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NMBA Monitoring
ANP1 Exam 3
| Question | Answer |
|---|---|
| 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
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