Cite this post as:
Scott Weingart, MD FCCM. EMCrit 201 – Deeper on Vasopressors and Athos 3 with Mink Chawla. EMCrit Blog. Published on June 12, 2017. Accessed on June 5th 2023. Available at [https://emcrit.org/emcrit/deeper-vasopressors-athos-3/ ].
Dr. Scott Weingart, Course Director, reports no relevant financial relationships with ineligible companies.
This episode’s speaker(s), (listed above), report no relevant financial relationships with ineligible companies.
Original Release: June 12, 2017
Date of Most Recent Review: Jan 1, 2022
Termination Date: Jan 1, 2025
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Hi Scott. of course i was a smidge skeptical listening to the CMO of the drug company that makes the med tell us about the med, but 1. i knew you would never have invited him unless you felt there was something worth considering, listening to, and 2. having listened, it was terribly thrilling to think we have a third arrow in our armamentarium.. a third pathway to consider to treat distributive shock, septic shock, perhaps. and third , how can i not listen to a NJ boy raised on philly cheesesteaks. he is a good, clear speaker, and as… Read more »
I believe it was his initial work on Angio II that led to the position.
This represents a potentially very exciting new receptor group to hit. Will need to keep an eye on this evidence but looks very cool.
Having listened to this, I don’t share Dr Chawla’s view on adrenaline (epi). Adrenaline has helped/saved my patients on many more occasions than it’s harmed them. Particularly, that sub-set who seem exquisitely sensitive to adrenaline as opposed to noradrenaline. This is merely my clinical experience.
Enjoyed this podcast
I too love epi, but for me it is an inotrope. But that could also be that I lack good options from other classes than beta. Milrinone essentially winds up on the same path. I wonder where epi fits in folks that have access to levosimendan.
1.What would you opt for a post cpr patient.Should we give epi infusion because this was used during cpr also or we going to use it again if cardiac arrest occurs again.
2.epi + levosimendan,why advocate this in sepsis(how leopard trial findings fit here)
I am going to listen to the Podcast in a few hours on my way home. I like them a lot, I am of course a big fan. But till then… 1. I am happy to see that the search for the ideal vasopressor goes on and on…I wonder how much it is going to cost, if we are going to actually have it here in Germany and what the future studies will show. 2. I am sure it will gain more popularity than vitC-B-Hydrocortisone Cocktail from Marik. When I tried to implement that “Cocktail” here where I work, everybody… Read more »
Pod cast on Angotensin 2 very interesting but with limited current role, very narrow marketing niche. Hence his interest in finding new applications. Hope he can do that, Otherwise my main take home point is to react immediately to low MAP. Anyone have experience with calcium bolus for low MAP? I learned this on the cardiac surgery ward and it works!
we have a bunch of patients who are maxing out on multiple vasopressors, if that is the only niche, still feel it would fill a valuable role.
i too was indoctrinated into the ways of calcium bolus and drip in the CTICU. I find in many patients the effect is brief–have you had lasting effects?
I was taught that calcium is the inotrope par excellence. Other inotropes act via their effect on intracellular calcium flux. Intravenous administration of calcium chloride will stimulate myocardial contractility and raise the BP no matter what the cause of hypotension. I use it not in a drip but a bolus and its effects last about 10 to 15 minutes. Use in in near arrest situations while searching for a cause.
I wonder when, in relation to the Marik study, this was recorded. I’d be interested in Dr. Chawla’s take on the relationship of Vit C and steroids. I have a feeling we will be repeating ADRENAL here in a few years to sort that out. If VitC+Steroids ultimately proves fruitful, what will be the role for ATII?
even if metabolic therapy pans out, surely there will still be reisstant hypotension on mult. pressors, no?
Perhaps a relatively simple question here. How are they identifying these “hyper-responders” with relative Angiotensin II deficits?
Fantastic work as always!
tiny dose makes huge change in map
I guess it’s like anything else in medicine….we are discovering phenotypes that have different responses to drugs/metabolites (e.g. codiene, coriander lol).
Really enjoyed this talk. Dr Chawla is very articulate and clear. I’m glad he is proud of his research but doesn’t overstate the use of ATII til he’s got the data to back it up.
I really enjoyed this episode. As a nurse, I’m a huge stickler for titrating drips to a MAP 65 and that there should be more of a sense of urgency when that MAP drops and not wait to react. There should be quick interventions for adequate perfusion.
Unfortunately I have come across many cases where I would be maxed out on both my vasopressin and norepinephrine drips and I can barely get to a MAP of 60. So I’m finding this discussion on Angiotension promising for another agent to add to distributive shock therapy.
Hi Scott This was a very enjoyable listen, thank you. I do though have some concerns regarding some of the comments regarding permissive hypotension. It was alluded to that the rationale for employing controlled/permissive hypotension was based on surgical need to decrease the amount of bleeding and that it lead to morbidity. We know that hypotension leads to worsening acidosis, impaired renal function and increasing lactate, but we also know (since Cotton/Bickell et al in late 90s) that being hosed with crystalloid and chasing normotension leads to increased mortality. I have rarely seen a subject cause more confusion and it… Read more »
I don’t think we are speaking about the same thing. I believe I made clear what Dutton’s concept of permissive hypotension was, but based on your comments I still may not have been clear enough. I believe you are lumping the just leave them under-resuscitated with high flow/low pressure normotensive strategy. May be worth listening to my original interview with Dutton on this topic.
Hi Scott, can I ask you about reference on the photo?
Im writing an essay on ras and I cant find a reference on that photo anywhere.. 🙁
Great episode. Came here thru SIR RFS, this podcast is part of the “CC curriculum.” Keep up the good work!
One of the discussions had occasionally in the Medical ICU where I work involves using MAP when the patient has a very wide pulse pressure. Some of my colleagues will use SBP to titrate whatever vasopressor we are using and I disagree with this when the MAP is below 65. If a patient has an arterial line which is functioning well and has a normal square waveform but a very wide pulse pressure do you still use a MAP goal? Is there any evidence supporting either approach?
makes no sense. map is the only value that retains accuracy in those circumstances