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.
brenna's dad posted as i was typing my dissertation.
i'm not sure but your rationale sounds good to me.