Physiology and Monitoring Neuromuscular Blockade Flashcards
prevents muscle contraction by interfering with the transmission of an action potential from the nerve ending to the muscle
action of neuromuscular blockers
- facilitate intubation
- decrease muscle tone to provide appropriate operating conditions
- alleviate muscle activity with ECT
- allow balance anesthesia w/o pt movement
- assist in controlled vent pts
uses of neuromuscular blockers
- impulse arrives at the motor nerve terminal
- Ca influx release ACh into cleft (synapse)
- ACh diffuses across cleft to nicotinic receptor
- ACh binds with alpha sites on postsynaptic receptor causing ion channel to open
- Na and K ions move across channel causing depolarization
- action potential spreads over surface of muscle fibers causing contraction
- ACh diffuses away from end plate region or is metabolized by acetylcholinesterase (AChE)
normal neuromuscular function
release of acetylcholine is ___ dependent and triggered by increases in concentrations of free ___ ions in nerve terminals
Calcium
opens calcium ion channels
cyclic adenosine monophosphate (cAMP)
what is the primary neurotransmitter?
acetylcholine
the principle site of action of neuromuscular blocking agents
“site of effect”
neuromuscular junction
what inhibits release of ACh
magnesium
synthesized in the motor nerve ending by acetylation of choline which is controlled by choline acetylase enzyme
acetylcholine
what is ACh rapidly (<15 ms) hydrolyzed by turning it into choline and acetic acid where choline is taken back into nerve ending to be used to synthesize more ACh
acetylcholinesterase (AChE)
- on nerve ending
- affects neurotransmitter release
- ion channel allow flow of Na
- activation mobilizes additional ACh for release
ACh presynaptic (prejunctional) receptors
blockade of presynaptic (prejunctional) receptors causes a __ in the release of ACh
decrease
- similar to those found in fetus
- receptors found throughout muscle cell, as call matures, less are formed
- not involved in neuromuscular transmission
- sensitive to agonists AND channels remain open 4x longer (hyperkalemia)
- creating supressed by nerve ending activity
extrajunctional (perijunctional) receptors
occurs if the muscle is damaged, diseased or denervated (burns, paralysis, stroke, muscular dystrophies, immobilization)
proliferation of extrajunctional receptors
[means there are more places NMB can attach to but will not have same effect]
- in junctional folds of muscle membrane
- made of 5 linear protein subunits (2 alpha, beta, delta, and epsilon)
- form a channel for flow of Na, K, Ca
postsynaptic receptors
- ACh binds to extracellular sites on alpha subunits
- channel opens
- Ca and Na flow in, K out
- depolarization occurs
- muscle contraction
postsynaptic receptor events
attaches to both alpha subunit sites and mimics ACh and causes depolarization
depolarizing blockers
attaches to one alpha subunit to prevent ACh from binding and thus prevents depolarization
nondepolarizing blocks
can occur with antibiotics (mycins), quinidine, tricyclic antidepressants, and naloxone
physically blocks an open channel or a closed channel around the extracellular entrance
closed channel blockade
time from administration to max effect
onset time
time from admin to 25% recovery of twitch response (1/4 TOF)
clinical duration
time from admin to 90% recovery of twitch respone
total duration
time from 25% to 75% recovery of twitch responses
recovery index
the dose needed to produce 95% of suppression of single twitch response
ED 95