Unit 3- Neuromuscular Blockers Flashcards
Competitive Nondepolarizing Agents
Block nicotinic receptors to prevent Ach binding
Depolarizing Agents
Cause initial membrane depolarization before paralysis
Nicotinic Receptors
Require ionic binding of 2 Ach, opens channel to allow Na+ in the cell
Tetrodotoxin
Decrease permeability of Na+ to cause muscle paralysis
Local Anesthetics
Inactivate Na/K channels to prevent action potential
Hemicholinium
Interferes with reuptake
Botulinum Toxin
Interferes with Ach vesicles with the plasma membrane to prevent Ach release
Cholinesterase Inhibitors
Decrease AchE activity, Ach accumulates at receptors
Magnesium Ion
Competes with Ca++ transport into the nerve, interfering with Ach release and decreasing postsynaptic Ach sensitivity
Aminoglycoside Antibiotics
Inhibit Ach release by lowering Ca++ availability at axon terminal, decrease postsynaptic Ach sensitivity
Depolarizing Agents Elimination
Hydrolysis by cholinesterase
Competitive Nondepolarizing Agent Elimination
Hepatic metabolism or hoffmann elimination
Hofmann Elimination
Elimination without enzymes affected by temp or pH
Benzylisoquinoliniums
Nondepolarizing competitive agents, atracurium, cisatracurium, mivacurium, doxocurium
Aminosteroid Agents
Nondepolarizing competitive agents, vecuronium, rocuronium, pancuronium
Asymetric Chlorofumarates
Nondepolarizing competitive agent, gantacurium
Atracurium
Muscle relaxation during surgery, intubation, safe in renal or hepatic insufficiency, urethral obstruction removal, minimal cardiovascular effect, pH and temp affect elimination
Cisatracurium
Similar to atracurium
Pancuronium
Muscle relaxation during surgery, intubation, inconsistent cardiac effects
Vecuronium
Muscle relaxation during surgery, hepatic metabolism, minimal cardiac effects
Rocuronium
Rapid onset, no cardiovascular effects
Gantacurium
Ultra short duration, degraded in plasma
Succinylcholine
Depolarizing agent, rapid onset with short duration, prolonged depolarization of end plate, phase I and II block
Phase I Succinylcholine Block
Open cation channel and depolarize , increased cation permeability, muscle fasciculation
Phase II Succinylcholine Block
Cation channel closes and repolarizes, junction resistant to depolarization, flaccid paralysis
Neuromuscular Blocker Paralysis Progression
Face, limbs, larynx, abdominals, intercostals, diaphragm
Dosing of Neuromuscular Blockers
Sufficient to paralyze limbs but not diaphragm
Margin of Safety
Large majority of receptors must be blocked to prevent muscle twitch
Reversal of Blockers
Initiate ventilation, withdraw administration, avoid synergistic drugs, use AchE inhibitors and cyclodextrin to reverse
AchE Inhibitors
Inhibit AchE to reverse nondepolarizing drugs
Succinylcholine
Reverses depolarizing agents
Edrophonium
AchE inhibitor used to reverse neuromuscular blockage