SCCM Resource Library-Year in Review: Emergency Medicine and Prehospital Care

Video Transcription

Well, I want to welcome everyone out. We are at the 4 o'clock hour for EM year in review. And we're excited to have somewhat of a crowd here. We figured Mickey Mouse and Minnie  might win as we ended the end of conference here, and Disney took over all of your interests. I'm excited to introduce our panel. I think our first slide deck will come up here.  This is our annual year in review. I had a nice conversation with one of our section mentors, Joe, who pointed out to me historically, EM has only had a year in review.  And this year, we actually had some roundtables that we sponsored. We had a session where they had a debate about palliative care. And so we've had a lot of different opportunities  for EM to shine and to talk a little bit about things we've done. This is kind of our landmark session that we do every year that we talk about pre-hospital care,  we talk about ED-based ICU care, and then how EM care is influencing upstairs care. So excited to have you all join us. Our panel of speakers, amazing guys.  We're very lucky to have all three of them here. I've heard all of them speak in the past. Probably the most energetic panel I've ever put together.  And so I'm excited to have them with us. If Keith ends up standing on the table doing his Rotem tag component, you'll understand that that's just  a normal thing he does when he does public speaking. He actually reminded me that his suit went all the way to Patagonia and back with him. He hasn't even been home.  He came right here to you guys to talk. So we're going to start off with our pre-hospital care talk. Dr. Amjad Musleh will talk about that. He's one of our faculty members at WashU.  There's only a small handful of folks in the country that have done EM critical care and EMS pre-hospital care. He's dual boarded in both of those.  And that's kind of a unique background. And hopefully, we'll bring a unique perspective on some of the things we can do prior to them getting to the ED setting.  We'll then transition over to what we consider time zero or ICU care downstairs in the ED. Dr. Keith Azevedo, currently assistant professor  at University of New Mexico, will take over there. And then finally, we'll end on a high note with Rod. Dr. Fontenette, who is an Air Force member out of UC Davis,  is going to talk a little bit about how EM care is influencing upstairs ICU care. He's going to be at WashU myself. And I'll be the moderator for the session today.  Disclaimers, I just want to make sure that we talk about Rod's. He was quick to tell me that while he is a US Air Force member, none of these comments reflect Uncle Sam, Donald  Trump, or anything about the government. So these are all just his thoughts right now that we'll be hearing. And the rest of us had no other disclosures to give out.  And then finally, I just want to let you know, the format will be all three speakers will go. Each of them will talk for about 13 to 14 minutes.  And then we'll take questions at the end as a panel session and hopefully provide some of that teaching points that you can take back to your own shops.  So without further ado, I'm going to hand it over and let Amjad start us off.  Hi, good afternoon, everyone. I know this is like 4 PM. You guys just ate. Everyone's a little sleepy and wants to go home.  So we're going to try to make it really, really lighthearted and easy to go.  And we're not going to beat you to death with stats. So without further ado, who is this? Disclosures, no financial. That's not the slide deck.  I think you got the one from last session. Well, we are covering Crash 3. So how about that? You're not going to saddle up Cowboys. No, I was like, yeah.  So I'll just start off just to get time going anyway. But we're going to talk about Crash 3, the first one for us. I'm going to kind of say, hey, not a bad idea  to have some TXA in your truck. And we're going to talk about Pamper and Combat, the post-hoc analysis of that. And we're going to end it off with a fun little Adenosine thing.  So here's some stuff to start off with. So everyone calls these paramedics ambulance drivers and they're amazing people. They get paid $17 an hour.  And at max, probably sometimes they get $22 an hour if they're critical care transport. But they do amazing work and don't get recognized for intubating grandma  on the back of a bathtub in a trailer park. So without further ado, this is kind of the three slides we talked about here. We're going to talk about Crash 3, TXA for TBI.  We're going to talk about pre-hospital plasma and then single syringe Adenosine, which I learned off the MCRIT website, but there was a nice little publication that just came out.  All of these came in in the last half of the year of 2019. The first one was Crash 3. So I like the little stylized logo that they have for it. And the question that they asked,  does TXA administration in under three hours  from TBI really reduce in-hospital mortality at 28 days? So that's what they were looking at.  TXA for the ER docs, we use this stuff like WD-40. We use it like duct tape. We use it on everything. If you have trauma, we use TXA.  If you got a nosebleed, we'll put some TXA in there. If you got postpartum hemorrhage, we put some TXA. Gums the other day, we put a TE in someone and they were bleeding.  We threw some TXA down there. I mean, one time we even nebulized TXA for DAH. So we'll use it for everything. TXA is awesome stuff.  And I see some nods back there of people doing the same. So I like a lot of infomercials because they're always talking about, this starts off with a random premise  of a guy doing something like sawing a boat in half or something like that. And they're always with the same premise. Like, what are you doing? Saving money is always the premise.  So here's the Flex Seal guy. That's my new favorite product. And the only reason I have this is we'll pop up and talk about how this stuff is like Flex Seal.  So it was invented or discovered by Utako Okamoto. I hope I'm saying it right. So she discovered this back in the 50s and published it in 62. She recently died.  She actually got to see Crash 2. So she recently died in 2016. And the reason she used to be, she went to dental school, hated it.  Then she decided to be a doctor in Japan post-World War II and people were not nice to women back then. So wasn't able to get a lot of research done.  And she was working on cerebellums. Her and her husband decided there wasn't enough cerebellums in the 50s to go around. So they were like, what do we have a lot of? Blood.  So they started drawing their own blood. And if they ran out, they drew out more blood and did research on blood. And they discovered Amicar first,  which was about seven times more potent than lysine to binding to the plasminogen, which we'll talk about. And then TXA, which is a whole bunch more potent.  And she wanted to promote it for postpartum hemorrhage, but didn't see the fruition of it till the later, like our century, I guess. So how does it work? TPA is floating around.  So I'm not gonna bore you with the big old clotting cascade. This is the backend of the fibrinolysis pathway. So you got TPAs floating around and you got plasminogen.  They bind together right here. And once they bind together, they break down fibrin.  It's just a competitive inhibitor. So that's why we do the whole one gram load and then we give you another gram over eight hours. It's just a competitive inhibitor  and it stops it from binding to the lysine binding site.  So what did the London School of Hygiene guys come up with? They built a massive network. They designed a pragmatic study with 175 hospitals in 29 countries.  Pragmatic studies are like a little rough around the edges, the real world studies. They did a double blind RCT and they ran it from July, 2012 to January, 2019.  They included a bunch of people. So if you're GCS, you had to have a brain injury. So it took a bat to the head or someone kicked you off some stairs  or definitely one of these things. And you had to have a GCS less than 12 or you had head CT signs of injury. So that's how you got randomized in.  There shouldn't be a knife sticking at you. So no major external bleeding. And you weren't sure if TXA was good for the patient or not. So those were the things that they looked at.  They wanted to randomize people initially when they started the study, they said we need 10,000 patients at the beginning to find a statistically significant answer.  And they realized later on, they were doing it within eight hours for randomization. Halfway through the study, they're like, no, the effects really die off at that point.  So they changed the outcome to within three hours. So you had to be randomized within three hours. No one got excluded. They were a very inclusive group.  So there was like no exclusion criteria listed on their study. And the intervention was basically, did you get TXA or did you get saline?  They randomized a pretty cool randomization. They had these like a box of eight of these and they were in envelopes. They looked the same. They didn't say placebo on them.  And you took the lowest number of a packet. You took it out and then you gave it to the patient and no one knew what you got until they got unblinded.  They had 4,600 patients analyzed in the TXA group within three hours. So that's the red. And then 4,500 analyzed in the other group  within the red, the placebo group. And this is a lot of busy slides. So you can just trust me. The groups are well, well matched, okay? Yeah, I don't have to go through these.  But one interesting thing is, remember I said GCS of 12? You see 13s, 14s, 15s here? Those must have been the patients that had CT injuries.  So that's why you have 13, 14, 15s right there. They had CT signs of injury and they got included.  This is where the big kicker busy slide is. So they basically, the results were not significant statistically. So they did a little bit of analysis of the groups.  I'm gonna break it down here how they did it. You had severe injuries and you had mild injuries. So GCS of nine to 15, GCS of three to eight.  These guys, the ones that were gorked basically did not do good. Didn't do well. It crosses midline here and there was no risk reduction or anything.  But if your GCS was mild, like nine to 15, you did okay.  There was some risk reduction right there. Or if your pupils were blown, you had a blown pupil, you probably didn't do good. And then if both of your pupils were reacting,  you did well. So that was their hypothesis there. And then really the actual risk reductions overall, 855 out of 4,613. So 18.5% and then 19.8% for the placebo side.  So TXA is in this side, placebo on this side. So if you had a mild injury, you did okay. If your pupils were reacting, you did okay with this. You did a little bit better.  And the reason I'm saying this is a EMS trial is you can do this in the truck. It's really easy. And there's a bunch of EMS agencies already doing this.  Here's what they also looked. Again, severe GCS, the guys under eight, eight and under. It didn't matter when you gave it to them. This was time. And this is the effect of error.  So nothing, didn't really matter. But the earlier you did it in the milder group, the better the patients did for mortality error. So just in case you thought, this is Billy Mays,  my favorite guy. He passed away from an MI. And this is why we're gonna talk about vascular, because everyone's wondering, do you get PEs from TXA? It's a antifibrinolytic.  Do you get heart attacks? Do you get strokes and everything? So if you look at the data, I'm just gonna look at it right now. There was 24 PEs on this side, on the TXA side,  32 PEs on the placebo side. Not really statistically significant. There was no difference between them. And it's all across the board. So MI, strokes, DVTs.  I don't know why they included renal failure and sepsis and seizure. Seizure is known because that one is actually, TXA can cause lower the seizure threshold, and that's in there.  But really, not very much harm came out of TXA. So if not only, it might, so I'm gonna give it a little seal of approval here. This stuff, if my family member had a TBI,  and they were early on in the TBI process, and they were in the back of a truck, and they had a mild TBI, I'd say go ahead and give them the TXA.  Not saying like it's a life game changer, but it's good to think about. It's a little cherry on top of your resuscitation. Now, my daughter wanted her picture in the slide,  and we're gonna talk about COMBAT and PAMPER trials. So you can look cool in PAMPERS. She got her picture in here. This is a post hoc analysis, it was a planned post hoc analysis.  So COMBAT and PAMPER were two RCTs basically. They weren't blinded RCTs, but two RCTs that wanted to see pre-hospital plasma. Now, the military's been doing plasma  as soon as possible for a while. Most EMS agencies aren't doing plasma as soon as possible. So we know there's a survival benefit with plasma.  We wanted to see in the urban setting here in the US. COMBAT was a negative study. They were from the Denver group. They had about 125 patients, and there wasn't that much,  there was actually no benefit to the pre-hospital plasma. Now, this is in Denver. You have a bunch of hospitals, trauma centers, and rapid transport times.  PAMPER was a little different. This is my old helicopter I used to fly on with lifeguard at University of New Mexico. And we had just red blood cells.  PAMPER wanted to add not just red blood cells, they wanted to give you FFP. Now, before we jump into why, they found a positive trial. So here's a little bit difference  people postulated about it, but there was gonna be a post hoc analysis that was pre-planned. They actually made the data sets very harmonized before the studies.  So with PAMPER, there was an older population. You had about 40, the patients were in their 40s, and at COMBAT, they were in their 30s. You had more saline in the PAMPER trial.  You had more blunt injury in the PAMPER trial. And you had, yeah, those are the main kind of differences.  And you had longer transport times in the PAMPER trial. So this is just the slides that they came up. Basically, they decided to look at a post hoc analysis, combine the data.  So they had 125 from COMBAT, and 501 patients from PAMPER, and they put them together. So you got 626 patients. You shove them together and you look at them,  and we're gonna separate them out in a group. So they just looked at general, all comers, plasma versus standard care. So standard care saline.  The guys that got plasma had a, they did better. Basically, 20% of the patients died in the plasma group, and 28% of the patients died in the standard saline group.  And these were well-matched patients, and the p-value was 0.02. So that's an 8% reduction. That's a huge, that's a big deal. Here's what they looked at, though.  When you looked at less than 20 minute transport times, that effect went away. Standard care was better, actually. Like, you just give them some saline, rock and roll.  Go as fast as you can.  If you look at greater than 20 minute transport times, yeah, the delay in getting plasma onto patients causes higher INRs, more issues later on.  So here's, before we jump all over this, I wanna talk about kinda like how to do this stuff. So it's really cool to talk about plasma being thawed and everything,  but the problem with plasma is, once you thaw it, you got five days. You have five days to use it. Imagine your blood bank guys, every time you throw out a bag of plasma.  They will murder you. They're just like, they don't like that stuff. Our hospital, Barnes-Jewish Hospital, we're massive, we give out blood like it's candy,  but we don't have, basically, we have FFP. There's other kinds of plasma. So let's just go through a little bit about the plasma. The first thing, just remember,  AB positive is your universal donor. All the antibodies are sitting in the plasma when you centrifuge it off. So AB positive is your universal donor.  A lot of MTP protocols use A positive male donors. So a lot of hospitals will have the A positive male donors because most of us, A positive males,  we're the majority of the population. AB is hard to come by. And most of us have low titers to B. We haven't been exposed to B unless you got a transfusion before.  So FFP lasts five days once you melt it. Okay, we've melted it, now we have five days. There's something called never frozen plasma,  which a lot of blood banks are not equipped to do already, but it's easy to go towards. Never frozen plasma is just like whole blood. They just take the plasma off whole blood.  Whole blood lasts 21 days. This has five extra days on top of that. So it lasts 26 days. This is something to consider before you jump into putting plasma on your trucks.  The other way that you can do it is our Air Force, our military guys have been doing this. And this was before World War II, we had freeze dried plasma.  Freeze dried plasma has really long shelf life and easy to set up and easy to administer. And they're using that. Only the French have it and the military guys have it,  got it approved by the FDA, but we don't have that here. So our options right now in the US, if you wanna put something that lasts longer on the truck,  you gotta use never frozen plasma. And if you already know how to use red blood cells, you can use never frozen plasma. So that was that.  I'm gonna give this one a begrudging approval. So not the full approval, because we're not ready for that unless your facility already does that. Cincinnati has that.  A lot of places do not have never frozen plasma. The problem you're like, why isn't everyone using never frozen plasma? Well, there's lymphocytes in the never frozen plasma.  When you freeze that off, it kills those off. There's other problems with never frozen plasma, but it's a good thing to think about. So last one, this is single syringe adenosine.  I learned this off of Scott Weingart's website back in 2015. I was excited when someone published a little trial. It's a very small trial. So they had 26 patients in one arm,  27 patients in another arm, but it's something that I've been doing and I tell my medics to do. And a lot of people don't have that in their protocols or know how to do it.  So first off, when you have SVT, you do the old school method. You lie to the patient and you say, you can blow this plunger out. You sit there, they blow for a little bit,  or you can mash on their carotid and launch a clot up into their brain. So those are your two options. The modified method right here is basically you have them blow in that syringe  and then you throw them head down and lift their legs up. And you hope it stops SVT. A lot of times it doesn't work, but sometimes it does. Your next step is just like a computer,  turn it on and off. The amount of faith that we have in cardiac physiology to sit there and give this stuff and turn off the heart and just watch it,  and everyone's watching the monitor and just watching the monitor and watching the monitor and then like, yes, it's actually worked. And you're just waiting there  wanting to see if the heart started. Well, the way to do it, the old school method was to have this complicated contraption. You got two or the three-way stopcock  and you're injecting one side and pushing the other side. And then I went and saw this on the MCRIP website was just fill this stuff up in one syringe.  Look at how complicated this side looks. We're gonna go ahead and it comes in three milligrams a mil. So let's say you're just doing 12 milligrams. That's gonna be four mils.  Pull it up into a 20 cc syringe, fill it up with water or saline and flush the whole thing.  Much, much simpler. And this is what their pilot study showed. Basically, they had 26 patients in the single syringe side, 27 patients in the two syringe method.  And they had the success rate of 73.1% for the first dose on the single syringe, 40.7% on the two syringe. It's just showing that it actually works.  And then 100% with up to three doses. So this one gets a Chuck Norris stamp of approval. Thank you guys. And then just to show you guys my family one more time,  this is a summary slide. TXA is safe, may help patients. Go ahead, think about it, putting it on your trucks. It could be the cherry on top. We should start making freeze-dried  or never-frozen plasma available to pre-hospital with long transport times. And then try the single syringe method. And my baby still does not look like an alien here.  He actually grew up and got a little cuter. So, thank you.  All right. You guys hear me okay? I promise not to stand at a table. I do have a mean backspin if you guys want to see that after. But I promise not to stand at a table. All right.  So my name is Keith Azevedo. I'm an intensivist at the University of New Mexico Hospital. I was asked to talk about time zero, essentially,  when folks come from the pre-hospital setting into the ED before they go up to the ICU. No, only conflicts. I suppose I'm a minor author in the first study.  Unfortunately, no financial disclosures, I'll give you guys. So I was asked to talk about, as you guys know, kind of pick three studies of 2019 that represent kind of time zero.  I was like, oh my gosh, yikes. There's so many studies to choose from. I don't know.  Yeah, there's a ton out there. I tried to choose two that were somewhat novel, maybe you hadn't heard about from other venues that you've been at here, and then one a little bit  more mainstream. Chose TE in the ED, eCPR, and TTM. I think to talk about three studies, all of us are like, oh my gosh, you're talking about three studies  in 15 minutes is super hard. So we're going to try to somewhat do it justice. But I'm going to also, like Amjad, try not to beat you to death with the statistics  or any of that stuff, or beat myself to death, I suppose. So TE and ED. First study here, single center study done by Dr. Ray at the University of New Mexico.  This study, what do we know so far about TE in the ED setting as well as the ICU setting? I think as most of, unfortunately, I had a bit of a participation slide  where I was psyched to hear about how much TE maybe you guys do, but they don't have internet. But at our place, we do a fair amount of TE, both in the ICUs and the ED.  I think what we do know so far is that in the hands of intensivists, there are pretty decent studies to say there are decision making parts that occur that it's somewhat helpful.  I think certainly in the ED, especially in the context of resuscitations, there is evidence to say that there are decisions being made  as well in the emergency department by emergency medicine folks that hopefully change management. What is a bit less known certainly  is the safety of TE, especially among folks in the ICU. What's even less known on top of that is the safety of TE in folks that are coagulopathic or high risk for bleeding.  I think for most of the folks we take care of,  that person that comes in, maybe they're arrested, maybe they have ROSC, but they're still, their hemodynamics are really poor, super undifferentiated.  You want a bit more information. They either have some type of trauma in their chest, not good windows on surface TTE, and you want to get a better look.  These folks inevitably, I think, that are critically ill tend to have some type of bleeding risk or some type of coagulopathy with these critically ill folks.  That's the real question is, is it safe among these folks? Is the risk benefit kind of pushed towards a benefit in these folks getting a little more information?  And that's what the question of the study looked at. Basically, they looked at, is it safe when performed by both intensivists and emergency physicians?  They were both intensivists and emergency physicians and just emergency physicians as well, and critically ill folks at high risk for bleeding. So what did they do here?  They looked at 228 exams. Out of that, 80 of these 288 were in a high risk bleeding group, kind of dumbed into that group. The second was 148 folks. They were in this low risk.  How did they define high risk? Anyone that was getting any type of anticoagulation, therapeutic anticoagulation, fibrinogen less than 150, INR elevated, low platelets less than 50.  Anyone, you just had a single one of these events, you were lumped into that kind of high risk bleeding group. So what did they come up with? Eight out of the entire group of 288,  that's both low risk and high risk. There were eight folks that potentially had complications related to TEE. Turns out that essentially, they were not  different between groups, four in the high risk bleeding group, four in the low risk. And the major complication was upper esophageal bleeding.  No deaths in either one of those groups. So what do the authors conclude? TEE can be safely performed in intensivists and by emergency physicians and critically ill folks  at high risk for bleeding. I think my takeaway for this, and I tried to hopefully include in each one of these at the end of each one of the studies, kind of a big picture  of my takeaway, I think if you have someone that comes in, once again, that is somewhat critically ill, maybe has, you get some labs back,  or by the time they're about to go upstairs, you find out they have low platelets or whatever the case may be that they're at high risk for bleeding.  I think if you need that information that a TEE will provide, I think you have some evidence here. This is the first study, as far as I know, that's looked at safety in these folks.  And I think you're somewhat safe to say you can go ahead with that. All right, second, eCPR, there's a talk going on by my boss here down the road  that I'm getting yelled at not being there. This looks, we do quite a, not a huge amount, but a decent amount of eCPR at my group and in our hospital.  One of the things we always talk about after a case is did we choose the right patient, are we doing the right thing, and so forth.  So 2019, of course, all these studies, as you know, 2019, it's a systematic literature review, meta-analysis, looking at the effectiveness.  Basically, it's going to be the superiority of eCPR. Remember, eCPR, I know you all know this, but just using VA ECMO versus conventional CPR and cardiac arrest, folks.  So what do we know? Survival's not great, right, in codes. And even worse than that is the neurological intact survival certainly is not great as well, right?  So the question this group asked with this systematic review and meta-analysis is, is there any superiority in terms of survival and neurological outcome in eCPR over cCPR?  And then kind of as a, in folks, of course, that are cardiac arrest, post-cardiac arrest from cardiac origin, and as a secondary analysis to look at, they said, you know what,  are there any parameters there that kind of predict survival in folks that received eCPR? Which is that question, I think, that for folks that do,  are there folks out there that are doing quite a bit of eCPR in their group? I'm not going to torch you guys with the raise of hands, but awesome, yeah.  So it sounds like there's quite a few folks out there that are doing that. So I think, I'm assuming, like your, all your folks' group,  as in our group, we always have that question over and over, you know, we're choosing the right folks, what are we doing? So what were the outcomes here?  Primary outcomes, survival to hospital discharge, as we talked about. Remember, survival to hospital discharge at 30 days of eCPR versus CPR.  Secondary outcomes, neurological function in survivors. And then that secondary analysis we talked about. Looked at key features that could be predictive of survival  in folks that have had eCPR. I think traditionally, you know, we think about these things that could potentially be parameters, like no flow.  That's that time from when the arrest occurs to when that patient receives CPR where there's no flow. That low flow being that time that they're receiving,  oh yeah, do I need to, am I okay? That low flow being that time in which they've received CPR. As you guys, folks all know, that chest compressions,  we think that cardiac output that's being augmented with chest compressions, somewhere around 20 to 30%, right? In the whole impetus initially behind this eCPR as well,  you know what, if we can augment more than 30% of that cardiac output by doing eCPR, by doing VA ECMO, maybe that ischemic reperfusion injury that we're having  that causes multi-organ failure and neurological damage potentially could be augmented. We can get some return from that. So that's the intent of that.  Of course, they looked at the initial rhythms and some bystander CPR. I hate to include inclusion and exclusion. The only important thing is the reason why I put a super quick  slide on here is to show that basically they looked at a bunch of studies. We'll look, but it's basically 118 studies. And they tried to look at folks that were on,  that received eCPR in comparison to eCPR and cCPR as well as folks that went on eCPR in any parameters that predicted survival. So those are really the two big things, all right?  118 studies, nine included. Eight of those observational, retrospective observational, one prospective in nature. Many, many, you know, lots of randomized,  no randomized control trials, right? And this is the other reason why I wanted to include this to hopefully get folks excited. We talk about it, of course, a ton in our shop,  but folks that are doing eCPR in their shop to, you know, if we can to put out as much data as we can for this because there's a paucity clearly of that data.  What were these folks finding in looking at these nine studies? They found that eCPR demonstrated improved survival and a better neurological outcome over cCPR.  Evidence super poor, right? Not great evidence for this, for that minor signal they could find. This is what they found. Interestingly enough, characteristics  that they found associated with improved survival in these folks that received eCPR, initial shockable rhythm, which is not terribly surprising in there,  and that shorter low flow time supporting that idea that hopefully, you know, if we can find the right patient that augmented cardiac output potentially is something we can  improve on there. All right. Conclusions for these folks. eCPR, sophisticated treatment option, certainly may improve cardiac output in selected patient populations.  And I think that's the key over and over and over again that all of us see is, you know, what the heck is that selective patient population?  We need to dial that in quite a bit more and kind of figure out what that is. And, you know, no surprise, their conclusion, further comparative research is needed to clarify.  Great. My takeaway for this, I think eCPR, like any advanced therapy, I think a lot of us work in centers that we have many, many options for things we can do to folks, right?  And trying to figure out those things that we do, if they're appropriate, and those patients that they are appropriate on and hopefully provide some sense of recovery for them.  I think we need to be mindful, of course, of that. I think determining who these patients are is challenging. And hopefully, I implore myself as well as, you know,  everyone else to continue putting out research to hopefully fill this gap that's in there to figure out who these folks are. All right, last study, pretty mainstream.  I think everyone is familiar with this study. We won't spend a ton amount of time. A bit of controversy, a bit of debate. We won't go terribly into that,  but we'll talk a little bit about it. So the TTM study for cardiac arrest, non-shockable rhythm. All right, background. I think for quite a while, folks have said, you know,  should we be cooling these people down with a little bit of sunshine in there and maybe not too cold? Or, you know, should we throw them at the bottom  of a crevasse here and really freeze them down? You know, what should we do? Their question here, just moderate therapeutic hypothermia.  So they define that as 33 degrees or normal thermia, right, 37 degrees, notably, not 36, which we'll talk about later. Improved neurological outcome in cardiac arrest patients  with non-shockable rhythms. I think as we all know, back in, you know, the early 2000s, there was some literature that came out that said, hey,  you know what, cooling non-shockable rhythms, there's some harm that we're doing. Papers subsequently after that said, actually, no, we're not doing any harm with these folks.  This group said, hey, we really want to look at those folks with non-shockable rhythms and see. They use 36 verse 37 here and see, you know, is there any neurological outcome data  for either one of these folks? All right, so outcomes, as we talked about, favorable survival in 90 days with a CPC score of 1 or 2. Remember that, I know you all know this,  but that CPC score runs 1 to 5, 1 to 2 being favorable, 5 not good. So they described the, you know, if someone was 2 or less being a favorable neurological outcome.  They had some secondary outcomes as well. These are all the normal stuff that they look for in these studies, right, infection, mortality, length of hospital stay.  I'm not sure why the slide is, you know, they bunch those together, but in any event, yeah, they looked at that. Earlier studies, as I think we all know, showed, wow,  maybe when we cool these folks down, there's some infection and ventilator-associated pneumonia, and then later studies didn't support that as well. So they included that.  Once again, I'm not going to beat us all to death with the exclusion and exclusion. Only thing important here to say, it was out of hospital,  in hospital, had to have a non-shockable rhythm. So that's the most important. You had to be comatose, defined as the GCS less than 8.  That downtime, or that no flow time, had to be less than 10 minutes. You had to have received CPR, and then you couldn't have a code go on greater than an hour, than 60 minutes.  A couple folks upset about this, you know, hemodynamic instability. They said, you know what, if you're on, I think they used a microgram per kilogram per minute  of norepi or epi, or greater than that. You were out of the study, and you had to be in the study enrolled within 300 minutes.  All right, so findings. Here's kind of the meat of it. So CPC score of one or two at 90 days. So folks, once again, that they looked at both groups  and said, hey, who had a better, in the survivors, had a better neurological outcome, defined once again as a CPC score of one or two. That was 10% in the hypothermia group.  Remember, that was the 33 degree group, versus 5.7, a lower amount, in the normothermia, that 37 group. No mortality difference between these adverse events, no difference.  What were the conclusions of the authors? Go here. In patients with comatose stat of post-cardiac arrest, non-shockable rhythms, the folks that got moderate,  meaning 33 degrees, led to a higher percentage of patients who survived with favorable neurological outcome at 90 days than was the normothermia group, 37.  All right, so what's my takeaway? Oh my gosh, lots and lots of holes to put, I think, into the study. A lot of folks said, hey, you had a real problem  with the fragility index being one in this, folks, and that there was a single psychologist that did a phone interview at 90 days and decided what their CPC score was  with that low fragility index. You said, oh my gosh, if you had one person that was different, these results are not even representative of anything positive during that time.  A whole bunch of issues with, you know, the folks that were cooled down to 33 degrees, they had less, they were less, they were afebrile longer than certainly a 37.  In the context of all of these different issues, and there's quite a bit more, my takeaway was, you know what, in folks, there's probably some type  of therapeutic hypothermia likely associated with folks that are post-cardiac arrest, comatose, non-shockable rhythms. I think shockable is, I think most of us can agree  that that's reasonable, and non-shockable, I think after this study, we can say, you know, I think it's reasonable to cool these folks. Search for what the heck that temperature is,  33, 36, I think it continues, of course, who knows what that is. This study was not, they didn't look at 36 versus 33, they looked at 33 versus 37 in non-shockable rhythms.  As I think we all know, the 36 versus 33 in the 2013 study, those folks, 80% of them were shockable, and about 20% were non-shockable.  These folks just wanted to look at the non-shockable rhythm, not the 33 versus 36. I think my final one there, you know, there's a litany of discussion out there.  Is it the ability of keeping them afebrile that actually predicts some type of neurological outcome? Is it actually the hypothermia? I think it's probably both,  but I think we need further studies, of course, to kind of parse this out, but I think likely there's probably benefit from both of those things.  Real quick on our takeaway from 2019, all three. So I think if you're in that context of having that patient that comes in at time zero and you need to have further information,  potentially about their cardiac output, their squeeze, you know, whatever it may be that you want to look at in the heart, and you can't get good surface pictures,  doing a TEE in someone that's potentially at high risk for bleeding, I think you're somewhat safe and it's reasonable. In terms of the eCPR versus CCPR,  certainly don't have enough information that's out there. Debate continues to go on, but I think there's some amount of literature  that's starting to form and we continue to work on that, I think, as a group. Finally, I think the debate will continue, 33 versus 36.  However, I think cool folks that are post-cardiac arrest and to maybe at least 36 and maybe in your non-shockable rhythms potentially consider 33.  Thanks, guys. Thank you.  Perfect. So again, I'm Rod Fontenette, one of the active duty Air Force EM intensivists. I spend all my clinical time in the ED and ICU at UC Davis.  And again, these are my views and not the views of the Department of Defense or the Air Force. So what I'll be talking to you guys  about in this last segment here is basically bridging the care between the emergency department and the ICU. If you guys follow Scott Weingart, he always says,  you know, bringing upstairs care downstairs, right? Because again, that patient shouldn't depend on where the patient is physically located to determine  and to decide if that patient is going to start getting their critical care, right? And so what I'm going to talk about is, though sometimes it seems  like the two specialties are very far apart, right, and the two departments are very far apart, what I want to kind of say is that sometimes the care and the things that we do  in the emergency department can also be translated upstairs. And that's what I'll be covering here in the talk. So we hit on four key areas. One is using the shock index  to predict post-intubation hypotension and cardiac arrest. Next is fluid bolus before intubation to prevent cardiovascular collapse. Does it really matter, right?  Push dose pressors as a bridge. And then again, talking about using peripheral vasopressors in those patients that are fluid refractory shock. And again, is that safe?  So again, just kind of throwing some vitals up there. I mean, I'm not really teasing out too much that's too bad. It looks stable at least from the door.  So what do you guys think, right? So hypotensive, tachycardic, hypoxic, tachypneic, almost everything is bad. I mean, the time is probably even wrong on the slide, right?  So there's nothing good on this slide at all. Hell, if the fever, if the temperature was up there it'd probably be wrong too. It'd probably be bad.  So, but we see these patients all the time in our department, right? So let's say for instance this patient is on a non-rebreather 15 liters flush flow.  I can hear it from across the room, right? Sats are 87% and they're working to breathe. I know, right, this patient probably needs to be intubated.  But are there some things that we can do to optimize hemodynamics before we start pushing our meds and getting ready to intubate this patient?  And that's one of the things we want to talk about, right? So using the shock index to determine or to predict the incidence of post-intubation hypotension  and post-intubation cardiac arrest. It's not a new thing, right? And that's what these studies are kind of looking at. The Journal of Critical Care back in 2012 they looked at it.  Resuscitation in 2013 and then again in 2017 they looked at it and what they found is that using the shock index that had very good correlation between in terms  of predicting who would have one, post-intubation hypotension and then two, who was likely to code following that intubation. And that cardiac arrest was noted to occur  within 10 minutes of getting the patient intubated, right? So why is it important though? Well, it's about a 22% risk of post-intubation hypotension  in the emergency department patient population. If you were to look at the ICU population that number is as high as 46%, right? So it's common, right?  35 versus 20% mortality, right? So basically folks that have post-intubation hypotension that increase in hospital mortality and it also leads to an increase in ICU length of stay.  All right, well what about peri-intubation cardiac arrest? Again, emergency department it's about 2 to 4, 2 to 5% depending on what you read and it's about a 5%  of inpatient emergency intubations that this occur and that's about a 14-fold increase in mortality in these patients that have post-intubation cardiac arrest.  So again, it's very important, right? So shock index, what is it? Right, so shock index is your heart rate divided by your systolic blood pressure, right?  I don't need a lab to figure out what my shock index is, right? I can pick this out just from the hemodynamics that I get from the door from walking into the patient's room  to evaluate the patient, right? 2019, Bulletin of Emergency and Trauma Care, that's what they looked at, right? So what they did was they first identified  and defined what was considered to be post-intubation hypotension, right? It was a systolic blood pressure that dropped to less than  or equal to 90 millimeters of mercury or greater than 20% from the patient's baseline or a MAP that was dropped to less than 65 or if the patient needed to be started on pressors  within 30 minutes following your intubation, right? And then they said, okay, let's apply this to all the different patient scenarios and patient settings, right?  So they're pre-hospital, they did emergency department, they did intensive care units, and they also did the operating room, right?  So this covers all the patients that we're going to see. What they found is that the majority of the patients and the majority of the studies were conducted  in the emergency department and in the ICUs and they said that shock index correlated pretty high with post-intubation hypotension and cardiac arrest.  I don't know why this kind of shifted, but basically what they were trying to do with this is kind of tease down to ICU studies in particular  to find what the best number was for the shock index, right? And these are the numbers they came up with. So a normal shock index is less than or equal to 0.7.  Patients that had a shock index of .8 or higher had a significant incidence of post-intubation hypotension. And those that had a shock index of greater than 0.9  or 1 had a significant increase in post-intubation cardiac arrest, right? So let's go back to our patient, right? Patient's heart rate was 178, systolic blood pressure was 69.  Our patient has a shock index, a pre-intubation shock index of 2.6. Significant risk of post-intubation hypotension and significant risk of post-intubation cardiac arrest, right?  So this is the patient that, though I do want to take control of the airway, I want to do it safely and I want to slow down, right? So when you get that intern, that second year,  that third year that's rushing in the room, calling out all their medications that they're ready to push for RSI, we also need to kind of say, look, let's just slow down  and maybe resuscitate before we intubate, right? And this is why, right? Will this alter my practice? I say yes, right? Because it makes me slow down and approach the patient safely  before I just start pushing medications to intubate. Right? And I know what you're thinking. Let's just give them some IV fluid, right? Saline saves everything, right?  I know that's what you're thinking. Well, that's what this study aimed to prove. Well, hell, let's just give them a fluid bolus, right? Fluid boluses is the key, right?  So what did they do? And this is a PREPARE trial. So what they did was it aimed at evaluating the administration of IV fluid bolus to prevent cardiovascular collapse  in the critically ill patients that I'm going to intubate. Basically saying that if a patient is found to be, say for instance has an elevated shock index,  me giving that patient an IV fluid bolus should prevent, hopefully, the patient going into circulatory collapse. Right? It's a pragmatic, multi-center, unblinded,  randomized trial done in eight ICUs in one ED. So it's applicable to us. And they also define what cardiovascular collapse was. New systolic blood pressure less than 65.  New or increased vasopressor use. And what did they find? Cardiovascular collapse occurred in the IV fluid bolus patient cohort just as often,  just as frequent as it was in the patients that did not get the IV fluid bolus. And if you look down at the very bottom, it says the data  and safety monitoring board actually stopped the trial due to futility. Right? Meaning that it didn't really matter if the patient got an IV fluid bolus or not.  The question is, though, will this alter my practice? So yes, no, right? And the reason why it's a yes, no is it depends on why I'm giving the patient the fluid bolus.  If I'm giving the patient a fluid bolus to prevent them from crashing once I push my medications, I think that's the wrong indication to give an IV fluid bolus.  If I'm giving a fluid bolus because I'm in the throes of resuscitation and I've deemed the patient to be fluid responsive, that's something completely different.  Then it's a thumbs up. But again, if I'm doing it only to prevent the patient from crashing, per this study, per the PREPARE trial, that's not the appropriate indication.  Right? So I say, just like any other medication, use your IV fluids wisely. Right? So then I know you like to say, what about push-dose pressers? How many of you guys out there  in the audience are actually using push-dose pressers? I like it, right? I like it, right? So I use it just because I like saying push-dose pressers. So the American Journal  of Emergency Medicine actually looked at this, right? And what they were trying to find out was evaluate the use of push-dose practice, right, looking at the patterns,  the efficacy, and more importantly, the safety in critically ill patients. And I think that last one is key because not everyone uses it the same.  Not everyone mixes up the dosages the same. Sometimes there's no consistency in how much you give. Do I get 50 mics of phenolephrine? Do I get 100 mics of phenolephrine?  Do I get 200 mics of phenolephrine? Right? So, and that's what this study was aiming to look at. Looked at patient demographics, medication administration details,  virals, pre- and post-administration, adverse effects, which we'll talk about here in just a moment, and then medication errors as well were collected.  It's about 146 patients were included. And the great thing is there was surgical ICUs as well as medical ICUs, and they also included emergency departments. And what did they find?  Well, they found that in patients that got push-dose pressers, you had an increase in systolic as well as diastolic blood pressures and an increase in heart rate.  Now, I'd say be very careful with the increase in heart rate because it just depends on which push-dose presser you're using, right? Because you could have a reflexive bradycardic  if you're using push-dose phenylephrine or neosynephrine, right? But if this is push-dose ephedrine, which is what they used in this study, or push-dose epi,  which is what some of us use, you can see a tachycardia. So, again, it's just using your push-dose presser appropriately. And then what did they find?  There were 17 adverse events, most often related to an excess increase in blood pressure and or heart rate. So, basically, if a patient's already tacking away  in a 130, 140 range, I probably won't use push-dose epinephrine as my push-dose presser of choice because I don't want to make that worse, right?  It increases stroke volume from decreasing diastolic filling time, decrease my cardiac output, have worse outcomes, right? Thirteen patients had a dose-related medication error,  right? Again, over 200 mics of phenylephrine and over 25 milligrams of ephedrine. Again, that's because a lot of this isn't really standardized, right? And then another one was 15%  of patients were given push-dose pressers and they were already on a continuous infusion of a presser, right? So, again, no true benefit.  And then there were quite a few adverse effects. And I think the reason for the adverse effects is because a lot of times, how do we mix these push-dose pressers?  I grab a saline flush, I squirt out one cc, I pull up one cc of epi or one cc of phenylephrine, I push it, I set that syringe down, I go on with my day, right?  I usually go grab a coffee before the coffee cup closes or something like that, but that syringe is sitting there and that syringe looks like just a regular syringe  of saline now, right? So, what I do is normally I try to label the medication for one, right, and then the next thing is that syringe goes where I go, right?  I don't just sit that syringe down and walk away from it, right? That increases the likelihood of error. So, what I say is that if you're going to do this,  do it appropriately and make sure you label your medication. So, the question is, will this alter my practice? Again, I say yes because it buys me time to do something else, right?  Especially if I need to emergently intubate this patient, I find that push-dose pressers can help. I know some folks say, well, why even do a push-dose presser?  Why not just start the patient on a presser, right? Why not just start them on levofad, right? How many of you guys are starting pressers on peripheral IVs? What? That's crazy.  But there's a study, right? So, let's see what the study says about it, right? And that's specifically what they looked at in anesthesia and analgesias.  Looking at levofad through a peripheral IV and looking at the safety of that, right? So, a study aimed to estimate the rate of occurrence of drug-related adverse effects that led  to surgical interventions, right? Meaning that I started a patient on peripheral levofad. How many of those patients had extravasation? And how many of those patients  that had extravasation had skin necrosis requiring some sort of surgical intervention? It was a retrospective cohort study done in Amsterdam and the Netherlands.  And again, they used levofad and they used some 14,000 patients in this study. And out of that 14,385 patients, there were five cases of extravasation.  Five. And how many of those patients had significant skin necrosis requiring surgical interventions? Zero, right? Meaning that this is safe, right? This is extremely safe.  So, will it alter my practice? I say yes, it'll alter my practice, right? So, instead of not starting pressers soon because I'm waiting to get at a central line of some sort  and a more definitive vascular access in, I can get these patients started on a large-bore IV. What I won't do, though, is probably start a dose  of phenylephrine in a 22-gauge hand IV, right? That's probably a party foul, right? I probably wouldn't do that. Hospital administration frowns on that.  It's just a bad day for everybody. So, a large-bore IV, whether it's an 18-gauge or whatever the case may be, in an antecubital fossa,  I say that's a good line to probably use, right? So, take-home is consider using the shock index in critically ill patients prior to intubation,  one, to prevent post-intubation hypotension, and more importantly, post-intubation cardiac arrest because what the literature shows is  that these folks have increased length of stays in the ICU, and ultimately, they have increased mortality. IV fluid bolus prior to intubation does not alter the  outcome if you are using it just to kind of ward off evil spirits and preventing the patient from becoming hypotensive after you push your RSI medications.  Just like any other medication, I say use your IV fluid appropriately. Consider using push-dose pressors for that hypotensive patient to kind of buy time, but again,  choose wisely and choose the medication wisely, and please be safe with your medications. Don't mix them and then set them down for someone to just pick  up a syringe that looked like a flush and push it, right? And then, infusing vasopressors through a large-bore peripheral IV has been proven to be safe,  but again, choose wisely and make sure it's not like a small-hand IV, make sure it's a large-bore IV that you know flows appropriately. And with that, that is all I have. Thank you.  Great. I want to thank our panelists and speakers. They did a lot of work over the past couple of months getting that together, and I think now we're all ready  to go home and load up our rigs with TXA and FFP and get our TEE probes in the ED and run our pressors upstairs. So, any questions for the panelists?  Please use the mics when you come up with questions.  I'll throw one out to you guys because I'm kind of curious. So, Amjad, you know, hearing the other comments that were made about potential low-yield interventions, in my opinion,  things like vasoactive agents, what's impeding that from going all the way backwards to something like the ambulance rig? Why can't we have that with our paramedics?  You can. I mean, they are running, so there's many ambulances outside that are actually running peripheral pressors already. Like, they've been doing that.  The funny thing about peripheral pressors, let's just say, like, in the rigs and stuff like that, how many of you guys have seen patients come to the ER  after they did an EpiPen to the thumb? Like, 300 mics of EpiPen to the thumb. I've seen it multiple times. And then we give phenylephrine in the penis to pre-epism.  Like, we're injecting end-organ stuff. So, this stuff about extravasation and people worrying about, there is sometimes skin necrosis. You do get issues, and I've seen skin necrosis  with, like, D50 and stuff like that. But this, I think, this has already been done by, like, in the rigs already, and it's something I advocate for.  But like I said, like, choose wisely, too. Don't run, like, the drip at a million. You know, use it as a fluid bolus into the 20 in the thumb or 22 in the thumb. Yeah, Tim.  With regards to the peripheral vasopressors, did you find, or in that study, did they actually look at monitoring? Were there protocols in place?  Because I think a lot of shops have utilized these. There are folks that do preach the safety of this. But there are clear monitoring paradigms. The nurses are trained to do this.  They're looking at peripheral perfusion modeling, and there's, like, an hourly check that goes to make this applicable. Were they deploying that?  And I'm assuming that if we're going to preach that as a standard mantra, then I think the safety aspect of it needs to come hand-in-hand, would you say?  Great question, and I agree completely. And in this study, they did. They were doing serial checks just to make sure there were no signs of extravasation.  And if there were, I can say in the five cases, they were in order to stop it immediately and then make sure, again, they followed it closely.  So the protocols were implemented in this study from all the patients that they used in those hospitals. So, great question. Thanks. One of the most... Oh, go ahead.  Let's alternate sides, if that's okay. Great talk. Thank you, everybody, for putting that together. The question I had was for you, Amjad, and for mild traumatic brain injury.  And in the emergency department, you see a lot of patients with mild traumatic brain injury. Has this changed your practice in terms of will you give TXA to these patients,  some of these patients we discharge home? Yeah. For me personally, it's been just realizing and remembering it, and it's been mostly in the ICU  because I have a little more time to think. But I have, when I thought about it, I have done it. I've changed it up a little bit now recently.  I've actually been using it in the ER and ICU. Did a one for one patient in the ER. I don't know if it helped, to be honest, but I'd like to think I did something.  So I made sure I told everyone I did it to. But, you know, like, so I would do it. I would, and it has changed my practice, and that says if I can remember to do it.  So if you're in the throes of resuscitation, I mean, that's not the first thing to pop up. It's not that big of a game changer.  Yes, sir. Yeah, one of the common causes of post-intubation cardiac arrest is dynamic hyperinflation. Do you have any recommendations for how to deal with automatically  preventing that in advance? In other words, dealing with the fact that you may have an issue, even an occult asthma patient or somebody with COPD nobody knew about.  So is there an approach you use to deal with the dynamic hyperinflation right up front?  Yes, sir. So for that patient that has like an obstructive lung physiology, is one is choosing the appropriate tidal volume, right, to set tidal volumes of 700, right,  and then set the rate too high in order to give them enough time to fully exhale.  And then I can lead to dynamic hyperinflation. Another one is setting my alarms appropriately on the vent, right? So I remember when I was transporting a patient  in Afghanistan, I went to pick the patient up. They had the highway pressure alarm set to 100, right? So that's probably not a good look. So again, just appropriate tidal volumes,  and then looking at and paying attention to my waveforms, and then setting my, especially in obstructive lung disease, something like asthma,  setting a rate closer to eight to 10 breaths per minute versus the 20 breaths per minute that we sometimes do. And then again, setting my alarms appropriately.  And then if I see an acute change in hemodynamics, alarms on the vent start to go off, have that at the kind of the forefront of my differential and to be potentially going on,  and then kind of getting the patient separated from the vent, but first seeing what the vent's telling me, and then kind of going from there. That's great, yeah. Yes, sir. Fine.  I would add a comment too. I think the idea that you're bringing up is a key one. I think all too often in the ED, in the ICU setting,  we underestimate the use of our monitoring devices. I mean, one of the first things I try to teach our fellows is when you go to intubate someone,  you get the tube and it's the not drop and walk out the room, but it's to look at the monitor and know what the initial end title CO2 was.  Knowing that existing data point right up front helps you then make some of those decisions about vent settings, monitoring, how I'm going to be aggressive with those things.  I think using the monitoring devices, we already have them hooked up to is huge. One of the things that we did a trial back at Ohio State where we looked at ventilation and CPR  and dynamic hyperinflation associated with CPR. And what we saw that in many situations, it's ventilation is excessive. They couldn't survive.  But the other point is that the excitement that often happens post CPR when they're bagging. And if you don't bag quick and give them a long exhalation time,  you know, you can stack them that way. So that's a big deal. Yeah, I want to add on that actually. So like, I remember being a EMT basic way back in the day,  and we get excited and we're bagging the patient. And the instructor will always tell you the breath of life, not the hurricane of death. Because the second you get that tube in,  you're just bagging away, bagging away. And another thing to pay attention to right after intubation too, I tell this to all the fellows,  a lot of times you're monitoring the waveforms don't always pick up everything. Listen for exhalations actually. Listen to the patient, blow off their breath.  Watch the end title actually finish off and taper off. But actually pay attention to those, like you're saying, on all the little data points. A lot of times I'll have the fellows,  when they walk out of the room after intubation, I'll ask them, what was the peak pressures? What were you getting on the, what volumes are we getting for those peak pressures?  And they won't know, basically. So pay attention to all your data sets on that.  Yeah, please. So where I'm doing fellowship in Denver, Colorado, there is a strong contingent of trauma surgeons who are diametrically opposed to the administration of TXA  in patients who do not have evidence of hyperfibrinolysis on a tag. How would you, or have you run into this problem in your institutions, and how do you recommend  mitigating that concern in the patient with TBI?  Oh, yeah, I basically, like I, luckily I haven't run into that actually in our group. And the point is, you're right. Are the patients benefiting if they're not in fibrinolysis?  And how many times have we run the tag actually and saw the tadpole? Like very, very few do we pick up on the patients with DIC,  yet CRASH-2 came out and they found a mortality benefit with that study, CRASH-2's coming out and they're seeing a little bit of benefit, and they are not showing you  that they're basing it off a tag. Like this was pragmatic world, like real world studies where we're giving this stuff early on and we don't have that data available to us.  We're in Pakistan in the middle of an ambulance somewhere, and they're giving this medicine, and they're saying, hey, what's the outcomes? That's all they're looking at.  So to say that basically you have to have hyperfibrinolysis versus not, like there was, I guess recently, what was it, TIC-2, T-I-C-H-2 came out  and they were looking at the expansion. Yeah, they were looking at the expansion on the CTs and they were seeing that there was some, a little bit smaller expansion of the bleed.  So I don't know if you have to have full-blown DIC or prove some fibrinolysis on a tag, wait that long to actually see a mortality benefit to this stuff.  So are they just not following CRASH-2 over there or? They, yeah, there is a body of literature. So where I work in Denver, Ernest Moore and colleagues  have a couple of studies they've published looking into tag-based TXA administration. And the theory is that in patients who don't have evidence of hyperfibrinolysis,  they may not benefit. Makes sense. And that if you do give the TXA, you can develop what they call lysis shutdown, where they just don't lyse,  and they might develop end-organ damage from thrombosis. All theoretical concerns, to my knowledge, the data supporting that as being a clinically relevant entity is weak,  but it is kind of annoying that it makes the tag look ugly. Yeah, yeah, true.  Yeah, I don't have a 100% conclusion to that question, but it's a good question. And we don't know the answer really yet. Like, what's the right patient to give this to  and should you wait that long to find the tag to see if there's any benefit to it? So, you know, more to come, I guess, on that. Thank you. Thank you. Well, we're at five o'clock,  so I'm gonna end our session. And I wanna thank everyone for coming and staying. And as it's the end of Congress, we'll see you all next year in Anaheim. So take care.

Video Summary

This video is a panel discussion covering various topics related to emergency medicine and critical care. The panel discusses the use of the shock index to predict post-intubation hypotension and cardiac arrest, the effectiveness of IV fluid boluses before intubation, the use of push dose pressors as a bridge therapy, and the use of peripheral vasopressors in patients with fluid refractory shock. The panel provides insights and recommendations based on recent studies and discusses potential changes to practice in emergency medicine and critical care.

Asset Subtitle

Trauma, Resuscitation, 2020

Asset Caption

The Society of Critical Care Medicine's Critical Care Congress features internationally renowned faculty and content sessions highlighting the most up-to-date, evidence-based developments in critical care medicine. This is a presentation from the 2020 Critical Care Congress held February 16-19, 2020, in Orlando, Florida, USA.

Learning Objectives

Identify prehospital care interventions that can improve clinical outcomes
Review best practices for care of the critically ill patient boarding in the emergency department
Describe resuscitative and pharmacologic management in the emergency department that impacts continued critical care monitoring in the ICU

Prehospital Critical Care

Amjad Musleh

Critical Care in the Emergency Department

Keith Azevedo

Emergency Care Impacting Critical Care

Roderick W. Fontenette

Meta Tag

Content Type Presentation

Knowledge Area Trauma

Knowledge Area Resuscitation

Knowledge Level Intermediate

Knowledge Level Advanced

Learning Pathway Emergency Medicine and EMS Care

Membership Level Select

Membership Level Professional

Membership Level Associate

Tag Cardiopulmonary Resuscitation CPR

Tag Blood Blood Substitutes

Year 2020

Keywords

emergency medicine

critical care

panel discussion

shock index

post-intubation hypotension

IV fluid boluses

intubation

push dose pressors

peripheral vasopressors

fluid refractory shock

Emergency Medicine and EMS Care

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