Dr Lacocque Post ROSC Hypotension (6/22/2021)

You did learn really well during your fellowship. I'm impressed. Okay, so good.

And then Paula Brijesh was there and he did it and he. He did a meta analysis.

Oh God.

Okay.

All right, we're good.

Sorry about the delay.

Okay. All right. Take it away, Angus.

All right, Angus. Okay if I go or you want to want me to wait?

No, go right ahead, Chris.

Okay, Yep, we'll get Jeremy on because that's what I know everybody wants to hear. Not my rantings and ravings. But anyway, I. I'm very pleased to introduce Jeremy Lecoq who thanks to Paul Pepe's approval is. Is now the newest Eagle as he is joining our clan as the medical director of the San Francisco Fire Department. He is a previous EMS fellow. So he was in what Amelia and Vijay are doing now previously and has since gone on to do great things as first the interim and now the full time medical director of the San Francisco Fire Department. He takes over for Clement Yeh, who is transitioning over to full time Department of Emergency Medicine or excuse me, Department of Emergency Management issues. So Jeremy is taking over for what Clement Yeh was doing with San Francisco Fire. He's already made some, some amazing additions to, to the fire department and has. Has made a fantastic transition already. And so is. Is a great new candidate to be a new Eagle. And then also at the same time doing all that had this, had this publication just coming out this week, which Peter picked up on and, and invited him for this. So we're excited to hear about that. A warm welcome to Jeremy to not only Eaglets, this group but, but the full. The full Eagles. And again thanks to Paul Pepe's approval, we're gonna, we're gonna move you into the Eagles group. So welcome Jeremy.

Great.

Thanks so much for the intro.

All right, so we'll jump into the paper. Thanks again for, for having me here today.

So the majority of the. The data diving for this was done while I was an EMS fellow. So part the of, part of our time, in addition to San Francisco, we spent in Alameda county with Carl Spohr. So this research comes from a mix of UCSF and Alameda county.

And the paper is about prehospital post Ross blood pressure and associated neurologic outcome. So it was just published in the American Journal of Emergency Medicine last week. I did the research with Lee Siegel, who's one of the paramedics at the EMIS Agency in Alameda and Carl Spohr, the medical director there. So as some background, as you know, about 350,000 people have out of hospital cardiac arrest every year and about 20, 30% get return of spontaneous circulation. More than half of those unfortunately die in the hospital. There's a lot of attention spent on research and quality improvement around cardiac arrest itself in the pre hospital setting, but not as much around post Ross care. Again especially in the pre hospital setting. A lot of hospitals in the emergency department have various protocols and both side but not as much in the pre hospital setting.

So you know, we were kind of wondering and developing this study, what ways can we maximize the pre hospital post Ross care to maximize favorable patient outcomes? So one potential target is focusing on the blood pressure. Does blood pressure right after Ross correlate with neurologic outcome and does maximizing that blood pressure have any potential? So most research to date focuses on vasopressors and hypotension in the emergency room or in the icu. But very few studies, if any, that we could find focused on hypotension in a pre hospital setting. So it was our intention to look at that. So we wanted to investigate the relationship between hypotension and neurologic outcome in adults with ROSC and out of hospital cardiac arrest. So this is a protocol. In Alameda county they did have a protocol for post ROSC. So in the beginning it's supportive care ABCs, make sure you titrate oxygen, end tidal, CO2, 12, lead glucose and then it goes on to treat not hypotensive so that you just monitor the patient and hypotensive with a normal pulse, you give a fluid challenge and then consider push dose epinephrine. In the beginning of the study, dopamine was the vasopressor of choice and then they switched to push dose epinephrine and then for bradycardia, atropine pacing and then eventually EPI if that doesn't work. So that's the protocol that the medics followed throughout the study.

So in an 18 month span, we looked at 781 patients who had ROSC.

After having CPR done in Alameda County. We looked at the transporting agency data including what drugs they gave and the first and last blood pressure that was recorded. Unfortunately, with the way that the data was mined and kept over the years, we didn't have any blood pressures other than the first one and the last one recorded by the crew. We link that PCR data with the CARES database, which as you know, includes the neurologic outcome recorded as a CPC score. And then we use multivariate regression to Compare the hypotensive patients with the not hypotensive patients and compared it with the neurologic outcome after controlling for several other confounding variables. So this is our chart. About 1800 patients had CPR performed on them in cardiac arrest. So we, you know, that number doesn't include the DOAS and everything. 781 had ROSC. 107 were hypotensive. 674 had a blood pressure systolic above 90. And of the hypotensive group, 61 got vasopressors and 46 did not. And the CARES database, again, we looked at the cerebral performance category, the CPC score, And we said 1 and 2 are a favorable good neurologic outcome. So this is all of our data. The big thing I just want to highlight here is the things we attempt to control for. So we had sex, race. This was kind of the thing we were excited to see. The systolic of hypotensive or not hypotensive vasopressure use and then initial rhythm, bystander cpr, first responder arrival, mechanical CPR not or manual CPR and then airways. So we attempted to control for all those things.

Basically we found after controlling for those things, patients who were hypotensive with a final blood pressure of less than 90 had an increased association with poor neurologic outcome. 23% of patients who were not hypotensive had a good outcome, neurologic outcome, compared to about 10% of hypotensive patients. About twice as many good outcomes with the not hypotensive group.

Of the 11 hypotensive patients that did have a good outcome, five of those got vasopressors, all of which happened to be dopamine and hypotensive patients who were treated with either vasopressor versus those who were hypotensive and not treated with vasopressors had no significant difference. So we found that hypotensive people with vasopressors and hypotensive people without vasopressors had similar outcomes. So vasopressors didn't significantly affect neurologic outcome for hypotensive patients. And we're thinking that's a reflection of the fact that the patient was likely in cardiogenic shock, maybe had a prolonged downtime, which is a poor prognosticator in and of itself. So whether we fix that hypotension or not, the patient still has a poor prognosis A large limitation for us was only having the first and last blood pressure. So there was no dynamic data available. We would have loved to see this is the blood pressure right after ROSC and then we gave fluids and then we gave a vasipressor and this is what happened with blood pressure. But unfortunately we didn't have that dynamic data so we just had the last blood pressure and we assumed that that was the post Ross blood pressure because everyone had ROSC and if they had a blood pressure, you know, it was after, after Ross. So that's how we treated the numbers. So we don't actually know if the vasopress has affected the blood pressure or not. We assume we did, but you know, again we didn't have the data to support that. And 43% of the hypotensive patients didn't get vasopressors. So that could have been for a lot of reasons. It could have been because they got fluid and by the time they finished that fluid their blood pressure was.

Improving or perhaps they got to the emergency room at that point. Obviously there's a lot of work for paramedics to do after a roster is EKGs and blood sugar and driving and packaging the patient and giving the run the ring down. So there's a lot of work to be done. And perhaps they just didn't get to that point of the algorithm or perhaps more importantly, perhaps it was a missed opportunity. Maybe they were hypotensive and for whatever reason they didn't give vasopressors. Perhaps there was a missed opportunity.

Basically we concluded that previous studies looked at hypotension, emergency department and icu, but not many looked at the pre hospital hypotension as a prognosticator. We found that prehospital hypotension was associated with a poor neurologic outcome and there was no significant difference in neuro outcome in hypotensive patients versus those who got vasopressors. So pre hospital vasopressors may not affect neurologic outcome. So we need to study this more with more patients so that we have better data on the hypotensive end and who got vasopressors. And ideally if we were to do this again, we'd have more dynamic data and include more than just blood pressure. Also include end tidal CO2 and pulse oximetry and all the other interesting data points that go with cardiac arrest. So thanks so much for having me. I'm happy to answer any questions.

Jeremy, this is Peter. Thank you. Great presentation.

My question for you is that this reminds me a lot of the EPIC for TBI trial where any episode of hypoxia or. And any episode of hypotension led to significant morbidity and mortality in those patients. And I wonder if the same, you know, physiologic mechanism at play here. I wonder if you have any comments on that.

I'm really sorry, but I got a phone call at the same time, so I missed the first part of your question.

No.

Okay, I'll repeat it. The study that was done out of Phoenix, the EPIC for TBI trial done by Barbro and Dennis Fate. Yeah. They found a significant increase in morbidity mortality with severe TBI when there was either an episode of hypoxia and. Or an episode of hypotension. And when you added in the hypotension, I think it was like a 17 fold worse outcome, if I'm remembering correctly. And I'm wondering if the same physiologic mechanisms are at play here, even though there's no TBI involved.

Yeah, I think the common denominator there is hypotension, is poor cerebral perfusion. If for whatever reason you get poor perfusion in your brain, obviously it's hard to come back from that. Poor perfusion in the brain, poor neurologic outcome. I think that's the common denominator here, as you're highlighting.

Peter, may I make a point? Physiologically speaking, this is something that Peter Safran and I were looking at back in the 70s and 80s, and you're on target about how important this is, that hypotension is a marker for the physiological state. A lot of people think of a CPR state as being this static, you know, thing. You're always the same physiology, but when you go into cardiac arrest, you have vascular tone. Right now, each one of us has blood pressure and our heart's pumping out against some resistance, and it creates the blood pressure that perfuses the coronary arteries over the course of several minutes. The oxygen is not getting out to those vascular, that peripheral vasculature. And so as a result, you kind of get into peripheral vascular relaxation. If your heart now is starting to beat again and it pumps out, it's pumping out against empty pipes, and it doesn't generate it. It just is a marker for being down a long time. CPR and the pressors, the way we give them, by the way, that's another issue is, you know, are ineffective under those circumstances. What we really need to do is restore better flow which we've now started to do with some of the head up cpr, ITD and all those kinds of things we learned about this past weekend. So. And I'm going to tell you that that 15 minutes in, that first 15 minutes after resuscitation is the key thing for the outcomes and sustaining it. And so anyways, this is just really another, you know, great piece of work that actually emphasizes that if you've been down a long time, you're not going to do well. So. Yeah. So thank you so much.

Paul, is there anything you didn't study in the 70s and 80s?

Well.

I didn't know anything about like Lady Gaga and things like that, you know, so I didn't learn those until later on.

Okay, so you didn't, you didn't study droper at all or ketamine in the 70s either, which I. I take offense to.

Yeah, I know exactly right. I don't think they existed yet, did they?

When I was round? No, but anyways, thank you though. But. Oh, the one thing I did study very well was best places to eat in San Francisco. So we can talk later.

Jeremy, I have a question related to Paul's point is do you have any timing of when that those vasopressors were given post rosc?

Even when we had like the time of administration, we didn't know when that was in relation to the time of arrest or time of Ross. The data that we were able to pull out of the charts was limited and it's just based on the way that the EMS agency stores and collects that data for quality improvement. To dig through that data and get what we really wanted again we'd have to look through every PCR individually and obviously there's time limitations to that. So we did not have that dynamic data.

But Peter, I think the time depressor is not as much as important as how long they were done and not getting. And so this is just a marker post resuscitation part started. It just can't be. It's not beating. Yes, it's what beating its wide open pipes as I was saying before. And that's. I think that's what it is. And, and you've seen something in the laboratory now with, with Keith etc. You've seen how with CPR alone, the cerebral perfume low. Okay.

Oh, there you are.

Call coming in and knock me out. So I'm apologizing.

Oh, okay.

I forgot where I look. But I was just saying is that the time out and you can't. And we showed Them. I know we showed the laboratory. You've seen those doing the head up versus active compression, ITD versus all three with the head up together versus just standard cpr. I mean, it's. You don't have very good cerebral perfusion pressure to begin with, going right away. And then it really falls off of the next five minutes. They just really probably don't have a prayer unless you're reperfusing them like. Like carry out there and keeping people alive and waking up before they even get. Get, you know, out of ventricular fibrillation. Right. So.

So speaking of Carrie, Kerry, you want to make a comment?

Welcome, by the way.

Hey, we can't hear you, Kerry. Just so you know, you're muted or something.

Maybe that's purposeful. Who knows? While we're waiting for Kerry to get on, it's 11. Just remember, it's 129. 83 is the CME number for today. 129.83. Okay.

KERRY ON yet?

No.

Anyways, whatever he says it's okay.

He's there and he's unmuted, but we can't hear him, so.

Got it.

That's a bummer. Any other comments or thoughts on this?

No, but thanks for doing the work. This kind of things, we need people to pay attention. And the best thing is be on the streets with them and watch what happens. You'll. You'll totally understand this. It's really cool. And then the other thing we are looking at, I think we discussed at the other meeting was what Jim Roach is doing down here in Florida is with the EPI drips, you know, that kind of thing, to maintain it. So you're not bolstering things. Okay. Alicia's go. Yeah, exactly. Right. That's right. Mean arterial pressure. Right. Is that. Is that. What's. What's the first one Go, Al. What was the top thing? Not sure if I can understand that one. We've been talking.

Type it in the chat. Kerry, if you. If you.

Yeah.

Especially in future studies, which I hope is the case, because that's what we were. That was a really good talk, that.

What's the deal? Oh, head up. That's probably what it is.

Okay.

Maybe that's what it is. So, so.

So, Paul and Jeremy. You know, I also don't want people to leave this talk thinking that we shouldn't be maximizing blood pressure post ROSC either. Right. I mean, that, that. That's not the takeaway here. Anyone want to comment on that?

Yeah.

I mean, my takeaway from this is we know hypotension is bad. This kind of confirmed in the pre hospital setting, which is kind of the newer part of the, you know, the, the data here. And then in terms of vasopressors, I think it's an interesting finding but I wouldn't change my practice based on it. And I think we need more patients and better data to make a more confident decision. But I do think it's interesting that there wasn't a clear benefit. But again, transport times aren't that long in Alameda county. So it's really hard to see the effects of these things.

I'm going to see if I can make an interpretation. What I think Kerry was trying to say is that you like when we do our head up cpr, you can't do it if it's hypotensive, if the map is low. And that's. But the whole point is if you do that per that performance of CPR and, and you know, and the head up and whatever all those things is that eventually really you get much better perfusion and you'll be in a better state the time it happens. So anyways, hopefully he'll straighten this out maybe next week or later on the call. On the next call. So I feel like I felt that's all here. What he had to say.

Didn'T that come out during the meeting that, that you shouldn't go into the heads up position until you had a map of 70 that came out?

Yeah, yeah, yeah. But what I'm saying is concentrate in before you get Ross. Concentrate on doing a better flow and you'll be better off once you get them back, that kind of thing. And then. Yeah, if you have a good map to take, you don't. That's a problem.

Is Keith, is Keith recommending.

You know, not, not to go? Hey, I mean obviously you guys are going heads up prior to rosc. Right, right, right. So how does that impact brain flow?

Well, the thing is like the cases we had last week for example, Even here in CFloor with Kerry is these guys are waking up before they even get Ross back. I mean they're, or at least coming around. And that's, that's, that's, that's the advantage. That's the whole thing is that this is a whole new dynamic. In the past we just had basic cpr. Even with mechanical cpr, it just wasn't as good as increasing flow and getting oxygen out to those peripheral vascular sites, that's all.

Yeah, it sure seems like there's two pieces to it. There's the initial brain injury which, whether it's traumatic or from the cardiac arrest. But then there's an injured brain. Really does not like hypoperfusion in the post ROSC phase.

Yeah, yeah, yeah, absolutely. But I'm not sure if it's. That's more of a marker than it is a, you know, a determinant of the outcome. That's all. Yeah.

Hey Peter, I'm gonna put a poll in the, in the FAEM SMD right now about what what post Ross vasopressor people are using in their protocols. I thought it was interesting that he was using dopamine. We can't even get dopamine here anymore.

Been on levophed for a while.

So I'm curious between epi, levophed and dopamine, what people are using. I'm gonna put that poll up right now.

Yeah, that's awesome. I think Jeremy said youyou said that you switched over to push pressor, right?

Yeah, they switched from dopamine to push dose epinephrine about halfway through.

But I thought I heard you say that everybody in the group got dopamine.

Everyone that was hypotensive, that got a vasopressor, that had a good outcome happened to get dopamine.

Oh, that's very interesting.

Okay.

Yeah, that was an interesting sick. I mean the question is that a signal or just. Or just random, right?

Yeah, I mean it was only 11 people, so again, the number isn't very high, but it definitely was interesting. You know, we noticed the number of people that got pushed dose epinephrine, even though it was an option for a long period of time, wasn't very high. And so it's hard to know. Like maybe there wasn't a lot of opportunity, maybe that was just less familiar. People were afraid to use it. It was harder to mix, you know, who knows?

The last question I had is, do you know how many doses? Is there an average?

The great work on the Twitter stuff.

That'S just copy and paste.

That's all right, Jeremy.

Sorry, there's some overlapping audio, so I didn't hear the end of your question.

I was just wondering, in the folks who ended up getting rosc, did you have the number of doses of EPI that they received versus those who didn't get rosc? In other words, just the quantity of epinephrine administered is also something that a lot of people are grappling with in the pre hospital region.

Yeah. It makes me think of the paramedic 2 trial, which I mentioned briefly in my Paper, I think. I believe we do have the data is to how many doses of resuscitation dose epinephrine they got, but it's not something we. We dug into.

Okay, got it. All right, well, it's 1128. I think it's good time for us to thank you. And Chris.

You want to make any last comments on Droperidol, because you have a captive audience while you're here.

Hey, before you go over, Chris, I got Peter, I got to get off and I was getting the other call, but is Ken on the call today? Do you know where he is? Is he available?

I don't know. I'm traveling today, so I don't see Ken.

I don't see Ken on the call here.

Well, I think he's out of town.

I think so, too. Okay, I'll see you over there on the other end. Okay, take care. Bye. Bye. Thank you. Great job, Jeremy. Welcome to the club.

Leave it to you, buddy. See you later.

All right, thanks.

Thanks.

No, thanks, everybody. Jeremy, awesome job. And I don't know, do you have the link to the next the meeting, Jeremy?

I do not.

All right, I'll send it to you and.

We'Ll get you on to introduce you to Eagles. So anyway, awesome job. Thank you for doing that and thanks everybody for having all of us on.

All right, thanks.

Chris coming on and we appreciate Angus. Thank you so much. And Angus, you're going to take everyone over to the Eagles, I presume?