Train of Four

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    I'm having a hard time figuring out why we shouldn't reverse a patient if we get 0 out of four twitches. I understand that if we do give a reversal in that situation, they can recurarize later, but I thought there was another reason why you shouldn't. Any takers?
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  4. 0
    Quote from Kason
    I'm having a hard time figuring out why we shouldn't reverse a patient if we get 0 out of four twitches. I understand that if we do give a reversal in that situation, they can recurarize later, but I thought there was another reason why you shouldn't. Any takers?
    label me stupid.....but what are you talking about? what is 0/4 twitches? is it a neuro assessment? and i could not find "recurarize" in any dictionary/medical reference. please educate me. just when you think you have heard most things you learn something else. :stone
  5. 0
    if somebody is 0/4 then how long do you think before they become 4/4 (and remember that 4/4 initially only means 75-80% of initial strength) ... depending on the drug it could be a long time... remember neostigmine lasts about 45 minutes (edrophonium about 20-30 minutes)... you can see the conundrum...
  6. 0
    Quote from Tenesma
    if somebody is 0/4 then how long do you think before they become 4/4 (and remember that 4/4 initially only means 75-80% of initial strength) ... depending on the drug it could be a long time... remember neostigmine lasts about 45 minutes (edrophonium about 20-30 minutes)... you can see the conundrum...
    thank you for clearing that up. i do remember the 4/4 category from my health assessment class in nursing school, but i don't remember the "twitches" part. i work in ED and we don't use such terminology. we do neuro assessments for muscles in a more general sense, such as strong, weak etc.. i'm sure we have protocols for certain drugs that require us to give a more accurate description of the patients progress but i have not stumbled upon it yet. thanks again
  7. 0
    Train of Four refers to monitoring a patient that has been given paralytics such as vecuronium, rocuronium etc. The # of twitches as well as the strength out of 4 gives an estimate of the level of paralysis. Usually the ulnar nerve is stimulated but the facial N. is also used as well as the posterior tibial nerve. Generally, what one is trying to do is detrmine the ratio of the 1st twitch to the 4th twitch. less than a ratio of 0.7 usually corosponds to the threshold at which resp compromise becomes apparent. It is used to determine intubating conditions, surgical relaxation (especially for abdominal surgery) and talso during emergance. Other modes of monitoring are the double burst and post tetanic count. There is more to learn about this than I can write so I'd refer you to any anesthesia text (or ICU text)under monitoring neuromuscular blockade.
  8. 0
    angel337

    for most surgical procedures a neuromuscular blocking agent (muscle relaxer) is given to allow better surgical access such as big belly cases. by giving these drugs you competively block the receptors that allow muscle contraction. each drug has different duration of action therefore need to be monitered using a twitch monitor. this twith monitor releases varying degrees of current. the ulnar nerve is frequently used to stimulate the adductor pollicus. when the anesthetist is monitoring a train of four (TOF), four bursts of current are fired from the stimulator and depending on how much drug is on board determines how many twitches are displayed. 1/4 twitch- 90% block 2/4- 80% block and so on. this allows the anesthetist to gauge whether more muscle relaxant is needed or not depending on twitch responce.

    finally at the end of the case the muscle relaxant need to be reversed in order to allow the patient to breath because we essentially paralyzed their diaphragm. these reversal drugs are called acetylcholinesterase inhibitors. in short they prevent the breakdown of Ach by certain enzymes, thus allowing excess Ach to displace muscle relaxants from receptor site (Ach is needed for muscle depolarization--contraction) but these reversal agent can prolong block if given too early b/c they themselves can get in the way and block receptor sites along with muscle relaxant thus increasing the competition for the Ach to due it's work.

    hope this helps scratch the surface
  9. 0
    Quote from ctbsurf
    angel337

    for most surgical procedures a neuromuscular blocking agent (muscle relaxer) is given to allow better surgical access such as big belly cases. by giving these drugs you competively block the receptors that allow muscle contraction. each drug has different duration of action therefore need to be monitered using a twitch monitor. this twith monitor releases varying degrees of current. the ulnar nerve is frequently used to stimulate the adductor pollicus. when the anesthetist is monitoring a train of four (TOF), four bursts of current are fired from the stimulator and depending on how much drug is on board determines how many twitches are displayed. 1/4 twitch- 90% block 2/4- 80% block and so on. this allows the anesthetist to gauge whether more muscle relaxant is needed or not depending on twitch responce.

    finally at the end of the case the muscle relaxant need to be reversed in order to allow the patient to breath because we essentially paralyzed their diaphragm. these reversal drugs are called acetylcholinesterase inhibitors. in short they prevent the breakdown of Ach by certain enzymes, thus allowing excess Ach to displace muscle relaxants from receptor site (Ach is needed for muscle depolarization--contraction) but these reversal agent can prolong block if given too early b/c they themselves can get in the way and block receptor sites along with muscle relaxant thus increasing the competition for the Ach to due it's work.

    hope this helps scratch the surface
    Thanks for such a quick response guys. I'm glad there are people out there that get this stuff. Does the anticholinesterase block the Ach receptors pre or post synaptically? Don't they also decrease the amount of plasma cholinesterase to some extent?
  10. 0
    Theoretically, Neostigmine can cause muscle relaxation at a high enough doses. This is a great clinical question.

    "If you anesthesia tray is completely devoid of muscle relaxants, which drug in your tray can cause muscle relaxation?"

    I'm can't remember the MOA, but theoretically at least the high Ach levels produced by Acetylcholinesterase drugs could cause a phase 1 block like Succinylcholine. Does anyone else want to take a shot?
  11. 0
    to also help determine how deep the paralysis is (if no tof twitches) you can do a post tetanic twictch count. this will help determine how soon you should get twitches back if you dont have any tof. supramaximal 100hz stimulation for 5 sec, then one twitch every second and count the twitch response. 8-10 post tt twitches will usually correllate tof 1/4. if less than 8 you have a ways to go before pt is ready to reverse, or return of any twitches.
    side note on tof. if the 4th twitch if 90% as strong as the first twitch then there is less than 70% blockade of receptors, if the 4th twitch is less than 90% of the first twitch then there is greater than 70% blockade of receptors.

    Does the anticholinesterase block the Ach receptors pre or post synaptically?
    anticholinesterases block the formation of acetylcholinesterase, this allows for greater amounts of circulating ach. the excess ach thusly has a greater chance to bind with ach receptors, competing with nmba allowing for muscle depolarization of muscle fibers (reversed paralysis), (while the nmba's are concurrently being metabolized in their normal fashion). this occurs at the postsynaptic membrane.
    however if you give an anticholinesterase to a person paralyzed with succs, it will prolong the block because the mechanism that breaks down succs is blocked, (cholinesterase) (succs is 2 ach molecules stuck together) this is why patients will fasiculate (depolarize) when you give succs.

    also of note when using pancuronium or vecuronium, these have metabolites that can prolong paralysis.
    vec's metabolite is 33% as potent as the parent drug
    pan's metab is 66% as potent this is significant if you talk reversal. the metabolits can cause resp depression after you take the patient to recovery.

    d
    brenna's dad posted as i was typing my dissertation.
    i'm not sure but your rationale sounds good to me.
    Last edit by gaspassah on Feb 29, '04


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