In this 214th episode I welcome back Dr. Gillian Isaac to do another ABA Keyword episode. We review non-depolarizing neuromuscular blockers and myesthenic syndromes.
Show Notes by Dr. Brian H. Park
Ted Lasso: https://en.wikipedia.org/wiki/Ted_Lasso
Amicus Podcast Interview with Michael Heller: Link
Barash Clinical Anesthesia 8th edition and Anesthesiahub.com
6 thoughts on “Episode 214: Keywords Part 17: Non-depolarizing blockers and Myesthenic Syndromes”
In regards to the question about the parturient with MG presenting with Pre-E I believe reason that bupivacaine was the preferred agent rather than 2-Chlorprocaine was because the patient was taking pyridostigmine. Although its primary therapeutic benefit is due to inhibition of acetylcholinesterase, pyridostigmine would also likely reduce the patient’s pseudocholinesterase activity as well. Since 2-chlorprocaine, an ester, is metabolized by pseudocholinesterase this could result in an abnormally prolonged duration of action of 2- chlorprocaine. Bupivicaine metabolism would be unaffected, which would make it the preferred local anesthetic.
Also, this is probably obvious but I definitely had to remind myself that in this scenario with a patient with likely Pre-E (time allowing of course), a STAT CBC would be certainly beneficial to rule out thrombocytopenia prior to attempting epidural placement.
Thanks for another great episode, love these keyword reviews!
Great points, thanks!
With regards to the question about which medication does magnesium not prolong, why don’t we see an impact with bupivicaine? I thought since magnesium is an antagonist of calcium and this can result in decreased release of acetylcholine at the synaptic cleft, that it would potentiate the effect of bupivicaine?? I am lost on this one
Great podcast! Concise and informative as always.
With reference to raised Parathyroid hormone ( without hypercalcaemia) causing prolonged block.
Altered hepatic metabolism – secondary to Parathyroid hormone may cause reduced CYP activity in phase 1 and impairs conjugation and acetylation in phase 2.
Not sure if I misunderstood this concept- but I interpreted it as raised PTH could itself impairs hepatic metabolism and therefore prolong duration of action on Rocuronium?
Reference: Applied Pharmacology in Anaesthesiology and Critical Care 2nd Edition-by Milner and Welch (South African authors) .
Hello ,Great lecture as always
I wanted to ask you something very basic , which i am strugguling to fully understand .
In myastenia gravis why do we need higher dose of sux but lower of NDMR ?
MG destroys acetylcholine receptors. Sux works by binding to these receptors and causing depolarization. So fewer receptors means they are resistant to sux. On the other hand non depolarizers act by blocking the receptors so less receptors means less to block.