Episode Chapters
- Introduction10:44Litigation and Stress Part 1Free Chapter9:33One More Film14:31Placental Abruption8:05Critical Care Mailbag - Cardiogenic Shock17:53Diplopia17:00Ketamine and Alcohol Withdrawal11:41Litigation and Stress Part 2Free Chapter11:03Trauma Surgeons Gone Wild: REBOA - Part 111:48Rabies11:33Community Medicine Rants – High Flow O29:52Pre-exposure Prophylaxis (PrEP)10:59Dental Trauma12:11Trauma Surgeons Gone Wild: REBOA - Part 212:50Pediatric Pearls – Pediatric Influenza20:27Mailbag8:33Summary24:03EM:RAP 2018 December German Edition1h, 34mEM:RAP 2018 December Spanish Edition1h, 14mEM:RAP 2018 December French Edition18:41
Nurses Edition Commentary
Kathy Garvin, RN and Lisa Chavez, RN
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EMRAP 2018 12 December Written Summary_V2 525 KB - PDF
EM:RAP 2018 December Full episode audio for MD edition 222:26 min - 208 MB - M4AEM:RAP 2018 December German Edition Deutsche 94:28 min - 83 MB - MP3EM:RAP 2018 December Spanish Edition Español 74:31 min - 102 MB - MP3EM:RAP 2018 December French Edition Français 18:41 min - 26 MB - MP3EMRAP 2018 12 December Board Review Answers 133 KB - PDFEMRAP 2018 12 December Board Review Questions 125 KB - PDFEMRAP 2018 12 December Written Summary_V2 525 KB - PDFEMRAP 2018 December Individual MP3 299 MB - ZIPEMRAP 2018 December Individual Written Summaries_V2 941 KB - ZIP
Whit F., M.D. - January 4, 2019 4:36 AM
Hey guys. Great segment.
I have a question on the relative uselessness of dexmedetomidine for ethanol withdrawal that you guys alluded to. When you say that dex masks the vital signs, do you mean that it isn't *really* reducing sympathetic tone? I know that dex (or clonidine) won't reduce seizure episodes alone, but aren't the labile blood pressures and crazy sustained tachycardia what really kills people? I always thought a big goal of GABA agonism or NMDA antagonism was to reduce the massive sympathetic surge as well as the seizures, and seems like dex would achieve at least part of that goal, just a little further down in the pathway.
Bryan H. - January 4, 2019 6:32 AM
Thanks for the comments. I think the key with dexmedetomidine is that it doesn't replace the other sedative agents we would be giving (benzodiazepines, barbiturates, potentially ketamine and/or propofol). I deep dive this topic on the ALiEM site: https://www.aliem.com/2013/02/dexmedetomidine-precedex-as-adjunct-for/. Dr. Lewis Nelson and I co-authored a letter to the editor about one of the dexmedetomidine studies that also discusses some of the issues: https://www.ncbi.nlm.nih.gov/pubmed/27139007. If you need an electronic copy, feel free to email me at bryanhayes13@gmail.com. It's not that dex doesn't decrease sympathetic tone, it's more that, by itself, it doesn't treat the underlying pathophysiology of ethanol withdrawal (at least from what we currently understand).
Whit F., M.D. - January 23, 2019 11:52 AM
Okay, but let me ask this. Our source of the problem is in the brain. Where the problem expresses itself is waaaaay downstream, in the cardiovascular system (what really kills people). Why does it matter to stop the crazy vital signs higher up in the brain instead of further downstream (sympathetic output)?
Put another way, isn't the he major problem is GABA receptor downregulation? If so, do benzos actually increase the speed of upregulation of the receptors, or just flog more out of the ones that are left? Would dex allow you to upregulate your GABA receptors more rapidly? Sorry for all the random questions.
Whit F., M.D. - January 23, 2019 11:54 AM
Oh wait. Just read that GABA depletion causes the problem, not receptor downregulation. Never mind.