscarinic receptors, moderate histamine release
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2
Q

Mivacurium

A

Isoquinoline class non-depolarizing neuromuscular blocker

  • competitive antagonists of nicotinic acetylcholine receptor at the NMJ- bind to same site as acetylcholine, prevents ACh from binding, non-depolarizing because prevents channels from opening
  • Onset 2-4 minutes; duration 10-20 minutes
  • Termination of action by plasma cholinesterase
  • no effect on autonomic ganglia, no effect on muscarinic receptors, some histamine release
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3
Q

Atracurium

A

Isoquinoline class non-depolarizing neuromuscular blocker

  • competitive antagonists of nicotinic acetylcholine receptor at the NMJ- bind to same site as acetylcholine, prevents ACh from binding, non-depolarizing because prevents channels from opening
  • Onset 2-4 minutes; duration 20-30 minutes
  • Termination of action is spontaneous
  • no effect on autonomic ganglia, no effect on muscarinic receptors, some histamine release
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4
Q

Cisatracurium

A

Isoquinoline class non-depolarizing neuromuscular blocker

  • competitive antagonists of nicotinic acetylcholine receptor at the NMJ- bind to same site as acetylcholine, prevents ACh from binding, non-depolarizing because prevents channels from opening
  • Onset 2-5 minutes; duration 30-45 minutes
  • Termination of action is spontaneous
  • no effect on autonomic ganglia, no effect on muscarinic receptors, no histamine release
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5
Q

Pancuronium

A

Steroid class non-depolarizing neuromuscular blocker

  • competitive antagonists of nicotinic acetylcholine receptor at the NMJ- bind to same site as acetylcholine, prevents ACh from binding, non-depolarizing because prevents channels from opening
  • Onset 4-6 minutes; duration 45-60 minutes
  • Termination of action by kidney
  • weak block on autonomic ganglia; some block on muscarinic receptors; no histamine release
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6
Q

Rocuronium

A

Steroid class non-depolarizing neuromuscular blocker

  • competitive antagonists of nicotinic acetylcholine receptor at the NMJ- bind to same site as acetylcholine, prevents ACh from binding, non-depolarizing because prevents channels from opening
  • onset 1-2 minutes; duration 20-30 minutes
  • termination of action by liver
  • no effect on autonomic ganglia, weak block on muscarinic receptors, no histamine release
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7
Q

Vecuronium

A

Steroid class non-depolarizing neuromuscular blocker

  • competitive antagonists of nicotinic acetylcholine receptor at the NMJ- bind to same site as acetylcholine, prevents ACh from binding, non-depolarizing because prevents channels from opening
  • Onset 2-4 minutes; duration 20-30 minutes
  • termination of action by liver
  • no effect on autonomic ganglia, no effect on muscarinic receptors, no histamine release
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8
Q

Succinylcholine

A

Depolarizing neuromuscular blocker

  • partial agonist of NMJ nAChR, depolarizes skeletal muscle membrane and initailly triggers muscle contractions (fasciculations) then blocks depolarization, inactivation of voltage gated Na chanels
  • Fast onset (1 minute), used in rapid sequence induction/ intubation for short procedures (or boost with a different longer lasting NMJ blocker)
  • rapidly metabolized by plasma cholinesterase (short duration of action)
  • agonist activity at other AChR’s- stimulates autonomic ganglia (hypertension, tachycardia); stimulates muscarinic receptors (bradycardia); histamine release. Specific to succinylcholine- myalgias, increased intracranial pressure, hyperkalemia
  • Prolonged block: seen with prolonged infusion/ repeated boluses due to desensitization of nAChR, open channel block of nAChR, competitive antagonism of nAChR; decreased metabolism by plasma ChE if decrased circulating levels of ChE as in liver disease, genetic “Kvariant” or decreased activity of ChE due to organophosphage (ChE inhibitor) poisoning or inheritied atypical enzyme variant
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