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Induction Doses in Shock

Rob Orman, MD and Bryan Hayes, PharmD, DABAT
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06:05
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Nurses Edition Commentary

Lisa Chavez, RN and Kathy Garvin, RN
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02:18

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EM:RAP 2017 January Written Summary 926 KB - PDF

In the shock patient, paralytic and induction meds don’t always behave how we want them to.

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Sam G., MD -

Hey guys,
Great convo on a super important topic. Wanted to touch base specifically on the dose of Etomidate in shock. There is some evidence that Etomidate doesn't really 'play by the same rules' as the rest of the sedatives in terms of dose alteration (reduction) to achieve comparable brain levels. Not sure what all data is out there, but check out this reference: http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1942673
-SG

Rob O -

Thanks for that Sam. Strange that etomidate seems to behave in a opposite fashion compared to propofol, fentanyl, etc. We will make this part of our pharmacology rounds and continue the discussion on the show.

Bryan H. -

Sam, thanks for your comments and for including the citation. There isn’t a lot of data to guide dosing with specific agents in shock states. I appreciate the editorial view from Dr. Shafer, though I still think using full-dose induction agents, including etomidate, can be dangerous for critically ill shock patients needing intubation. There are a few major issues with this 2004 paper that, in my opinion, significantly limit any application to clinical practice. First, hemorrhagic shock is very different pathophysiologically from septic shock. Second, this is an author trying to present his work in a non-peer-reviewed (or, at least, very limited) fashion by submitting it as an editorial. Third, what the author presents is not human, or even animal, data. It is a series of simulations based on the pharmacokinetics derived from a separate set of papers. Fourth, it is not specific to intubation, which is the discussion we had on this episode. These were laboratory animal models suffering severe hemorrhage who were given various sedatives/analgesics. The second-to-second changes in an actual patient with shock in the peri-intubation period cannot be extrapolated from these models. While the data surely demonstrate propofol to be the worst offender with regard to negative hemodynamics response, I don’t think this exonerates etomidate. To me, it just affirms that etomidate may be one of the agents that has less potential to cause significant BP drops compared to others.

Sam G., MD -

Hi Bryan,
Thanks so much for the thoughtful response! We are totally in agreement that this paper represents nothing close to robust data. It is interesting, however, and makes one think... perhaps the pharmacokinetics of sedatives in profound shock are not necessarily universal across medications and may be more complex than we think. I think the major driving force behind reducing/preventing per-intubation arrest in shock is largely the result of simply widespread awareness of the phenomenon. As discussed, Ketamine & Etomidate will both have little direct drug effect on hemodynamics but the resulting sympatholytic insult is a problem. I have no idea where that dose range is for Etomidate. For that reason (amongst others) I generally try to avoid Etomidate in shock states. If what this paper suggests turns about to be true however, I would hate for people to be giving say 10mg of Etomidate (instead of 30mg) thinking they are providing comparable levels of sedation.

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