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NMBA Monitoring

ANP1 Exam 3

QuestionAnswer
Neuromuscular junction components 1. Pre-synaptic nerve 2. Post synaptic muscular membrane
Neurotransmitter involved in NMB ACh - acetylcholine
What class of neurotransmitter is ACh? quaternary ammonium ester
What does an impulse at the motor nerve terminal cause? 1. influx of Ca 2. release of ACh
What does ACh bind to? nicotinic cholinergic receptors on post-synaptic membranes
What happens when ACh binds to nicotinic cholinergic receptors on post synaptic membrane movement of K and Na ions that ↓ transmembrane potential
what happens when movement of K and Na ions ↓ transmembrane potential? an action potential propogates over skeletal muscle leading to muscle contraction
What does acetylcholinesterase do? It works at cholinergic receptors to hydrolyze ACh into Acetic acid and choline
What does choline do? re-enter the nerve terminal where it participates in the synthesis of new ACh
agonist binds to receptor with a confirmational change ~ like a key to a lock, and the door opens
competitive antagonist binds to a receptor with no confirmational change ~ like a key to a lock that doesn't open a door - blocks the lock for other keys
Depolarizing NMBD Succinylcholine (ACh agonist)
Non-depolarizing NMBD's (competitive ACh agonists) pancuronium, atracurium, cisatracurium, rocuronium, vecuronium
How does succinylcholine depolarize the post-synaptic membrane? mimics the action of ACh (movement of K and Na ions) when it occupies the postsynaptic nicotinic cholinergic receptor - muscles contract, then relax (fessiculate)
How does succinylcholine prevent ACh from binding to nicotinic cholinergic postynaptic receptors? Hydrolysis of SCh is so slow that the postjunctional membrane does not respond to subsequently released ACh - prolonging NMB (5-8 min)
How is SCh hydrolized? It is diffused away from NMJ and hydrolyzed in plasma and liver by pseudocholinesterase (nonspecfic cholinesterase, plasma cholinesterase)
How do non-depolarizing NMBDs cause NMB? bind to post-synaptic nicotinic cholinergic receptors WITHOUT causing activation of ion channel permeability. Block depolarization w/ ↓ ACh availability at receptor leading to NMB.
How are NMBDs reversed? 1. redistribution 2. gradual metabolism & excretion 3. administration of reversal agents
What do NMBD reversal agents do? ↑ amt of ACh at NMJ to compete with non-depolarizing NMBDs
What do we use Peripheral Nerve Stimulators (PNS) to assess? NMB
PNS Single Twitch supramaximal electrical stimuli: 0.1-1.0 Hz
Hertz ~unit of frequency ~equal to one cycle/second
PNS TOF ~4 consecutive 200 microsec electrical stimuli in 2 seconds
PNS TOF depolarizing blockade ht of all 4 twitches ↓ by similar amt - only have a fade with OD
TOF ratio amplitude of 4th response / amplitude of 1st response
PNS TOF non-depolarizing blockade ht of 4th twitch ↓ than 1st twitch bc AChis depleted by successive stimulations
TOF > 0.7 1.complete return to control ht of a single twitch response 2. evidence of pts ability to sustain adequate ventilation - BUT pharyngeal musculature may still be weak and uppoer airway obstruction remains a risk.
% blocked w/ 4/4 twitches 60%
% blocked w/ 3/4 twitches 75%
% blocked w/ 2/4 twitches 80%
% blocked w/ 1/4 twitches 90%
ETT NMB suitable when all responses disappear ~ 0/0 twitches
TOF % for safe extubation > 90
TOF Double Burst Suppression ~2 bursts, 750 ms apart ~each burst has 3 (200 microsec) bursts separated by 20-msec intervals (50 Hz) ~ easier to feel the fade
TOF Tetanus tetanic (continuous) electrical stimulation for 5 sec (50 Hz) ~ intense stimulus for ACh release at NMJ
TOF Post Tetanic Facilitation ~d/t ↑ ACh at NMJ after tetany, subsequent twitches are transiently enhanced ~ post-tetanic twitcch indicates ACh is starting to work again ~time until 1st response to TOF is related to # of post-tetanic twitches
Best mode to document 100% paralysis when NO response to Single Twitch, or TOF ~ tetanic stimulus followed by a single twitch stimulus at 1 Hz starting 3 sec post tetanic
what muscle is innervated by the ulnar nerve? adductor pollicis ~ causes adduction of thumb and finger flexion
where does the negative lead go for ulnar nerve PNS negative (black) lead - 1 cm proximal to the pt at which the proximal flexion crease of wrist crosses the radial side of tendon to the flexor carpi ulnaris muscle
where does the positive lead go for PNS of the ulnar nerve positive (red) lead - 2-5 cm proximal to negative electrode
what muscle is innervated by the facial nerve? (temporal branch) obicularis oculi ~ causes movement of eyelid ~ most corollation w/ diaphragm muscle
where does the negative lead go for facial nerve PNS negative (black) lead - at tragus or posterior to orbit (over nerve)
where does the positive lead go for facial nerve PNS positive (red) lead - somewhere else on forehead
what muscle is innervated by the posterior tibial nerve? flexor digitorum longus ~ causes plantar flexion of big toe
where do leads go for posterior tibial nerve PNS inner malleolus and heel
what muscle is innervated by the external popliteal or peroneal (fibular) nerve? tibialis anterior muscle ~ causes dorsiflexion of foot ~ unlikely to ever be used
where do leads go for external popliteal or peroneal (fibular) nerve? behind the head of the fibula at inner side of tendon of biceps
PNS electrode placement over the course of the nerve and not over the muscle itself
how does the negative (black) electrode generate its action potential by depolarizing the membrane ~depolarization vs hyperpolarization (positive lead) makes it easier to stimulate the nerve ~ maximal twitch ht w/ neg lead closest to path of the nerve
what will cause increased skin resistance & affect reading of PNS electrode placement on dirty, hairy, cold skin
stronger or weaker twitches when electrodes on a limb paralyzed by a stroke stronger
optimal placement of electrodes in relation to OR personnel out of the surgeon's way but visible to you
when not to stimulate PNS during delicate part of surgery ie under microscope
NMB in awake pt consciousness / sensorium unaffected - SEDATE FIRST
most sensitive (blocked 1st, recover last) to most resistant muscles (blocked last, recover first 1. extraocular 2. pharyngeal 3. masseter 4. adductor pollicis 5. abdominal rectus 6. orbicularis oculi 7. diaphragm 8. vocal cord
diaphragm NMBD requirements 2x's dose for adductor pollicis muscle blockade
which is paralyzed 1st? small, rapidly moving muscles (fingers, eyes); or diaphragm small, rapidly moving muscles (fingers, eyes) are paralyzed 1st and recover last
is adductor pollicis monitoring a good indicator of cricothyroid muscle (laryngeal) relaxation? NO
what causes underestimation of blockade at vocal cords or diaphragm? monitoring the most sensitive or least resistant muscles to blockade -
when to place PNS induction BEFORE giving NMBD
when to give NMBD induction after induction drug and single burst or TOF for control measurement
when to intubate induction after NMBD given, single burst or TOF at 0/0
changing from succ to non-depolarizing NMBD return of muscle function by TOF or clinical signs should be verified before giving non-depolarizing NMBD
when to reverse not until at least 1/4 twitches, preferably 2-3
spontaneous recovery from non-depolarizing NMBDs w/o reversing NOT recommended (except mivacurium) d/t 60% block w/ 4/4 twitches
most sensitive tests of adequate muscle strength return after NMBD sustained head lift 5 sec ~ grip strength ~ follow commands ~ 33% blocked
Depolarizing NMBD in hemiplegia severe hyperkalemia d/t exaggerated response - pushes out more K (caused by up-regulation)
up-regulation 1. chronic ↓ in ACh release causes compensatory ↑ # of ACh receptors 2. ↑↑↑ response to succ 3. ↓↓↓ response to non-depolarizers ~ prolonged inactivity, sepsis, dennervation or skeletal muscle trauma
down-regulation 1. ↓↓↓ ACh receptors in MS, myasthenia gravis 2. ↓↓↓ response to succ 3. ↑↑↑ response to non-depolarizers
Created by: girlnamedsharon