Anesthesia Pharm EXAM 3 NMB Reversal – Flashcards
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When don't you have to give a NMB reversal?
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Must be 5 half life At 4 half life, you must reverse the patient to wake them up even if they have 4/4 twitches
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What's the half life of fast, intermediate, long acting NMB?
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Duration of Action Succinylcholine: 3-5 min Intermediate: 30-45 -Rocuronium Cis Atricurim (Nimbex): 20-35 min Pancuronium (Pavulon): >1H
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If you give 1.5mg/kg Rocuronium (Zemuron) 2H ago and check for twitches 4/4, what would you do?
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1/2 life of rocuronium is 30-45min, so at 2H, it's not at 5 1/2 life yet, I would give NMB reversal agent to wake the patient up by best practice
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What are the most DIAGNOSTIC test on a NERVE STIMULATOR?
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TOF and 100hz Tetanus -it also has "Double Burst" mode
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A single twitch on a NERVE STIMULATOR indicates what? Name 4 cholinesterase inhibitors.
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a single pulse of 0.2 msec Anticholinesterase 1. Neostigmine (Bloxivers, Prostigmin) 2. Pyridostigmine (Mestinon, NAPPS) 3. Physostigmine 4. Edrophonium -Anticholinesterase agents are usually administered during spontaneous neuromuscular-blockade recovery aka acetylcholinestease inhibitor
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What is the TOF?
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is what we use intraoperatively how much NMB do I have on this patient. so I gave my 120mg Rocuronium RSI dose, checked TOF. preceptor comes in. You can either check it at the FACIAL or ULNAR nerves. That 120mg after 30 minutes, probably not going to get any twitches still but at 45 minutes, 1 twitch. So TOF is just that, once you press that 100 Hz, you get a series of 4 twitches lasting 0.2 sec long. click click click click. Once 4 twitches are back, you would VERIFY by hitting the TETANY for 5 sec and get the "eeeeeerrr" HOLDING without FADE. So the TOF is the MOST DIAGNOSTIC
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What is titanic stimulation?
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-it's taking the NERVE STIMULATOR, press 100 hz and hold it for 5 sec. The same is true for POST TETANIC FACILITATION. Easy, applying exogenous electrical current to STIMULATE the preS terminal, increase Ach release, more Ach at postS jx, allowing more IMPULSES (potentially) unless 1-heavily block with NDNM 2-completely saturated with Depolarizing Succinylcholine related drugs where Ach is already saturated at the postS jx -in that case, the stimulus cannot get through
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After I give 120mg of Rocuronium (Zemuron), ETT, 2 min later, what happened?
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I would anticipate no stimulation, that I got complete competitive antagonist on PostS Jx. No Ach could go through to create a response. checking with a nerve stimuli on the "obicularis oculi" I would not see a "eeeeeerr" response. However, 1H later, after a few 1/2 life. I would see a "eeer...." FADE, because now there is enough released of receptors at the postS jx site that increased flow of Ach from PreS terminal would create a transmission then I'll get an "eeer..." but it will FADE so that's what TETANIC STIMULATION is, it's HOLDING..
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What is post tetanic facilitation or count?
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aka tetanic stimulation
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TOF 100 hz test followed by Tetany HOLDING test for 5 second for confirmation after Rocuronium for instant
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bowel surgery, surgeon gets mad because the muscle is all tense, needs to be deep with NMB. back to the example of 120mg Rocuronium, 1.5H gets 3 twitches, ooo too many, telling us there's less than 75% at the NMJ that's saturated so we need to redose at this point (keep in mind 90-100% required for optimal surgical incision) if we get 4 twitches, that's in 50% we definitely need to give more Rx.
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Redosing NMB is about how much of intubating dose?
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10% so if you give 50mg of Rocuronium standard induction and you got 3 twitches back, you need to REDOSE at 10% of 50mg and that's 5mg. Not 50mg, too much additive effect because there's some receptors are still blocked, you just need to block the rest of them. so give 10-15% is fine.
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If you're reducing, how many cc would you give?
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1cc for redosing, you're not going to go wrong because that's 10mg of rocuronium, 1mg of vecuronium, 2mg of cis atricarium. in 5 minutes, reaccess nerve stimulation, probably no twitches then back to q15min check nerve stimulation
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post tetanic count all that is
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is HOLDING 100 hz for 5 sec to see if you have FADE
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Double burst stimulation is to see if you have
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burst burst or twitch twitch, it's 2 really really fast one, combo between TOF and POST TETANIC COUNT, doesn't have a lot of clinical value
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What's the different between post tetanic count and tetanic stimulation?
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post tetanic count is just that the number how long, HOLDING for 5 sec and count goes eeee 1 2 3 and HOLDING RELEASED, you don't have a full 5 seconds (the eye releases) post tetanic count again, you hOLD 100 hz and you anticipate you will not get a FADE of your NMB. alternatively, oh they're cool.
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Evoked réponses during NDMB and DMB
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Posttetanic potentiation is different from posttetanic count* Ex. Succ = all or none after 1-2 minutes, Top column Phase I, shouldn't shown anything -fasiculating still twtiches folow by paralysis Nondepolarzing block Ex. Vecuronium, twtiches fade (top R) After 5 minutes, competetively antagonize, n twitches Posttenanic FADE = POSTTETANIC COUNT = same thing
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when we're looking at NDMB and DMB, there is a
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big different with DMB with succinylcholine -at fasciculation you will get twitches but afterward, lets say in 1-3 min, you will NOT get any twitches because Ach is completely saturated at the NMJ, see nothing "it's all or none" versus NDMB with Rocuronium -as it sets in, it will weaken...until paralysis versus Succinylcholine, they'll fascinate then full paralysis Ex. 10mg Vecuronium -at 5 minutes with TOF, see nothing because all is completely competitively antagonize but -at 30 minutes, few receptors site opened up through metabolism, probably 1/4 twitch with TOF -at 45 minutes, 2/4 with TOF so from 30-45 minutes, you will get a post tetanic FADE or COUNT same thing -at 1H, 4/4 twitches no FADE
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What is post tetanic count or fade?
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there's tetany then loosen up -all the count is account for how long that tetany was -how long did it take before you get FADE when the muscle released
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With succinylcholine, how could you go into phase 2 block? and why you only get 2/4 twitches on TOF when succinylcholine is all or none
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you could have 2/4 if you -redose -give a priming dose -give a defasiculating dose -if you lets say give 10mg rocuronium + succinylcholine -with succinylcholine, it's all or none unless you do infusion which you won't do
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With succinylcholine, it's all or none unless
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you get 25% receptors back therefor impulse is back as well
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Chart talks about Fraction of occupied and non occupied receptors by NDMB
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90-100% optimum surgical condition
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99-100% indicates
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that 99-100% of the receptors are saturated or there is completely competitive antagonism, no response, so this is your 0/4 twitches, total flaccid so you will NOT get a post tetanic count or stimulation, NOTHING
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95% indicates
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so 5% are opened versus 95% occupied -you can get post tetanic facilitation meaning you won't get a TOF, however, if you HOLD that nerve stimulator at 100 hz, you will get a POST TETANIC FACILIATION
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What is post tetanic facilitation?
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you may not get the muscle to move with the 100 hz current for 5 seconds, but if you immediately do a TOF right after, you may get 1 small movement of facial muscle or ulnar or hypothenar (ulnar side) -your diaphragm muscle could move a little bit so on your CO2 capnography waveform, you could start to see a curare cleft so the diaphragm is getting a little impulse back, spasm like a hiccup or tried to contract, autonomic fx diaphragm is the 1st to want to come back, inate ability to survive, last to go to sleep but 1st to come back, at plateau of ETCO2 waveform, see a dip, you know NMB comes down a little bit, curare notch, so if you get a long way to go with procedure, give more NMB
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What's the 1st clinical diagnostic sign indicating patient is waking up?
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curare cleft or notch on ETCO2 waving and that's that diaphragm pulling it down
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at 90% saturation or 10% availability, you will get what
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you get post tetanic facilitation and 1/4 TOF theoretically -still optimum surgical incision from 100-90% range when NMB required intrabdominal, intrathoracic, hips, when you need NMB relaxant
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dropped to 75% you get
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4 twitches because only 75% of the receptors are blocked, 25% free, you get VT and normal tidal capacity so you mean to tell me that if I get 75% of my receptors blocked, I can breath? Yes you can. Which is why if it's not 5 half life, you have to reverse the patient because of this. yeah, i can get a few VT and vital capacity but I am weak, out of energy, ETCO2 build, CO2 narcosis, arrest.
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Important point, when you get 4 twitches, indicates what
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75% of your receptors are blocked, dangerous to extubate here with just this criteria alone, you need to check post tetanic count as well, especially last dose of NMB is only 45 minutes ago for instant. Post tetanic count is going to be your diagnosis from 75% to 30% so there is no way to tell with TOF if you get 25% opened or 70% opened
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With TOF alone, can you tell whether or not your patient is ready to be extubated, you have 4/4 twitches, can you extubate?
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Hip NO! TOF alone does not tell me whether there is 25% or 75% receptor opened, I need a sustained tetany for at least 5 seconds to confirm. The only way to know is to do a post tetanic count after your TOF.
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So you did TOF and get 4/4 twitches, you know that at least
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25% of my receptor site are opened -heck it could be 50%, 100%, don't know for sure -you need to follow up with post tetanic count as differential diagnostic -if tetany test HOLD for 5 sec, you're cool to extubate because 75% of your receptors are opened, enough receptors site opened be strong enough to breath.
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TOF is okay to titrate intraoperatively when you
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working with 1 or 2 twitches to maintain optimum surgical incision such as checking to make sure you are at least in the 90-100% range. *TEST
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when 30% occupied or 70% free, you're cool
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they get 5 sec head lift, grip your hand *GOLD STANDARD for extubation is a 5 second head lift
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What's the gold standard for extubation?
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5 second head lift for certification exam but in reality if the patient is bucking, take the tube out
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When you are not really sure if the patient is ready to extubate or not, what would you do?
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reverse the patient even if they get 4/4, sustained tetany but VT are just low, 4cc (remember we want 6-8cc/kg) to extubate, she's awake so you don't want to zap her again, you already did that, why is she weak? do secondary diagnostic: is she still weak?, too much opioid? residual inhalational agent off the fat? anesthesia take a hit on her? other diagnostic head: help her out, work with her, make her cough, probably get atelectasis lower lobe, give her + pressure with breaths, lung recruit her, cough and carrying on and do that, stay in OR.
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Optimal surgical condition is how many twitch
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1 twitch for a whipple procedure abdominal procedure -don't let it go to 2 twitches, surgeon will say "patient is waking up" means muscle is tightening up so you need to give 2mg of vecuronium or 5-10mg of rocuronium, 2mg of cis atricarium (10% is for redosing)
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you will do an infusion for
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unlike a lap chole may 1-3H (you bolus) procedure don't need infusion but an 8 level laminectomy because 1-1.5H per level which means every 30-45 minutes required redosing or intermediate acting NMB, we get lazy, 1cc each time too much so what you do is an induction dose follows by MAINTENANCE INFUSION of whatever NDNM. let it run for 7H, the hour before they start to close. -cis Atricarium or Vecuronium: very very stable for infusion, reliable unlike -Rocuronium infusion becomes very tricky, not accurate in their timing, lots of variances, unstable, unreliable. TOF and sustained tetany is not dependable
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What is the best NDMB to run an infusion for an 8 levels lamanenctomy?
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Cis Atricurium you learn to love, because you turn it off after 20-30 minutes, the patients wakes up. Makes you look good, efficient. 0.1mg/kg intraoperative to maintain at 0-1 twitches optimum surgical incision, after 20-30 minutes will have 2-4 twitches back
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when we talked about antagonism of NMB, how do we reverse them?
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opioids and IAs, did you reverse them? in the world of anesthesia, reversal means NMB, not opioids or benzo. of course I did, she's talking to you. fine motor fx of trachea to talk, you wouldn't be able to breath right. anticholinesterase, activity at NMJ.
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Name 3 anticholinesterase we use for reversal?
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1. Neostigmine 99.9% of the time -onset 3-5 min but can take up to 10-20 minutes 2. Edrophonium (Elon) 3. Physostigmine -crosses BBB, tx cholinergic syndrome*
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Which reversal agent crosses BBB?
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Physostigmine -treats cholinergic syndrome -saturates the brain
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if you don't have 4/4 twitches after you gave Neostigmine, what does that mean?
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that patient is not ready -either you reverse before any twitches or -phase 2
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Name an intermediate acting anticholinesterase.
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Neostigmine -inhibits cholinesterase at the NMJ to allow more Ach to bind at the PostS jx so you get nerve impulses -1/2 life of Neostigmine parallels that of the intermediate acting NDMB which is 30-45 min, say 40 minutes standard acceptance, and so I would need a reversal agent at 5 half life to pair with that -think same way as opioids and narcan reversal have to give similar dosing or you get resaturation of the opioids on that receptors right -same with NMB, you get a recurization of the NMB if you give a short acting reversal with an intermediate acting NDMB
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What happened when you give a short acting reversal agent to reverse an intermediate acting NDMB?
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you will get a recurization of the NMB, curare notch say you gave Rocuronium (intermediate) or even Pancuronium (long acting), you have to at least pair it with an intermediate reversal agent of Neostigmine hence used 99.9% of the time because Edrophonium is ultra short acting anticholinesterase used for NMB reversal
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Why don't you want to use Edrophonium to reverse Rocuronium?
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because Edrophonium is a rapid acting reversal only to reverse rapid acting NMB, in Rocuronium you would need to use Neostigmine (intermediate) to reverse an intermediate acting drug can also use in long acting as well in Pancuronium as reversal
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If a patient received 50mg of Rocuronium
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30-45 min later, you see 2/4 TOF, how many twitches minimum you must have to give REVERSAL? 1one -that makes sense because 1 twitches equates to 10% of junctions are opened 90% occupied so we got to have some receptors open for Ach to get to and anticholinesterage prevent breakdown of Ach, thus Ach binds to receptors (10% in this case), now we can get impulses.
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so if it's completely competitively antagonize the Rocuronium, there's no impulses getting through
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doesn't matter how much Neostigmine you give, it's not going to work, you must have some receptors open hence at least 1 twitches to give reversal -must have some receptor availability
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how many twitches create optimum reversal condition?
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2 twitches you can give with 1 but ideally is 2 -remember the whole time your body is metabolizing and everything else is working at the NMJ -so as this being metabolize away so is this and fall at the same time too
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Edrophonium take home point
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it's a 20 minutes reversal so in practice if 4/4 TOF, they are comfortable giving Edrophonium because they know in another 20 minutes, the body even metabolize more of the Rocuronium and have a sustain tetany, probably say they have 70% open at that point. however, Edrophonium is a tricky one, use for diagnostic criteria for myasthenia gravis as anesthesia standby, could create floppy fish syndrome -very short acting -99.9% of the time you will use Neostigmine because of the 1/2 life is pairing with the intermediate acting of NMB
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Physostigmine is a
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anticholinesterase -use as reversal -intermediate acting -crosses BBB -Treats cholinergic syndrome
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Which cholinesterase inhibitor (anticholinesterase) freely crosses the BBB?
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Physiostigmine -no quaternary ammonium therefore its lipid soluble -the ONLY one in its class that can do this
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Patient that has severe alchalasia needs esophageal surgrical repair lost 100 lbs, cachectic, which Rx MOST expect to prolonged DOA?
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Succinylcholine -pseudocholinesterase deficiency aeb malnutrition, ESLD, ESRD, Malignancy, burns, super old, pregnancy -decrease metabolism of Rx -Mivacurium (no longer use) -Ester local anesthetics
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Regards to cholinergic syndrome, say you gave Neostigmine all by itself
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-Muscarinic, Anticholinesterase, SA node, bradycardia, yeah yeah yeah but why -*Ach: tremendous anticholinergic response because Neostigmine is an anticholinesterase, inhibits the break down of Ach, thus tons of Ach are available at the cleft -that's why you MUST give an ANTICHOLINERGIC drug ATROPINE to combat the increase Ach (cholinergic response causes BRADYCARDIA) Thus, reversal of Agent is just as complicated as induction. -reversing NMB allow Ach to flow to receptors to get impulses from nerve to nerve BUT by shear action of this cholinesterase inhibitor inhibiting Acetylcholinesterase -tons of Ach available at the jx, create ParaS responses due to the Muscarinic stimulation (M2 heart, brady) -Prevent bradycaria: give ATROPINE or GLYCOPYRROLATE
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Glycopyrrolate aka
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Cuvposa Glycate Robinul Robinul Forte anticholinergic used to increase HR, treats bradycardia, after using reversal agent (anticholinesterase/cholinesterase inhibitor) results in massive amount of Ach at the cleft causing CHOLINERGIC response so Glycopyrrolate will counteract that causing TACHYCARDIA due to its anticholinergic effect -so HR 80 will not be in 100's is what you will see
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What are the 2 drugs used to treat cholinergic response (BRADYCARDIA) from Neostigmine (anticholinesterase)?
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1. ATROPINE pairs with -EDROPHONIUM (ultra short acting) 2. GLYCOPYRROLATE pairs with -pairs with NEOSTIGMINE due to (longer half life than atropine) NEOSTIGMINE (BNP) -Bloxiverz -Prostigmin -Do not have to use for Physostigmine because it's centrally acting (BBB), no affect the HEART, no BRADYCARDIA
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Do you have to give an anticholinergic drug to treat bradycardia in Physostigmine?
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No, it's centrally acting crosses BBB -has no effect the the heart -doesn't cause BRADYCARDIA
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How do you pair an anticholinergic drugs to treat BRADYCARDIA due to anticholinesterase drug?
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1st: you must know that Atropine and Edrophonium are short acting 2nd: glycopyrrolate and neostigmine are long acting 3rd: anticholinergics (atropine, glycopyrrolate) 4th: anticholinesterase (edrophonium, neostigmine) 1. ATROPINE pairs with -EDROPHONIUM (ultra short acting) 2. GLYCOPYRROLATE pairs with -pairs with NEOSTIGMINE due to (longer half life than atropine)
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Can you pair glycopyrrolate (long acting) with edrophonium (ultra fast acting)?
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Glycopyrrolate (long tachy ATC) It will work but 20 min after, Edrophonium (short brady Cholinergic) have been metabolize away, all you have left is CHOLINERGIC drug TACHYCARDIA. Conversely, Atropine (short tachy ATC) + Neostigmine (long brady Cholinergic), it will work BUT the 1/2 life is shorter than that of Neostigmine. After 20 min, HR be in the 40's, BRADYCARDIA -due to atropine wears off 1st while Neostigmine still available to cause a cholinergic response of low HR
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Neostigmine is always pair with ___ while Edrophonium is always pair with ___
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Neostigmine is always pair with Glycopyrrolate. (long_long) Edrophonium is always pair with Atropine. (short_short) If patient's HR 80 drop to 70's, I want you to give 0.1mg of Atropine or be called PACU with HR of 35 all r/t anticholinesterase = cholinergic response BRADYCARDIA
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Scopolamine is also
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a cholinergic drug -but not use for reversal
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Glycopyrrolate comes in standard 0.4mg/2cc vial, how much do you give and with what anticholinesterase Rx?
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Glycopyrrolate (ATC), I would give 0.2mg of Glycopyrrolate for every 1mg of Neostigmine -Neostigmine comes standard 1mg/1cc in 10ml vial -Match 1cc:1cc (Glycopyrrolate:Neostigmine) Ex. given 3mg of Neostigmine, how much Glycopyrollate would you give? 0.6mg = 3cc (0.2mg/cc, needs 2 vials) Ex. pt has 1 twitch and you have to reverse, gosh why can't he be 2 twitches IDEAL for reversal. but he can give a FULL reversal, he CANNOT with 0 twitch, sit there in the OR waiting until you get at least 1 solid twitch. 1 twitch: commit to maximum reversal dose
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What's the maximum dose of anticholinesterase NDMB reversal drug, say Neostigmine?
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Maximum you can give Neostigmine is 5mg. -more will get you in trouble -Neostigmine (long Cholinergic/ATC_esterase brady) always pair with Glycopyrrolate (ATC long tachy) -Answer 5mg Neostigmine + 1mg Glycopyrollate because 0.2mg Glycopyrollate for every 1mg of Neostigmine. -so it's 1cc:1cc right, so you just draw up 5cc of Glycopyrollate is 0.6mg and 5cc of Neostigmine is 5mg. -These can be mixed together, ideally. -Take 10cc, draw up 5mg of Neostigmine and 1mg of Glycopyrollate. -If some cases, you give the Glycopyrollate (tachy) 1st then the Neostigmine (brady) 2nd, Neostigmine may stay in system longer and BRADYCARDIA so ideally mix them.
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They have 4/4 TOF twitches but when checked for sustained tetany, they have immediate FADE, how many receptors do you think are blocked?
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75% receptors is blocked 2/2 FADE 25% receptors is free because of 4 twitches How much do I give? 1 twitch: get full reversal 2 twitches or more: give 3mg of Neostigmine and 0.6 of Glycopyrollate (always paired) -Atropine + Edrophonium: Tensilon
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Patient has 1 twitch, how much reversal do you give?
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with 1 twitch, patient is still very deep -go ahead and give FULL reversal 5mg of Neostigmine + 1mg of Glycopyrollate 1mg/1cc 0.2mg/1cc
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What is Tensilon? aka Enlon Plus
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It's mixture or combo in 1 syringe, that's cool Atropine + Edrophonium "E+A=T"
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So, the consequence of Neostigmine is what? What does Neostigmine do?
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We know that it create a ParaS effect 2/2 being cholinesterase inhibitor -less Ach broken down, more Ach free -more Cholinergic, more Bradycardia *OR bed blow out, make sense, parastalsis waves, cramping, 3-10 minutes, we have a situation -OR nurse mad at you, you gave too much reversal -given FULL reversal 5mg dose of Neostigmine.
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Neostigmine can also be use at low dose 1mg mixed into 100cc bag for what?
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paralytic ileus surgeon ask 1mg of neostigmine to see if the ileus to move before bowel resection -slow enough that you don't see bradycardia from cholinergic response but every now and then you have to give 0.2mg of glycopyrollate for 1mg neostigmine, for anticholinergic activity helping to increase the HR -if it starts to move, they don't have to resect the bowel "stimulate poop storm"
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With reversal we want to make sure what
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protect the airway, breathing
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Extubation criteria must be methodical, must have
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ETCO2: 65, not ventilating well enough RR: 4 or 24, either end is not good VT: 80 or 800, both are rough on the spectrum so IDEALLY EXTUBATION criteria must include: optimum ventilation meaning VT, appropriate RR, FULL reversal, and PATIENT AWAKE, take deep breath and pull ETT out. -very diagnostic for recovery
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When you give NMB or muscle relaxant, 10mg of Vecuronium or 20m of Cis Atricarium, how does it work, the pathway?
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top to bottom correct thus explain lost of LASH reflex, diaphragm last to go away 1st to lose: LID, Facial m., tracheal or glottic m. relax -Diaphragm inate animal, fight NMB, last m. to lose On REVERSAL: the opposite is true for reversal, diaphragm is 1st to come back
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When we do an RSI, do we really care about the diaphragm and musculo skeletal muscle?
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not really -we just need to glottis m. to relax so we can pass the ETT 1-3 minutes after succinylcholine, diaphragm will stop tugging, paralyze last -same for Rocuronium
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When do you see the diaphragm starting to come back, % wise?
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at 10% of receptors opened -diaphragm begins to come back as Ach receptors unblocked from NDMB, 10% free, Ach binds, partial reversal
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On induction, what muscle lose 1st and last? how about on reversal?
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Induction 1st to lose: GLOTTIS, diaphragm is last. Reversal 1st to win: DIAPHRAGM, glottis is last. -curare notch THM: onset gear down, recovery gear up
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Anytime you have ESLD, ESRD, critically ill patient, you use what NMB
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Cis Atricarium
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Tell me about the additive affect if you redose intermedate NMB if patient has 2 twitches and you want the patient to only have 1 so you give a full dose of NMB again
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with 2 twitches, the patient maybe have about 10% receptors opened lets say, so your FULL dose of NMB is too much, say you gave another 50mg of Rocuronium. -10mg is all you need to cover that 10% receptors free -now you have 40mg waiting at the cleft to binds so if the case if over, you will have to wait until the rest of the 40mg is cleared before the patient wakes up again because essentially, you took them back to 0/4 TOF instead of 1/4, overshoot your dosage essentially is what's happening
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when talking about accumulation of drug, what are we talking about
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say IAs accumulating in the fats, dermis, etcs that's when we talked about "accumulation" to the body tissues
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Review of Nerve Stimulator: 2 ways to be utilized
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Nerve stimulator has 2 probes to connect wires: red & black, EKG electrodes connect to face or hand, then leave your nerve stimulator by head or feet of patient. -hit your TOF and don't have to get out of your chair -Single twitch, TOF -FADE in twitches looks like, you can have FADE in b/t twitches, tall to shorter waveforms (so the switches would be: STONG, Weak, Weaker, barely noticeable FADE)
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Which NMB exhibits FADE? DMB or NDMB
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NDMB (Non Depolaring Neuromuscular Blockade)
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At 90% saturated or 10% free, how many twitches will you have
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-will have 1 twitch and either no other twitches -significant FADE when checking with 100 hz HOLDING 5 sec
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At 75%, you probably have 4/4 twitches with TOF, how about FADE?
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TOF: may have 4/4 twitches 1st -4th stronger to weaker When you do post tetanic stimulation -definitely have FADE because 75% still blocked
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But with Depolarizing muscle relaxant, what do you see?
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All or nothing EXCEPT for -priming dose -defasiculating dose
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What's priming dose?
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talking about NDMB -give 10% dose before as smaller dose -then give FULL dose as larger dose *if you want a faster ONSET: additive effect Ex. doing lap chole, wants to do priming dose of Rocuronium so he can intubate this patient quicker (GERD, DM, hiatus hernia, obese, taco bell) -do everything possible, RSI with cricoid pressure -good Rx principle we can give priming dose as well 10% -use 1.5mg/kg Rocuronium
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What's defasiculating dose, priming dose, redose? what %?
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10% is MAGIC for -priming dose -defasiculating dose -redose With Rocuronium at 10% of standard intubating dose -10mg as priming dose in theory: after versed, fentanyl, 10% Rocuronium of 10mg will probably get 30% of receptor blocked, took out 30% of the NMJ with that essentially -could creep up higher depending on patient, so you do not give a PRIMING dose in PREOPs, NMB only lives in your hand given in OR right during INDUCTION
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When do you give the 10% priming dose?
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-during or after your induction drugs -after versed fentanyl -10mg for 10% priming dose will weaken the pt -but when you give the other FULL induction dose of 120mg of Rocuronium, it will work really fast, because you're already block 30%, after 120mg, will block 100%. -you can prime all of them EXCEPT succinylcholine, you don't prime a depolarizer or redose, phase 2 block
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on 200kg morbidly obese patient above, weight base dosing of Rocuronium of 1.5mg/kg means 300mg/kg, how would you give a priming dose to that patient
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even though 10% meant 30mg priming dose base on 10% of 300mg, DO NOT GIVE *Use STANDARD intubating dose of 100mg, not weight -your patient is not going to breath hence -10mg is the MAGIC dose for priming for standard intubating dose
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What about the defasiculating dose?
answer
defasiculating dose is 10% of the intubating dose of SUCCINYLCHOLINE, because it is the oNLY Rx that is a depolarizing -you can use any of the intermediate Rx -any NDMB, any of the nondepolarizer Defasiculating doses *you can give 10mg/1cc of Rocuronium + Succ *2mg of Cia Atricarium + Succ -Not Pancuronium, too long, slow onset, not going to help your Succ onset of 3-5 minutes, plus potential TACHYCARDIA so NO NO NO NO
question
If you got TOF response of 4, 3 on a nerve stimulator, break down the % of NMB
answer
TOF 4/4: 75% 3/4: 85% 2/4: 90% surgical relaxation wants > 90% -so you want 10% available or less, not too much 1/4: 95% -intubation ideally 95-100%
question
What's the intubating dose for Rocuronium?
answer
0.6mg/kg BUT K 6.2, no GERD, need ETT for quick removal peritoneal dialysis catheter via laparoscopic, renal patient, don't want to use Succinylcholine, but if you use Rocuronium intermediate you will have to be there 30-45minutes, renal patient so 1H before you can reverse it. Could you drop that dose significantly as intubating dose? YES, for right now, know 0.6mg/kg but next POA2, you can cut that dose in 1/2 for renal patient so 25mg of Rocuronium instead of 50mg Do you think it will take longer or the same amount of time for intubating condition? -takes LONGER since we cut dose in 1/2 -standard 0.6mg/kg takes 1-2 minutes onset -renal dose 0.3mg/kg mask pt solid 3 minutes so add gas when you mask them, that way they will have less drug on board systemically, have metabolize quicker, and be able to reverse the, same with all the other INTERMEDIATE NMB
question
Double burst is not very diagnostic
answer
all it is is to see if there are 2 synchronous burst -check for FADE TOF is better to use follow with sustained tetany
question
intubate with Succinylcholine with a defasculating dose of 10mg of Rocuronium (10% of INTUBATING DOSE of 100mg for succinylcholine), 100mg proppofol, ETT, check twitches, remember you gave 10mg of Rocuronium and 100mg of Succinylcholine, you have a FADE, explain
answer
FADE: 1st strong, 2nd strong, 3rd weak, 4th super weak What the heck did that come from, I got a FADE but I gave Succinylcholine (depolarizer) when FADE only occur in NDMB. Answer: because you gave Rocuronium also, 30% blocked Remember 100mg succ gets fasiculation, muscle contraction, then it relaxes. -doesn't maintain full muscle relaxant with Succ fast acting allowing receptors to open up and the intermediate acting out lasted the fast acting so NDMB or Rocuronium still there to binds and you get a FADE as 10% dose is not strong enough to completely eliminate the FADE
question
After you given Succinylcholine and see masseter muscle rigidity, explain
answer
With succinylcholine, normal rigidity is 5-10 seconds but after 1-2 minutes and you still have masseter muscle rigidity with high ETCO2, treat for MH MH crisis: masseter regidity -not phase 2: that's flaccid *check CO2 and HR: 1st signs, temperature is dead 30-60-90-120 Anytime you see ETCO2 80, you either not ventilating or MH, freak out!!!
question
Explain Phase 1, Phase 1, DMB and NDMB, why do you get a PHASE 2 block if you did not redose Succinylcholine?
answer
with Deplarizer redosing, super saturated receptors at the NMJ, create that phase 2 block, that's that, how about? -Nha said, it's not a curare cleft, patient not waking up so I'll just reverse them anyway but doesn't have any twitches meaning sitting at 95-100% saturation, Nha said give him MAXIMUM REVERSAL of 5mg Neostigmine and 1mg of Glycopyrrolate with 0/4 TOF, check nerve stimulater after 3-4 minutes, 1 twitch, gas came off, ETCO2 35, ET agent 0.1 Sevo, Tachycardic, why? -patient is aware now but they are paralyze because you gave Max reversal -yell open your eyes, take a breath, she's paralyze because you gave an anticholinergic and anticholinesterase Rx, what happened? Answer: there were no free receptors (Glycopyrullate competes for receptors), no where for Ach to get on then you inhibited the Acetylcholinesterase with (Neostigmine) allowing more Ach to come in while all receptors blocked so as soon as 1 opened, all these Ach wants to bind to it, creating PHASE 2, can you imagine just one receptor at a time opened and got blocked again? create PHASE 2 block just like redose Succinylcholine -so much surplus of Ach, pt can't move, made your block worst -that's why you must wait for at least 1 twitch and ideally 2 or you will create what look like a PHASE 2 block -you may get a twitch because you got all those Ach there but they will NOT be able to move
question
Conversely, you may have 1 twitch, so you gave FULL reversal, you checked you nerve stimulator, get 4/4 twitches, sustained tetany talked into being into 5 sec, 1...5, reality you get a FADE
answer
We said that's your differential from 30-70%, well she's breathing, VT 300-350, that's alright, you extubate, to recovery room, how're doing mame? can't talk, can't open her mouth. she doesn't have her fine motor fx back from her trachea. Pick up your arm, get "FLOPPY FISH" Weak and floppy like a fish 2/2 your NMB is not fully reversed or you gave too much reversal when it's not time yet. -handle the situation, now pt is hypoventilation, needs to reintubate, you got all these neostigmine anticholinesterase drug there, what NMB do you use? -if you give Succinylcholine gives you PHASE 2 block -if you give Rocuronium or other intermediate Rx, worsen Answer: you don't give another NMB, because the patient is already paralyze. give another dose of propofol and ETT -glottis is already weak and will stay open -put them sleep again, ETT, sedated until they metabolize off their NMB, solid 1H, not looking hot
question
When they have no twitches at all and you tried to reverse when they have no receptors opening, explain what will happen
answer
so they're still paralyze, just cannot breath unlike FLOPPY FISH -you have 1, maybe 2 (rare), weak twitch, you need a full reversal, all that is is creating all that saturation of Ach there, now you got a pt in PHASE 2 block, you got some impulses going through very small amount but not enough -hence very weak and flaccid -similar to "organophosphate toxicity" exactly the same thing, that's what neostigmine is organophosphate
question
What happened in organophosphate toxicity? what Rx does it act similar to?
answer
like in pesticide inhaled warmer get flaccid, can't breath -15-20% FLOPPY FISH occurs when you tried to reverse the patient with lets say Neostigmine when they only have 1 twitch, not a good one either -that's why it is highly recommended that you wait for 2 twitches before reversing the patient -wait 5-10 minutes: get bed in the room, move over gurney, burn enough of that drug so you can have 2 twitches -say you use Sevo, Des, they're still weak, you can speed up by using N2O
question
IAs potentiate/agonize what
answer
IAs potentiate/agonize the NMB, so to get the Sevo gas off quicker to 0.1 MAC awake, you can essentially use N2O to speed up emergent to get the gas off Des > Sevo > Iso -get that gas off with 50-70% N2O so your antagonist gas can get off that NMB -2nd gas carrier effect, at the same time keep their brain amnestic -get 2nd twitch back faster with N2O, reverse them then
question
how long do you wait to see if your NMB reversal agent work?
answer
it should works after 3-5 minutes after that, you have a situation NDMB have FADE while DMB is all or none
question
Placement local of EKG leads for nerve stimulation
answer
Ulnar Nerve -hypothenar flexus -diaphragm Facial Nerve -obicularis oculi -glottis -canthus of the eyes CN5 Trigeminal branches comes off their, mandibular branch so TOF, you see jaw movement, a good thing Leads color doesn't matter: 1 is current, 1 is ground, doesn't matter p Dorsadis Pedis or PD -in cranial surgery, rotate full 180, all you have access to is their feet, heads in pin
question
when in doubt, do you reverse? got 4/4, got tetany, if you're asking yourself, then what?
answer
GIVE IT FOR THE LAWYER -if you have all that: 4/4, sustained tetany, but not more than 5 1/2 life. -GIVE IT, it wouldn't hurt but help the patient -Small dose of 1mg of neostigmine and 0.2mg of glycopyrullate to document "REVERSAL AGENT GIVEN" -they will blame us and say it's anesthesia "prevent residual paralysis" *if it hasn't been 5 half life, "gave it for the lawyer"
question
do you need to reverse Cis Atricarium (it's eliminated by non-organ dependent)?
answer
intermediate acting -you still need to reverse the agent *mom arrested anoxic brain injury died *if it hasn't been 5 half life, reverse it
question
Do reversal agent causes PONV? Yes reversal agent increase PONV, what would do you for super high risk with retractable N/V?
answer
DON'T USE NMB for minor procedure -ORIF ankle: do regional nerve block or -LMA and propofol + opioids general while avoid Etomidate, STP, the NMB reversal so they less likely to have PONV
question
if you reverse succinylcholine, what happened?
answer
in 3-5 minutes, you just bought a PHASE 2 block *NEVER EVER reverse succinylcholine -say you use succinylcholine and intraops you need to give intermediate NMB Rocuronium, do you check twitches before you give? 100% YES to see if they are heterozygus or homozygus because 1 in 30 versus 1 in 300, you have to make sure that patient has no such issues -you can check twitches after succinylcholine and they have 0/4 no twitches, 30 minutes 1H goes buy, no twitches, you now know they have TYPE 2 so you WILL NOT GIVE ANOTHER NMB because you know TYPE 2 they are still blocked due to their heterozygus homozygus genetic
question
how do you check to see if the patient is heterozygus or homozygus when given succinylcholine? why do you check for that?
answer
with succinylcholine and genetic defects -pt could go into PHASE 2 block -so before you give another NDMB like Rocuronium -check TOF to see if you have twitches 1st -Yes twitch, good, can give -No twitches after 5 half life, they are considered in PHASE 2 block 2/2 genetic THM: all your muscle relaxation needs to be gone after succinylcholine before you can give another dose of NDMB
question
tell me about central cord damage and NDMB
answer
cord separation, major damage to cord, cachexia, burns -who bunch of new receptors -Burns: applogiatic by metablism but let's talk about -you have all these immature extra junctional receptors affecting your NMB: easier or harder to block them? HARDER: due to immature receptors taking up space, but they don't have any function -this is chronic it, happened awhile, takes weeks for them to develop these EXTRA JUNCTIONAL RECEPTORS
question
Duchanne Muscular Dystrophy or cerebral palsy, anything along the line of loss of myelination, muscle weakness, giving a NMB would do what to these patient?
answer
profound loss of neuromuscular function and connection -weak already so do you think an intubating dose of Rocuronium is going to last a long time or short time? -A LONG TIME losing nerve terminal, muscles, diffuse demyelination loss of muscle -the impulses are going to what ever muscles are left, the rest are just dying versus Central Cord injury produces immature extra junctional receptors little bit of NDMB goes a LONG way so THM: low dose* *avoid succinylcholine due to MH (triggers by succ and IAs except N2O)
question
tell me the difference b/t Rx metabolize by non-organ dependent and pseudo esterase
answer
non-organ dependent metabolize by esterase in the blood depends on renal hepatic fx -Cis Atricurium, Atracurium, succinylcholine, mivacurium These are NDMB but metabolize in the same fashion Which one are eliminated by pseudocholinesterase? -succinylcholine, mivacurium *Be able to differentiate b/t non-organ dependent metabolism and pseudocholinesterase metabolism.
question
what's the metabolizing NZ of succinylcholine?
answer
pseudocholinesterase metabolizes succinylcholine in the plasma does it happened at the NMJ? NO -it diffuses out and plasma and metabolizes by pseudoC. -don't get confuse with Achetylcholinesterase, not that
question
we gave neostigmine 5mg and glycopyrullate 1mg
answer
in recovery room, pt is BSC, nuts, screaming -tachycardia, red, freaking out, rip out their IVs, HTN What happened? Answer: they're in a cholinergic syndrome 2/2 glycopyrullate (anticholinergic effects) giving them fight or flight response. or they got atropine + edrophonium. Tx for cholinergic syndrome is: physostigmine -get into their mind 1mg/1cc, also treat post ops delirium -don't give anymore anticholinergic with it -crisis as result from too much ATROPINE or GLYCOPYRULLATE
question
Standard of Drug labelings
answer
Blue: Opioids Orange: Benzo Yellow: Induction Agents (Ketamine, Propofol, STP) Gray or White: Local Anesthetic (lidocaine) Red or Dark Orange: NMB Checker pattern: Reversal Agents (Neostigmine) Green: Anticholinergic Purple: Vasoactive drugs Reversal syringe has neostigmine + glycopyrullate -Color: Checker pattern + Green (anticholinergic) 5mg Neostigmine + 1mg of glycopyrullate
question
Dalton's Law
answer
Each gas exerts its own that's important -partial pressure O2, Sevo, N2O -all those exert their own pressure -then there's the sum of all pressure Dalton's Law of Partial Pressure (PP) states: pressure of a gas mixture is the sum of the PP of the individual components of the gas mixture. Pnitrogen is the PP of the nitrogen and Poxygen is the PP of oxygen.
question
What's acetylcholinesterase's function on succinylcholine?
answer
NOTHING -because succinylcholine is metabolize in the blood by pseudocholinesterase -Ach does NOTHING to succinylcholine Succinylcholine acts like Ach so a fake cholinergic NZ of pseudocholinesterase metabolizes it in the blood
question
healthy 17M femur fx playing football, open fx, eaten lunch 1H prior, ETT, uses Succinylcholine, immediate pulseless VTAC
answer
Treatment for Hyperkalemia: ACLS -calcium gluconate: stabilize membrane -insulin + glucose: takes awhile -bicarbonate 1 amp IVP -Hyperventilation: increase to 20 bpm CO2 to 20's -albuterol into ETT: resequest K back into the cell -diuretic: long time same with saline Drop pH to pull K back into cells the likelihood that it is is very high, so treat it like it is
question
when can you give succinylcholine to a burn patient?
answer
NO SUCCINYLCHOLINE w/ BURNs EVER!!!! -post induction VTAC/VFIB 2/2 elevated K unless laryngospasm: -hold positive pressure APL 70 -lidocaine -slug of propofol amnestic loosen larngeal m. (LMA) -10-20mg/1cc of succinylcholine not associated with hyperK (that's induction dose 100mg) if they decline quickly, give Succinylcholine. if need RSI, use Rocuronium
question
What are the 2 classifications of NDMB-nondepolarzing and DMB-depolarizing?
answer
1. Benzisothiazolinone (quinolone?) 2. Benzoisothiazole (isosteroid?) Can you give them interchangeably during same procedure? yes but VERY ADDITIVE EFFECT, POTENTIATION VERY MUCH Can I start with Cis Atricurium and switch to Rocuronium? -say RSI with Rocuronium and want to switch to Cis-Atricurium. you CAN but very ADDITIVE EFFECT where your Cis Atricurium have a functional 1/2 life of 20-30 minutes, due to additive effect, it's going to be 30-45 minutes at least until that Rocuronium completely metabolize off and all you have left is Cis-Atricurium THM: if you stay within the group and you should be fine
question
Last Week FINAL and Case Study review
answer
talk about MH Do some case study, pull things together. Vascular repair: absolute MESS (especially GSW)
question
For obese patient, how do you dose them?
answer
go off of IBW
question
What's Isoquinoline vs Iso-Steroid Derivative?
answer
Isoquinoline derivatives Tubocurarine Atracurium (Tracrium) Doxacurium (Nuromax) Mivacurium (Mivacron) Steroid derivatives Pancuronium (Pavulon) Vecuronium (Norcuron) Pipecuronium (Arduan) Rocuronium (Zemuron)
question
Succinylcholine aka (how is it metabolize)?
answer
aka Anectine: rapid hydrolysis by plasma cholinesterase (butrylcholinesterase/pseudocholinesterase)
question
The primary use of anticholinesterases is to
answer
reverse NDMB
question
__is the NT for the entire paraS NS (paraS ganglions and effectors), parts of the SympatheticNS (sympathetic ganglions, adrenal medulla, sweat glands), some neurons in the CNS, somatic nerves innervating skeletal muscle
answer
Ach __is the NT for the entire paraS NS (paraS ganglions and effectors), parts of the SympatheticNS (sympathetic ganglions, adrenal medulla, sweat glands), some neurons in the CNS, somatic nerves innervating skeletal muscle
question
NT transmission is blocked when
answer
NDMB compete with Ach to bind to Nicotinic Cholinergic Receptors. "competitive antagonist" The cholinesterase inhibitors indirectly increase the amount of Ach available to compete with NDMB thereby reestablishing neuromuscular transmission.
question
In excessive dose, acetylcholinesterase inhibitors can paradoxically potentiate a NDMB.
answer
In addition, these drugs prolong the depolarization blockade of succinylcholine because the Rx's increases Ach competing with Succinylcholine.
question
What can increase the DOA of a cholinesterase inhibitor?
answer
renal or hepatic insufficiency resulting in prolongation of NDMB's action NDMB is a competitive antagonist competes with Ach for receptors site thus increase DOA of cholinesterase inhibitor
question
A reversal agent should be routinely given to NDMBs unless
answer
full reversal can be demonstrated or the postoperative plan includes intubation and ventilation
question
the suggested end points from a NMB are
answer
sustained tetanus for 5 sec in response to 100 Hz stimulus in anesthetized patient or sustained head lift in awake patients If neither is achieved, pt should remain intubated and ventilated
question
Sugammade exerts its effect by forming tight complexes in a 1:1 ratio with
answer
steroidal NMBs
question
___ causes inactivation of gantacurium via metabolic degradation and adduct formation.
answer
Cysteine causes inactivation of gantacurium via metabolic degradation and adduct formation.
question
Factors potentiating NMB
answer
Electrolytes and acid-base disorders HyperMg HypoCa HypoK Respiratory Acidosis Hypotemperature Lasix Lidocaine CCB (Verapamil) Dantrolene IAs Aminoglycosides
question
the quaternary structure is what prevent what
answer
quaternary structure prevent that drug from crossing the BBB Drug such as NMB doesn't cross BBB only skeletal m. -same for anticholinergic Glycopyrrolate has NO CNS activity and NO opthalmic activity On the other hand, anticholinergic Rx Physostigmine does not have quaternary ammonium -able to cross the BBB -treats cholinergic syndrome -the only 1 cholinesterase inhibitor cross BBB
question
2 Major Classes of NDMB
answer
*TAM-D is Isoquinoline *PP-RV is Steroid Isoquinoline derivatives (TAM-D) - Tubocurarine - Atracurium (Tracrium) - Doxacurium (Nuromax) - Mivacurium (Mivacron) Steroid derivatives -- e.g. (PP-RV) - Pancuronium (Pavulon) - Vecuronium (Norcuron) - Pipecuronium (Arduan) - Rocuronium (Zemuron)
question
Route of elimination-- important determinant of duration of action of NDMBs
answer
Renal elimination: - Long half lives; long durations of action (> 35 min) Hepatic elimination: - Shorter half lives: (< 30 min) THP: the liver eliminate faster than the kidney
question
Antagonist-assisted neuromuscular-blockade reversal: acetylcholinesterase inhibitor, more Ach available
answer
-Edrophonium (Tensilon), neostigmine (Prostigmin), or pyridostigmine (Mestinon)-- effective by increasing acetylcholine availability of neuromuscular junction {secondary to acetylcholinesterase inhibition} Atropine + Edrophonium Glycopyrrolate + Neostigmine -Physostigmine (Antilirium): not used because dosage requirement is excessive
question
Reversal of phase II block following infusion of succinylcholine or redosing may be reversed
answer
with edrophonium (Tensilon) or neostigmine (Prostigmin) in patients with normal plasma cholinesterase In patients with atypical plasma cholinesterase, phase II block reversal may not be reliable, requiring mechanical ventilation until blockade subsides.
question
if you start with Succinylcholine and Switch to an intermediate NDMB say Rocuronium
answer
you will have a great NMB -additive effect BUT if you just use 0.5mg/kg LOW dose of succinylcholine -you will not have an additive effect
question
Combinations of NDMB provides the same degree of blockade at smaller dose of each drug but the benefit is
answer
Benefit: fewer dose-related side effects - Example: BP/heart rate effects of pancuronium (Pavulon) + metocurine (Metubine Iodide) < with pancuronium (Pavulon) monotherapy
question
Do Women required more or less Vecuronium and Rocuronium than Men
answer
Clinical significance: -Normal rocuronium (Zemuron) dose should be reduced in women compared to men, same with Vecuronium *men have a greater skeletal muscle mass percentage-- requiring a higher neuromuscular-blocking dosage
question
Pancuronium is the only Long Acting NDMB, think 0.1mg/kg intubating dose
answer
onset: 3-5 minutes duration: 60-90 minutes -no histamine -no autonomic ganglia blockade?? Pancuronium (Pavulon) block enhanced by respiratory acidosis which opposes neostigmine (Prostigmin) antagonism Beneficial for long duration paralysis needs in cardiac suite Tachycardia balances narcotic induced bradycardia via blunt sypathetic response CV: increase HR, MAP, CO Increased heart rate r/t vagolysis at post ganglionic nerve terminal, muscarinic blockade and catecholamine release Inhibits plasma cholinesterase Often used in cardiac surgery Inexpensive Aminosteroid compound Onset 3-5 minutes, duration 60-90 minutes Intubating dose 0.08-0.12 mg/kg *heavy on renal 80% elimination make sense long acting drug makes kidney work long hours
question
Pipecuronium (Arduan) intermediate NDMB drug overview
answer
Pipecuronium (Arduan) -onset: 3-5 minutes -DOA: 60-90 minutes -No histamine release -no CV changes Pharmacokinetics: -similar to pancuronium (Pavulon) in terms of renal clearance -Hepatic cirrhosis -- no effect on pipecuronium (Arduan) pharmacodynamics/ pharmacokinetics
question
Succinylcholine and Duchennes
answer
Succinylcholine is contraindicated in Duchennes due to risk of rhabdomyolysis, hyperK, cardiac arrest response to NDMB is normal however -avoid general anesthesia and succinylcholine -Duchennes: X link recessive disorder
question
2 anesthetic drugs exhibit prolonged DOA in patient with MG taking anticholinesterase
answer
Succinylcholine Ester local anesthetics Because these drugs inhibit plasma cholinesterase, can prolong DOA in drugs metabolized by plasma cholinesterase.
question
use of muscle relaxant with Huntington's disease
answer
they are extremely sensitive to NDMB herefore should be titrated very carefully -also because of decrease plasma cholinesterase, they exhibit increased sensitivity to succinylcholine -THP: increase sensitivity to NDMB and succinylcholine
question
MG patient taking pyridostigmine (anticholinesterase), you should
answer
expect a potentially exaggerated response to NDMBs and DMB in succinylcholine -monitor NMB at oculi muscle MG have decreased functioning Ach receptors -Rx helps alleviate skeletal m. weakness -but may have prolonged response to DMB -external ocular m. affected 1st
