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Regarding cocaine mimicking a 1c antiarrhythmic it is my understanding that it most closely looks like a 1b class, ie lidocaine and mexilitine. (like lidocaine it is a local anesthetic with similar properties). In this context I learned years ago that lidocaine was contraindicated with cocaine OD and use of amiodarone would likely be drug of choice, once bicarb, cardioversion etc were entertained. Given it's properties to my knowledge lidocaine would add toxicity to the mix.
Also the concept of QTC prolongation (negating the scenario of co-ingestion viz a vis methadone) it is my understanding that cocaine will prolong the QRS duration and as a secondary event cause QTC prolongation.
No one has ever clarified this for me, however is there not a difference between QTc prolongation due to widening of the qrs vs prolongation of the S-T segment alone. Are the implications different from the region of channelopathy whether the qrs is long by default from a widened qrs vs true QTC prolongation via widening from the s-wave to the end of the T-wave. Aren't we talking a different issue with depolarization vs conduction delay and in so doing changing the risks of torsades. QRS widening is not a torsades risk, but S-T prolongation vis a vis a primary QTC prolongation is.
Are these differences relevant and do we need to view the QTC in the context of secondary QTc prolongation due to QRS widening vs QTC prolongation via S-T prolongation.
The argument to use lidocaine in this presentation makes no sense to me. You are using a local anesthetic of type 1b class to "fix" toxicity of a 1b anesthetic via cocaine which is working on the same sodium channel and likely to add insult to injury.
Andy, I'll followup with our tox folks about whether the article was correct vs. your comments. My discussion was based on what was written in the article, so it might be worth sending your comments in a letter to the editor for them to address. Thanks for taking the time to write.
Thank you :)
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