Good afternoon. My name's Sheila Alexander, and I am an associate professor from the University of Pittsburgh School of Nursing and Critical Care Medicine. I'm going to be your moderator today and also give talk number two. This session is the Cardiopulmonary Resuscitation, Do It Right and Save Lives session. And we have four talks planned. The way we have this set up, each of the first three talks are going to be about 20 minutes. In the fourth talk, we're going to have some vignettes and some Q&A. So we're hopeful we get some good participation from everyone. With that, I'm going to introduce our first speaker. Our first topic is CPR, why we need to do it right. Our speaker is Paul Pepe, professor emeritus of medicine, surgery, pediatrics, public health, and ranks family chair in emergency medicine at the University of Texas Southwestern Center at Dallas. Hi, everybody. Good afternoon. I hope everybody's awake, because I need to be woken up myself. I want you to know, I used to work there at the University of Texas. I'm now part of the Orange County Convention Bureau. And we wanted to whisk you to the session on mouse to mouse resuscitation here. I know that may sound goofy, but whatever, couldn't resist doing one of those mini faux pas here. So here we go. So the session was called CPR, we need to do it right. And CPR is a more generic term, which is cardiopulmonary resuscitation. And it means the whole gamut of it. And what we're going to talk about is some really cool new, I mean, things are working in terms of technological advances and all that. But I'm going to actually stick to the basics, to some extent, then talk about the actual act of doing CPR and how to do it right, maybe, and why it's so important. And not everybody has believed that this is true, but I hope to convince you that this is going to do it here. So as a conflict, I have no conflict of interest, except one, I'm not a morning person. And two, I was a young child. I was early interested in mouth to mouth as a young child and explored the universe early. And that set me up for ACLS. Everybody knows what ACLS is, right? Alternative Clinical Lifestyle. And that's me. So I actually was originally on a critical care doc. And we started doing things and thought sepsis was not just positive blood cultures, but maybe a syndrome, maybe an inflammatory thing. So I wanted to get blood work and sequentially follow it, whether it was leukotrienes or arachidonic acid. And I actually wanted to get the blood work. We just started this new program with paramedics in Seattle at the time. So I actually went out on the streets with them. And I came across the concept of the earlier the intervention, the better the results was kind of my thing. And what was interesting, I was also out there and I could see that the quality of what I thought was good CPR or the quality of how they ventilated or whatever was not as good as we thought they'd be doing. So maybe they didn't make it because of that. So we kind of improved things and did very well. And what we've learned, particularly in the last two decades is that chest compressions are critical to resuscitation in sudden cardiac arrest in those particular situations. And the classic laboratory studies show that you got to prime the pump, that if you stop to ventilate or anything else, check pulses, that you fall off the pressure head and you got to build it up again. And you're going to see some evidence about that today. So that eventually led us to the fact where even I was part of the papers back in the 90s where if they're gasping, OK, then that's a great way to enhance circulation, enhance oxygenation, enhance ventilation. So we would just do compressions only. And that sort of got to be the thing. In fact, early studies showed that key finding of early studies during the 2000s to 2010 were that the chest compression fraction, that means the amount of time your hands are actually on the chest wall, you know, was correlated with better survival. So the more time you had your hands on the chest, the better off you are. So this ended up being, by 2010, when the guidelines came out for CPR, what did they tell you? Push hard, push fast. Do it right. It was important. So I have to take a quick commercial break here. With the new CPR jackhammer. Now, you'll not only meet but exceed the American Heart Association guidelines for compressions. After all, don't you think more is better? Deliver an average of 3,542 compressions per minute with the new CPR jackhammer. CPR jackhammer, because more is probably better. And maybe not, OK? And the reason why I say that is that when we were seeing this, we wanted to see if this, we've seen people, we were getting records back because we were starting to actually have machines that would give us feedback or we can monitor how fast CPR was going, how deep it was, what the recoil was like. And we were finding out it wasn't that great. And some of these people were going up like they were doing CPR jackhammer. And one thing that happens if you go, for example, too fast, you may not get deep enough or create enough of a recoil. And then sometimes if you're going deep enough, you may be going too slow. But we came up with a concept of looking at chest compression rates as a first delve into this. We published it in 2015, where we looked at survival. And this is the paper a lot of people refer to as the sweet spot. Right now, I'll ask you, what rate should you use for CPR? Most people will throw out, oh, I think it's 100 to 120 or whatever. Well, it came from this paper, and here's why. So when we looked at this, the sweet spot of CPR was compression rates being 120. It was indefinitely associated with better survival. And so what's interesting, if you look at this thing, you actually gradually increase. And then you fall off the map as you go faster. So hard and fast, too fast is too much. So the quality is related sometimes to that. But then that begs another question. And for example, you'll see here in just a second. By the way, what we ended up doing is we got this high-tech piece of equipment. What do you call these things? The thing you put on a piano, what's that thing? A metronome, right? We put it on the defibrillator and all that, and it worked. Now, this leads us to one of the themes of today about quality of CPR. And it's going to lead to the theme that people talk about various interventions. Do you use epinephrine? Do you use ECMO? Do you use this? Do you use your goal-directed therapy? Whatever it is. And then people get almost animus there about it. They'll get into contentious fights about something's good or bad. And you're going to see a theme I'm going to have today that binary thinking is bad. It's not something's good or bad. It depends. And you're going to see why here. And it's all related back to the quality of CPR and some other things that happen during CPR. So in ITD, if you don't know what that is, for example, if you're pressing on the chest or you're squeezing during CPR, it's kind of like a turkey baster is released. That's why the recoil is so important. It helps suck air and blood back into the chest as you compress. What the ITD does is very kind of cool. It's like a little valve. And so what happens as you compress on the chest, and then what you do is before you release, this is blocking the airway. It's a little valve. And it goes, mm, mm. It's like you sucking through a straw. And it creates more vacuum. So what it actually does is tugs a little bit more blood in, out of the brain, into the chest, or whatever it may be. And it's just a second. It's like minus, I don't know, 16 centimeters of water for a blip. It just goes like that. But it's just enough to tug some more blood in. And it was very interesting. So in the laboratory, it works fabulous. And we said, hey, let's go take this to the streets. So we did a very, this is a classic gold standard study. It was sponsored by the NIH. It was in multiple countries, let alone about 150 EMS agencies. It was elegant design. Everybody got an ITD, except half were inactivated. Then you got to see later which ones were. So it was well-controlled, well-designed, published in the New England Journal. Cool thing. But it showed no advantage to the ITD. So we're going, hmm, that's weird. Meanwhile, right about the same time, another paper was published in The Lancet where it was combined with something called an active compression decompression pump. Now, an active compression decompression pump that looks like that looks like a toilet plunger, because it's kind of a toilet plunger. And that's where the idea came from in the first place. So you're not only compressing, but then you're actually decompressing, creating more of a vacuum on the upstroke, as you can see here. I actually took this video in 1999. This is how long this thing's been around, et cetera. And interestingly enough, they were able to get back asystole patients in Paris with this, even though, because it took so long to get to the patients and through traffic and various other things. All right, here's the deal. So they did this study in The Lancet where they had the two of them together. And they improved outcomes, even at one year, neurologically intact outcomes, favorable outcomes, 50%. So why the discrepancy? Why didn't the ITD work before? Is it because it's just a passive animal in this thing, or it requires the other thing to work, or whatever? Well, one of the first questions we asked, by the way, there's several answers as we get to this, okay? One of the first things we found was we said, hey, we just did this study on the quality CPR. And they had data from that particular study that actually looked at the ITD versus non-ITD. And we looked at this quality. So we said, could it be the quality CPR? So what interesting thing we did is this is a thing where we just raw data, where we're looking at rate. At the bottom here, you see 90 to 99, 100 to 109, 110 to 119. And so what you're looking at here is that this is the sham valve, okay? And it looks like the best place is here, but it doesn't make much difference. But if you put the ITD on, the survival rates went up dramatically if you're in that sweet spot that we were talking about before. In fact, you were worse off if you went too fast. So this thing, in retrospect, even though this is a little bit of data dredging perhaps, but it's not. We applied a new question. We went back and looked at a prospectively collected data set. And it was pretty impressive to see that. That led us on to other studies that we did later on and looked at the quality of CPR, even using very liberal criteria. So we decided to go back and look at that original study. In fact, this thing actually showed that you really had better outcomes if you're doing quality CPR. So this summer, to take it a step further, I wanted to ask another question. You know, is the quality CPR, is the rate and depth of CPR for you the same as me? Because we know rate affects depth, depth affects rate. So what's the optimal combination of the two? And more importantly, is the optimal combination if I'm a big man with a big chest, et cetera, the same compliance as if I'm a small woman, or if I'm older, or if I'm using a device, or is it, you know, does it? So we were looking for signals. So this thing, we actually said that previous studies have indicated that both chest compression rate and chest compression depth are each, you know, independently associated with survival probability. However, an optimal combination of the two has yet to be identified, particularly respect to age, sex, presenting cardiac rhythm, because if you're down for a while, maybe it changes your, you know, hemodynamics a little bit. And then CPR adjunct use. So since we knew about this ITD and they had collected the data, we went back and included that data set. So this is really interesting. I like this, because what came out in this paper is a whole new approach to things. It's called a contour plot, and a contour plot are used in other things like architecture and various other areas. But we decided to use this as a three-dimensional model. And what you're looking at is on the, what is this called, the y-axis, right? So 80, 100, I'm learning this new scientific stuff. It's really cool. So 80, 90, 100, 140, et cetera. And then over here is the depth, 4 centimeters, 5 centimeters, et cetera. So what you're looking at is this color-coded thing. It's cool, because guess what blue is? Blue is like not too good. You're cold. So zero survival rate. A little bit of darker blue is, but it's not bad. It's like maybe a 1% neurologically intact. You get up there in the greens, you're up there in the 5, 6% range, maybe even 7. And look at this, getting up maybe in here with a little bit of yellow is like 7% neurologically intact. This is all comers, by the way, and not just VF and not people with C. It's just all cardiac arrest cases here. It turned out in the original study, 80% of the people did not get quality CPR. And that's what's interesting. But we have the data to look at it retrospectively that they were not getting. So we took the group of people, the 20% that were getting relatively good quality CPR, and wanted to identify those. But we actually got the whole group here, and we looked at people who had combination of all this. And that's what's cool about this. So this is your standard CPR, the sham ITD. And look at this, here's your sweeter spot that's there. Right about, well, whatever that is, 100, 107, 108, I think we got. Or maybe 100, you know, it's that same thing we showed you before. So it makes sense. But if you put this impedance threshold device on, look what happened here. It's a hotspot. And this thing was over 10%. What the point here is, it's not that the ITD is good or bad. And there was nothing wrong with that New England Journal study. I was on it. It's accurate. It says, if you don't account for quality CPR, you ain't going to get good outcomes with this thing. It's not going to work. It even could be harmful. But if you use it right, meaning quality CPR, getting in the sweeter spot, you can actually double survival chances, or more so in this particular case. So this thing is highly dependent on quality CPR, but it can make a difference in your outcome. And by the way, we saw some differences, but there was no major signal coming out of the age six or whatever. I think we need to look closer at other things like BMI or something like that. But the point was that I think one of the best takeaways from this paper was that the quality of CPR really drives. And you can do it real time. You can get feedback on the spot. And I've learned to do this where it says, slow down. And I go, slow down. And they go, oh, push harder. I go, OK, slower and harder, and I got it. So you can actually improve your quality of CPR. All right, so maybe it was not such a neutral trial after all. It's an accurate study, but it doesn't say that the ITD is not good or bad. It's how you use it, just like everything else. And that applies to things like, for example, if you take the CRASH-2 study at face value, TXA, is it good or bad? People get contentious about it. Well, if you take the CRASH-2 study at face value, it's great for you upfront in the first hour, but if you wait till three hours, it's harmful for you. So I'm just giving that as an example, whether you believe that particular study or not, that the concept of thinking about, is epinephrine good or bad? Again, or goal-directed therapy. OK, so Tom Ofterheide, who's just a brilliant man, he's the research director at the University, conducted a couple of these studies. We wrote a paper called Evidence-Based Medicine Versus Experience. And our experience tells us something's wrong here. And we went back and looked at it. So what we kind of came to the conclusion for was that research is spelled wrong. It should be R-E-S-E-A-R-C-H. And the things that are key issues are timing. Things are confounding variables. For example, in CPR, the confounding variable may be poor CPR, but it may be one other thing which we're going to talk about next, et cetera. And so that's why people get contentious. If you're not with me, you're my enemy, he says. Only a Sith deals in absolutes. So remember that, OK? It's a lesson from Obi-Wan. OK, I'll move on. OK, next concept, timing and synergy. OK, so some things need other things. We're all talking about bundles of care. And it turns out in CPR, bundles of care. So if you use this ITD, that's compression and decompression, plus something else. What we added in is since this stuff pulls blood, say, out of the venous side into the heart and out of the brain, it actually, during CPR, you're actually ejecting pressure heads both on the right side, meaning, let's say, the arterial side and the venous side. So obviously, the arterial side wins out, because eventually we get better with CPR. But it's not the most efficient system. What if we could pull blood out of the head and then increase cerebral perfusion pressure? And that's what we did. So guess what? All of you that work neuro-intensive care, you taught us a great lesson. We have a big R&D department, rip off and duplicate, right? And what we did was we took the head up thing. And what we found is that we really improved outcomes. And I gave this at the plenary talk last year for those who were there. And we confirmed that actually you did much better when you use this head up approach as well. Here's the problem. If you go right to head up, it's harmful, because you're not priming the pump. And we found later that as you go gradually up after a period of time, after you've got developed, prime the pump and then gradually go up. So this year, we actually added in in the laboratory this thing. I think it's called the Eligard. I don't even know. I call it DAX-y is my thing, because I'm a generic person. I have no conflict with this. But it's a machine that actually over a period of time gradually raises the head up where you're about, I don't know, 22 centimeters up above the ground, etc. And so it really, we found as we did it gradually, we got even better outcomes. What you're looking at this graphic is cerebral perfusion pressure. As you can see here, over 20 minutes, you start losing, so it was standard CPR supine. Why is that, by the way? Why does it go down? We're using machines. They're not getting tired. And what it is is that you start, there's no oxygen going out your tissues, so you start getting, your vascular tone goes away. So you get vascular paralysis and the pressure head goes away. But if we use the active compression decompression pump with the ITD, what I call enhanced CPR, it actually does much better and it sustains it. And we found with head up, it actually was somewhere right in between, but it also falls off. When we added head up, we get something that looks like this, a cross thing. And now with this gradual elevation, we're getting a next level, a next increment in terms of proving the quality. But this is a point, this one, is that if you add up the contributions from the head up, the active compression, et cetera, even if you add them up, this thing is far better. It's synergistic because you're using a bundle. They all do the same thing. They pull blood out of the brain and into the heart, but they basically have different mechanisms to do that. So together, they're synergistic. It was really impressive. And that's the thing that's really been, I thought, phenomenal with that. Okay. Last part for this thing is one more thing and not necessarily a small matter. You'll see is pediatric cardiac arrest. And this leads us to a little bit about one other confounding variable that we'll talk about. So what's the conventional wisdom? We're doing much better in hospital with pediatric cardiac arrest. What about out of hospital? What's the common, you know, conventional wisdom with that now? First of all, grim outcomes. We just don't get them back. Part of the reason why kids don't go into sudden cardiac arrest and they're loaded with oxygen. They basically get hypoxemic. Generally, it's a respiratory cause. They get hypoxemic, and therefore, they get hypoxic. And then, all of a sudden, the heart goes bradyastolic. They're way behind the curve, okay, already by the time we're called out to see them many times. It's volatile scenes. The family are saying, get him to the hospital, get him to the hospital. Paramedics are, you know, don't get to do this for you. It's a difficult anatomy and relatively small veins or whatever it might be, infrequent skills use. And so, what happens? Kids are easily left. What do you think happens? It's basically a scoop and run mode. And so, that's what's happened. So, the general practice across the United States is just get them loaded, get out of here, or if we just even go the ambulance, just get them out of this scene, okay? Well, physiologically, does that make sense? Doesn't, because they're already hypoxic. And then, every second, wasted. So, what we did in Polk County right here, you know, we did this study right here in the politically, a lot of people think Korea is the most politically unstable peninsula. We actually use Florida here. And so, and we wanted to give it a try, and we decided to focus on on-scene care. Go right to an I.O., get some epinephrine on board while you're going right to an airway, and we actually got people well-trained in doing airways, even if we use this in IGEL or endotracheal tube. We got a small cadre of people who are highly skilled to get it in, and we trained them in verbal judo to deal with families, so they get to give the confidence that we've got to do it right now and here. And they're right, because if you don't do it here and now. For many years, the survival rates in Polk County were zero, okay, in terms of neurologically intact. So, that leads us to confounding variable three. We talked about quality CPR, we talked about timing of things, but the other thing is how we ventilate during CPR. And kids have had this thing where they're telling them, you know, it's respiratory, so bag them. So, I don't know who trains them in this stuff, and you guys work in ICUs, you understand the physiology better, that lung inflation's great for oxygenation purposes, but over-zealousy ventilating knocks out positive pressure ventilation. So, what these guys have been doing is they're going like this, they're not even giving a good lung inflation. And the problem with that is if you're doing CPR, you're actually, you know, getting rid of some dependent lung zones and you're deflating. That's a problem. And in fact, we've shown in the laboratory now that by not having a good lung inflation, you're increasing pulmonary vascular resistance. You don't get good flow through there. You've got to have good lung inflation to have that happen. Just don't do it often. So, these guys were trained to give a really good squeeze and then release it quickly, and maybe only one every 10 seconds. Maybe a couple up front and then release it. So, they're maintaining really low intrathoracic pressure, but keeping intrathoracic pressure mean low, but yet keeping good lung inflation, which helps with CPR. All right, so this is what happened. The first couple of years, there were no survivors for several years, and we're just using for sort of a comparative two years before and after. And with this thing where we're going right to it, getting the EPI on board, et cetera, and so on, we actually got 23% going home neurologically intact. And it was profound. So, what did it? Was it the EPI? Was it the airway? I think it was all the above. We're just doing it better. And the quality of CPR, if you're scooping and running, what do you think the quality of CPR is under those circumstances? And I just showed you how important that was. So, this was published earlier this year for the first two years. Then we came up with another concept, which is system one thinking. So, right now, if you had to go in, you see a kid, and you have to give these four years old. So, you go, okay, 1.01 milligrams per kilogram, and then you got to figure out, you know, whatever, how many pounds is he, and, you know. So, decrease airway and also make it quicker. If I told you, what's 50 times 50, you'd go, 2,500. But if I said, what's 55 times 55, now you're going to system two thinking. So, what we said is, hey, it's a nine-year-old. As we're coming to the scene, we knew it was a nine-year-old. So, okay, we'll get 0.3 out. If it's a, you know, whatever, a one-year-old, get 0.1 out. So, we prepared it on scene. And look what happens the next thing using the system one thinking. So, now it's up to 35% in the following two years. And you're seeing the timing of when epinephrine got on board. It had been 60 and a half minutes when they were scooping and running, even if they were doing it in the ambulance. And then got it down to seven and a half when we were going right to the IO. And then now, recently, as we're getting it ready before we went in, it was down to five minutes. We're getting it actually down lower and we're getting better outcomes there, in fact. So, anyways, that'll be published, hopefully, fairly soon. And so, the bottom line here is that they're not dead. They're just mostly dead, you know? Look who knows so much, huh? Yeah. Well, it just so happens that your friend here is only mostly dead. You got it. All right. So, the overall conclusions here I hope you take away are that, on the road to the 22nd century, that we'll find out if we do better quality CPR and we monitor it, we do it on real time and get feedback, if we can control for better ventilation, if we know the timing of all these things. As you can see, the kids thing was a real good example, bringing it all together. And there are bundles of care. And that the new things that we do, we need to rethink maybe the right heart rate and, right, I mean, start right in depth, maybe different depending on what it is. So, as we move on, remember that research is spelled wrong. It should be R-E-S-E-A-R-C-H. So, with that, we'll make life better for future generation. Oh, wrong slide. Sorry. We'll make life better for future generation. So, I'm Paul Pepe, and I approve this message. Thank you very much. Okay. So. We're going to go to questions later, right? Okay. Good. All right. Let's go. Thank you. Yeah. So, thank you, Dr. Pepe. That was awesome. I learned two things. One is, next time I'm asked to follow him as a speaker, I'm going to refuse, because that was fabulous. And two, I probably need to stop teaching CPR and telling people that, well, just try it. You're not going to make them more dead, because that's my line. So, apparently, I need to teach them to do it right. My name is Sheila Alexander. I'm going to do the second talk in this session, which is really about keeping patients at the right temperature post-cardiac arrest. I am from the University of Pittsburgh School of Nursing. I have a secondary appointment in critical care. I am primarily a researcher, but I am also practiced for a very long time and have done a lot of therapeutic hypothermia. And we're running a little mini-trial today to try to induce therapeutic hypothermia in all of you in this room. At least I'm cold. So, I have nothing to disclose, no conflict of interest or any financial interest related to this content. My basic overview and objectives for this talk is to try to review some of the data, and a lot of it's heavily weighted on the guidelines. And I'll explain why when we get to that. But I will give you some definitions. So, we're all talking about the same thing. Talk about how hypothermia and temperature management can, the mechanism of action through which it likely modifies outcomes after cardiac arrest. Talk a little bit about some population-specific, who it works for and why we think it works for them. Some therapeutic goals, including comparing the sort of two temperature ranges that are often discussed in the literature and in meetings like this. That would be 32 to 34 degrees Celsius versus 36 degrees Celsius. And then finally, give you a little bit of an overview of approach in case you want to introduce this and you aren't currently doing it. Particularly in places that might be resource poor. And some considerations for when and how to use it. So, beginning with our definitions, targeted temperature management is sort of a very broad term. That just means we're trying to control temperature, keep it at a certain range. This is often used within the literature, but not so much clinically because it kind of gets broken down into a couple things. Induced hypothermia is where we are taking action to control the temperature and usually bring it down to a target. Therapeutic hypothermia is what you hear much more often. It's the same. It is induced hypothermia. We are usually trying to reduce temperature to 36 or sometimes below. Now, if you're trying to use any method, whether it's pharmacologic or environmental, to just bring the temperature down to normal, prevent fever or hyperthermia, that is still targeted temperature management. It just doesn't fit into these other groups that are hypothermias. Protective hypothermia is a specific type of therapeutic hypothermia that I think is sort of relevant, but mostly to lab people or rat people doing rat research. Protective hypothermia, by definition, requires that we get temperature and control within 15 minutes of return of spontaneous circulation after cardiac arrest, which is really not a feasible target in humans in real life. So that's why you hear people talk about protective hypothermia, but it's really not clinically relevant at this time. Maybe get there someday. So how does cooling the body, the brain, parts of the body, how does that maybe serve to improve outcomes after cardiac arrest? And primarily what we know, and this is from cardiac arrest literature, but there's also a large body of literature looking at therapeutic hypothermia in neurologically injured populations, whether it's a stroke, traumatic brain injury. So there's a pretty good body of literature in all of these populations and some of the take-home messages. We know it slows metabolism. You can get as much as a one degree, for every one degree drop in Celsius that we can drop the temperature, we get a decrease in metabolism by 5 to 7%, which if someone has a struggling brain, either due to a brain injury or because the heart's not getting blood there, that can actually work well to save brain tissue and improve function. We know it decreases cerebral blood flow. It does protect the blood brain barrier, sort of keeps it firmed up so it doesn't get as leaky as quickly and decreases intracranial pressure, which can help particularly for a very acute swelling of the brain after a cardiac arrest or in these neurologic emergencies. At the cellular level, we believe it promotes cell membrane stability. So a lot of the cell membrane has a high lipid content. If you think about that Thanksgiving turkey and the gravy that maybe if after Thanksgiving you throw it in the refrigerator, it gets that nice hard layer of fat on top a couple hours later. That's sort of the thickening of the lipid in the gravy where you get kind of the same thing for cell membranes. That lipid membrane firms up a little bit so it's more stable and you don't get the same ionic flux in and out. We also know that therapeutic hypothermia decreases neurotransmitter. Production, in particular, it decreases glutamate, which is an excitatory neurotransmitter. So we're decreasing neurotransmitter, but also it decreases free radical production, which is really important after a hypoxic condition like cardiac arrest where the brain's not getting oxygen. So you get a lot of free radical buildup when we apply therapeutic hypothermia. We're decreasing that production of free radicals that's going to suppress inflammation and ultimately improve patient outcomes. We know it decreases apoptosis at the cellular level, so we have more cells surviving. And I want all my brain cells to survive if I ever have a situation like this. So the more we get surviving, the more brain we got functioning. We do, there is a considerable amount of literature that therapeutic hypothermia also increases functional outcome. It is partially about ADLs and just getting back to physical functioning, quality of life. But we also know it improves survival and improves actual brain functioning. There does seem to be, it does seem to be preserving cognitive function as well. So when we think about who we are using therapeutic hypothermia in, most of the literature on cardiac arrest has been in comatose adults with return of spontaneous circulation after cardiac arrest. A lot of this has been in the out of hospital arena. There is more literature exploring the in-house, the effects of therapeutic hypothermia after an in-house witness cardiac arrest. The important piece about coma is therapeutic hypothermia is not comfortable if you are the person receiving it. It's not something we typically do in someone who's awake and alert. It's best if someone's comatose, it helps prevent sort of some of the irritation. And then when they do finally wake up, they won't punch you in the face for making them so cold. Yeah, so it is also, as we're learning more about cardiac arrest, we know that we've looked in some other populations. It does seem to be saving brain if it's in or out of hospital cardiac arrest. As long as we get return of spontaneous circulation, ideally, the sooner the better. In kids, there has been more research coming out recently, and it, the evidence does suggest that in kids, who get, have cardiac arrest and return of spontaneous circulation, if we cool them, it does help improve outcomes. If we look far, far back into the infants and hypoxic ischemic encephalopathy, they've actually been doing therapeutic hypothermia for a while in these infants, and it really does help improve cognition considerably, which is really important because, you know, they're infants, so they have a whole lifetime. So, in addition to sort of knowing what patients to apply, we need to consider the ideal temperature, and there is a lot of literature around this area. How cool should we be making patients? The initial research was done looking at cooling someone to 32 to 34 degrees. And that was, so that sort of became, this is our target goal. And it did seem to improve outcomes in cardiac arrest, but other neurologically injured populations as well. Well, then subsequent studies started comparing that and looking at actually comparing maintaining temperature of 33 degrees Celsius versus maintaining the temperature at 36. And indeed, it was found not to be superior nor inferior. They seemed to be equivalent. So that's kind of what has led in the American Heart Association guidelines and most guidelines now. The class one evidence suggests that keeping the ideal temperature should be between 32 and 36 degrees. There is some evidence, particularly for kids, suggesting 32 to 34 degrees initially for the first 24 hours, and then maybe letting them get to 36 up to 37.5, which is normal. We don't want them hyperthermic. Or in kids, maybe we just stick with the 36 to 37, keep them slightly cooled to normothermic. In no instances do we want people to be getting fevers. So right now, the state of the evidence, there have been some subsequent studies published since the American Heart Association guidelines and the pediatric guidelines. But there's nothing still convincing to suggest that there are differences between maintaining 32, 34 degrees Celsius versus 36. So I think our evidence just isn't quite there yet to say one is better than the other. So you're probably OK using anywhere within that range. So that brings us to ideal timing. And what we know about that is, one, the literature about pre-hospital cooling strongly suggests it is not helping if the paramedics are trying to cool and get them in, and it may be causing harm. It may be actually having a negative influence. So the goal is really just to get them, one, return of spontaneous circulation as quickly as possible, and then get them to the hospital where we can start cooling, ideally getting temperature to target range within four to six hours as quickly as possible, and then maintaining it for at least 24 hours. After that 24-hour period, after cardiac arrest, we then shift the focus to just maintaining normothermia. So we don't want to keep someone hypothermic for more than about a day, but we also don't want to let them get fever or hyperthermic, which just increases metabolism and causes more problems. So in kids, we have less evidence. We don't have a clear ideal temperature. We think cooling is good. We don't have much on timing either. The recommendations are just not as strong. The evidence that is out there suggests 32 to 34 degrees for the first one or two days is probably helpful in maintaining brain tissue and optimizing outcome. After that 48 hours, shift to maintaining normothermia for at least three days and probably beyond. Fever's not good for any of us. Additionally, there have been another more recent review that says, or just keep them from normothermic to low-level hypothermia, that 36 to 37 and a half degree range for the full five days. Don't have clear guidance because we just need more research in that area. So regardless of the population or our target goal, temperature, or timing, we don't ever want to see fever in any patient who has a neurologic or potential for neurologic injury, whether it is post-cardiac arrest, stroke, or traumatic brain injury, adult or kids. Fever is bad. It increases metabolism, requires more energy use, and promotes actually more brain damage. So if you're thinking of cooling and you don't already do it, or maybe you do, but you want to know how the best way to do it is, there is some literature looking at different methods. I'm just going to give a very quick overview of the devices available. We do have intravascular cooling is sort of the most commonly used because it is the strongest. It cools quickly and it maintains the temperature in a tight range. This can be done in one of two ways. Old school, which I am, frankly, this cold saline, we would just keep saline bags in the freezer, hang them up, our normal saline, and give more fluid. We don't always want to give that much fluid. Now there are these internal cooling catheters, which are sort of best practice. These are central lines that go in. They have a, at the tip of them, they actually circulate cold water or a cooling solution and will cool the blood as it passes by. So you're not introducing additional fluid. So because of this, these internal cooling catheters get really fast cool down. So you get to target temperature rapidly and they keep the target temperature there. Most of these devices actually have a thermometer that will attach to them. So it can tell you what you can set it to keep your patient's temperature at 36 or wherever your ideal is. And that allows it to be very consistent. It maintains that temperature right where you want it. So that's your best bet. If you have the resources, they are expensive. If you maybe don't have those resources, there are a number of other ways. There is external or surface cooling where we cool the body or part of the body. You can do that. If you're really old, we used to try to do that. The days before they had all these devices, we used to try and do this with just passive air. We would have naked patients on the bed and just take off the sheets and run fans over them. That doesn't work very well. There are circulating blankets that can circulate air or fluid. Those work a little bit better. The gel pads, which you can see here, usually they look sort of similar to compression devices, but they are filled with a gel that's going to cool someone. They tend to be good for getting to target temperature and sort of keeping someone there. They're not as good as the intravascular devices, but they're a good second choice. If you are a neuro person, they do have this device, a cap that will cool just the head. I'm not sure that one works very well. I haven't seen it work very well in my experience. And then super old school, we just used to do ice water baths as well. Problematic, but it will get you there. It's just hard to maintain that because it takes a lot of manpower. So really what you want to try to do is the most advanced technology that you can afford. And it may be, if you can't go with the intravascular device, these gel pads are a good second choice. The others may or may not get you there. The passive air and bathing are thought to be inferior. So gel pads are probably the way to go. There is this newer technology. This device is still in research. It's still in trials, so it's not quite ready for primetime, but I think the evidence seems to be building in this area. It actually is a transnasal cooling method. So it circulates coolant oxygen mixture down into the nose and into the upper airways in the lungs. Thus far, the early evidence seems to suggest it is equivalent time to target temperature and suggests that maybe it can maintain. These patients may not need to be kept quite as sedated or comatose. So that's sort of what's on the horizon. So some of the pearls, if you're considering this and you don't currently do this, you do need to consider your resources. Some of the devices are costly, but they require less staff time. If you're trying to do the bathing or even the gel pads, they can require a lot more staff time because you need a person to do that. The gel pads, you can get skin breakdown. You just have to watch them and check them and change them. It is important to cool within hours, preferably four or less if you can get your patient there. It is vital to monitor your temperature continuously. Even with the intravascular devices, you don't want to overshoot and have your patient be below 32 degrees. You also don't want to be trying to keep them between 32 and 36 and find out that your device was malfunctioning and your patient's still sitting there at 37.5. It is important to try to maintain your temperature as tightly within the range that you choose as possible. Monitor for shivering. There are some pharmacologic as well as non-pharmacologic methods to control shivering. We do see patients shiver when they are cooled, even to 36. Sometimes you see that when shivering actually is working against your therapeutic hypothermia because it generates heat. If you are adding this, you need to consider drug efficacy. We know that hypothermia actually changes drug absorption, metabolism, excretion. So it is important. The guidelines give you some direction on that. There's also some references at the very end of this talk that will give you more references on what you need to watch out for. You need to continue to monitor other vital signs as well. Make sure we're not inducing bradycardia or other hemodynamic instability, which can rarely happen. Labs are important, particularly potassium. Hypothermia can cause potassium to shift into the cells. So then when we re-warm, the potassium shifts out of the cells. And if it's done too fast, it can cause some cardiac instability. So we need to re-warm slowly and then always prevent fever. And I would just, in summary, I think therapeutic hypothermia and temperature modulation are definitely beneficial for comatose patients. We do need to consider resources because not all facilities can actually use this, particularly with some of the more expensive devices. Cool in a few hours. Keep it for one or two days. And above all, save brain by preventing fever. And that is it for me. And we are saving questions. So I'm going to ask our general here to just bring up our next talk. So for the, thank you. For the third talk in this session, we have Jake Jenser, who is assistant professor and director of the CIC research at Mayo Clinic in Rochester. So he's probably kind of used to the temp in this room. He is going to talk to us about you have to go to the cath lab and coronary care. And coronary angiography after out-of-hospital cardiac arrest. Well, thank you so much for the kind introduction. And thanks to all of you for being here this afternoon. I would understand if you wanted to go outside and get some sunshine. But thanks for being here anyways. So I am a cardiologist and an intensivist. And so I have a little bit different perspective here. And I'm here to talk to you about one specific aspect of post-resuscitation care. I don't have any disclosures related to this presentation, although I did participate as a site PI in one of the clinical trials, which I'll talk about. But that was a nonprofit-funded trial. So I'm going to start by talking about the epidemiology of coronary disease in patients resuscitated from out-of-hospital cardiac arrest. I'm going to talk about coronary angiography and PCI, which is percutaneous coronary intervention, and their timing and how that relates to outcomes after cardiac arrest. And then I'm going to talk about how I select patients for coronary angiography after cardiac arrest. So coronary artery disease itself is probably the single most common cause of out-of-hospital cardiac arrest. And in studies of coronary angiography after cardiac arrest, up to 70% of patients have some degree of coronary disease. And in many cases, this is complex or multivessel coronary disease. Coronary disease is more common in patients with shockable rhythms. And so a lot of the research is focused on that aspect. And in patients who are resuscitated from an out-of-hospital cardiac arrest with a shockable rhythm, about a quarter or more have ST-elevation myocardial infarction, STEMI. And these patients almost all have coronary disease. And in the vast majority of cases, there is an acute coronary lesion causing the arrest. Even in patient populations without ST-elevation, coronary disease is very prevalent. About 2 thirds of patients, but fewer have an acute coronary lesion, somewhere on the order of a quarter to maybe a third. Now, in the refractory VF population, these are patients who are not immediately resuscitated after a few shocks and a couple doses of drugs. Those who are put on ECMO, supported, and then receive coronary angiography have very high rates of coronary disease and very high rates of coronary lesions, similar to an ST-elevation MI population. And there are a number of predictors of acute coronary occlusion, in particular, that it's relevant to know. And the reason that I focus on this is if you have an acute coronary occlusion, that means that you have a large area of myocardium that's going to be ischemic and that's going to become damaged if you don't open that vessel. And so these are the patients who are most likely to benefit from a coronary angiogram and from revascularization. So ST-elevation itself is very specific for acute coronary occlusion. The problem is that the other types of EKG abnormalities that we've learned to recognize, they're very nonspecific. They're also very common. And so as few as 10% or 20% of patients who've been resuscitated from out-of-hospital arrest actually have a normal EKG. And even in these patients, a significant minority have acute coronary lesions and even coronary occlusion. As many of you know, troponins are almost always elevated after cardiac arrest. And even in patients whose first troponin on presentation is normal, some of them still have acute coronary occlusion. So you can't rely on the EKG and the troponin alone to rule out the presence of acute coronary occlusion. Now, there are a number of other predictors. So the big ones that I've already highlighted are ST-elevation on EKG. That's probably the most specific. We know that a shockable arrest rhythm is a big predictor as well. And a prodrome of chest pain or angina before arrest is also highly suggestive. There's a number of other predictors that are not quite as specific. Obviously, if someone has known coronary disease, then yes, you know they have coronary disease. Also, specific risk factors like smoking or diabetes seem to be associated with acute lesions. Patients who have heart failure, either on examination or imaging, have higher prevalence of coronary lesions. Patients with brief arrests, a lot of times these are the one-shock wonders. They come back after a single shock for VF. A lot of them have coronary occlusion. Again, these other EKG abnormalities are associated with acute coronary occlusion, but they're just not that specific. Patients with high are rising troponins as well. And one of the tricky ones is a lot of times we'll do echo. We'll look for LV dysfunction. We'll look for wall motion abnormalities. And these are very common. But it's hard to know if they're new or if they're old. And so the predictive value is not quite as good. Now, importantly, just because you have coronary disease or an acute coronary occlusion, identified at coronary angiography, that doesn't necessarily mean that you're going to have a mortality benefit from PCI. I'm going to talk about why. The primary reason is, of course, that people die after cardiac arrest predominantly from brain injury. So when we look at large populations of patients with cardiac arrests, these are data from the Nationwide Inpatient Sample, we see that patients who are selected for coronary angiography are substantially more likely to survive. And when we look at more detailed studies and meta-analyses, this is a consistent message that patients who get early coronary angiography after out-of-hospital cardiac arrest have better outcomes. They're more likely to survive. And because most cardiac arrest survivors are neurologically intact, they're more likely to have neurologically intact survival. And these number needed-to-treat values of 3 to 4, honestly, they're too good to be true, right? You're saying that if you do three coronary angiograms, you have one neurologically intact survivor? I mean, even my interventional cardiologist colleagues don't believe that. But when you look at these studies, you'll find that the patients who get coronary angiography, they are different. They tend to have better arrest characteristics. They often have STEMI, et cetera. Now, when you look at patients without STEMI and also, to some extent, in patients without shockable rhythms, again, the same trend is seen, that patients who get coronary angiography have a lower risk of adverse outcomes and better neurologic survival. The problem is selection bias. These studies are all heavily confounded by selection bias, as are many observational studies in critically ill populations. Interventional cardiologists know how to select patients for coronary angiography who are going to do better. Now, maybe we all can do a better job. But the patients who get coronary angiography are consistently identified as lower risk patients. They would do better whether they got a coronary angiogram or not. And the reality is that the coronary angiogram itself is not beneficial unless the patient gets revascularized. If they get PCI of an unstable lesion, yes, that could have a benefit. But we actually know from the chronic coronary disease literature that revascularization of chronic coronary lesions, for example, stable angina, is not associated with a mortality benefit. And the same is true in cardiac arrest. Finding chronic coronary disease and treating it won't necessarily help your patient. It's really the acute lesions that matter. And in particular, there's several studies, and this is one of the best ones, showing that it's really the revascularization that actually drives the benefit of coronary angiography after out-of-hospital cardiac arrest. Now, these are data looking at long-term mortality and long-term survival, but the short-term survival data are the same. And what you see is that patients who get a PCI, they do the best, short-term and long-term. Patients in the middle group who got a coronary angiogram but didn't get a PCI, they do better than patients who didn't get a coronary angiogram until you account for the differences in their baseline characteristics. And once you adjust, all the selection bias goes away, and the outcomes are the same. So just squirting radio contrast into someone's coronary arteries doesn't help them unless you find something that you can fix. So this calls for the need for randomized trials. And fortunately for us, a good-quality, good-sized randomized trial was published last year. And this is COACT. And they took comatose patients with VT or VF out-of-hospital arrest who did not have ST elevation myocardial infarction or shock. And I'll tell you a little bit about why that is later. And they randomized them to either immediate coronary angiography as soon as possible or delayed coronary angiography after the patient woke up from their coma. And this was done in Europe. And so the population is pretty typical of European cardiac arrest populations. They have a high prevalence of witness arrest by standard CPR. Overall CPR durations weren't too long. But importantly, most of these patients had some ischemic EKG abnormalities. And what they found is that the prevalence of coronary disease was about the same as in all those observational studies, about two-thirds of patients. But notably, the patients in the delayed coronary angiography group received coronary angiography about a third less often. And that's because those patients who didn't get coronary angiography were the ones that didn't wake up. And in fact, the most common cause of death in this population, as in essentially all other cardiac arrest populations, was brain injury. Again, the rates of PCI, about a quarter to a third, are the same as in these observational studies that I was talking about before. Unfortunately, this study did not show any difference in 90-day mortality between the two groups. And they've actually shown in abstract form the later mortality, one year and beyond, which also wasn't different. If you actually look at the point estimates for mortality, the delayed coronary angiography actually did slightly better, which is probably play of chance. But there wasn't even a trend to benefit with early coronary angiography. So the question is, is this a definitive study? Does this answer the question once and for all? And the answer is no. But it does apply to a lot of our patients. And we should apply it in those proper subgroups. This was a very good study. This was a well-designed, well-executed study. And I think we have to trust the results. Importantly, this population, in most ways, was very similar to the patients represented in observational studies. This wasn't some weird, unique population where we wouldn't expect this to work. But importantly, they excluded patients with ST-elevation myocardial infarction or shock. And these are two of the populations we think are most likely to benefit from early coronary angiography. In addition, all the patients were comatose. So this doesn't apply to patients that are awake. But they didn't really talk much about coma severity. Now, I'm not a neurologist. But I know that not all comas are the same, particularly in post-arrest patients. And so they did not stratify their randomization or their results reporting based on the severity of coma, which I think would be important. Although they didn't include non-VF patients, I don't really know how much that matters because we think their prevalence of coronary disease is lower and their outcomes are worse anyways. The one thing that is very strange about this study is this study has the lowest prevalence of acute coronary occlusion in any study of coronary angiography after cardiac arrest. And because I've told you already that these are the patients we think are most likely to benefit, it does raise some questions. But I choose to be an optimist when I interpret this study. And I believe that the best way to interpret this study is that deferral of coronary angiography in hemodynamically stable, comatose, VF, out-of-hospital cardiac arrest patients without STEMI is safe. It will not increase mortality and is not associated with a higher rate of adverse events. It avoids delays in initiating targeted temperature management, which Dr. Alexander already told you is important. And finally, from a health economics standpoint, you avoid the need for the coronary angiogram in that third of patients who never wake up. The PERL study, which I was one of the site PIs in, was conceptually similar. It was smaller. And we also included non-shockable rhythms and patients who had mild to moderate shock. And we found, again, a higher prevalence of culprit lesions and PCI. But unfortunately, as you can see from these survival curves, there wasn't a difference in mortality between the two groups. The red is the early coronary angiogram group. And you can see that it's numerically better survival, but not statistically significant. So what do the guidelines say? The guidelines say that emergent coronary angiography is most appropriate for patients who've been resuscitated from cardiac arrest, who have ST elevation on their EKG, even if they're comatose. Also, if you have, for example, a STEMI-equivalent pattern, like a true posterior MI, that would apply. A slightly weaker but still strong recommendation is for patients with hemodynamic or electrical instability. And so these are the patients that were not represented in COACT. And we still think that they need early coronary angiography. Non-emergent coronary angiography. And again, the timing, a little bit uncertain. I used to think within 24 hours. Now maybe you can wait till they wake up. For patients with ischemic EKG changes, shockable rhythms, and other indications like LV dysfunction, higher rising troponins, or other strong predictors. But the big problem with making these decisions about going to the cath lab in the early phases, which is usually when the patient's in the ED, is you have to balance the likelihood that they have an acute coronary occlusion, which is what drives the benefit, and the likelihood that they have a bad brain injury that perhaps they won't survive. And that will prevent them from benefiting, because having an open coronary artery isn't going to prevent you from dying if you've sustained a terrible anoxic brain injury. Now there was a paper that came out a few years ago that talked about using known predictors of adverse outcomes after cardiac arrest as a way to identify which patients might not benefit from coronary angiography. And you can't rely on any of these individually. You have to have a combination of multiple factors. And you have to make a distinction between saying, I'm not going to do a coronary angiogram on this patient right now, and saying, I'm going to withdraw care. The latter is not appropriate. That's a very different discussion, and that's not at all what I'm saying. But we know from several studies that patients with multiple risk factors, like I've listed here, do very, very poorly. They're very likely to die of brain injury. And so it's less likely they're going to benefit from a coronary angiogram. As an example, there's a nice study from France where they took almost 800 patients, and they found that among the patients who had a non-shockable rhythm with an unwitnessed arrest and a prolonged resuscitation, and they defined it as getting at least three doses of epinephrine during resuscitation. There was not a single survivor out of almost 800 patients. So taking a patient like that to the cath lab, it's hard to think that's going to benefit them. There's a number of other adverse prognostic signs that many of you are familiar with. A couple that are, you have to be very careful when you apply, but are still important, is the early neurologic exam. So as I said, not all comas are created equal. And if you have a patient who's completely unresponsive to pain and doesn't have quite all their brainstem reflexes on their best unsedated neurologic exam, that's someone who's going to do poorly. It doesn't mean that there's no chance of survival, but it does suggest that maybe they're not going to benefit from a coronary angiogram. The same is also true with unresponsive patients with myoclonus. And I know the neurologist will tell me that there's lots of different types of myoclonus, and I'm very, very simple, but I know that if they have a bad coma and they have myoclonus, that's a poor prognostic sign. So this is a very important study, and this is from the University of Pittsburgh. What they did is they stratified patients by their coma severity and then looked at the influence of coronary angiography on survival. Overall, across all patients, coronary angiography was associated with higher survival. That was true in patients who were awake, who didn't have a coma, and patients who had a mild coma. These are patients who had either some motor response to pain, or at least they had all their brainstem reflexes. But when you look at the patients who had a deep coma, these were unresponsive to pain and didn't have all their brainstem reflexes. They had very, very poor outcomes. That's less than 10% survival, and there wasn't a benefit of coronary angiography. So I think this demonstrates that the neurologic injury alters the ability of coronary angiography to improve outcomes. So how do I select patients now that, you know, with all this data, putting it all together? So first of all, you want to exclude non-cardiac etiologies. You're not going to do a coronary angiogram in a patient with PE or drug overdose, right? Now, the first question is, do they have STEMI? If they do, you bring them to the cath lab unless there's really significant extenuating circumstances, maybe a no-code status or hospice or something. If they otherwise are hemodynamically or electrically unstable, then again, you're probably going to bring them for a coronary angiogram. Now, remember that not all shock after cardiac arrest is cardiogenic shock, so you have to be a little bit thoughtful here. If they don't have either of these strong indications, then the next question is, are they awake or not? If they're awake, I'm much more likely to bring them to the cath lab because I know they're not going to die of brain injury, and I know that they have much more potential benefit of a coronary angiogram, so my threshold's much lower. If they had a VTVF arrest and they're awake, I bring them to the cath lab. It's very straightforward because you're going to be asking questions later about defibrillators, et cetera, and you want to know the coronary anatomy. Likewise, if there's other reasons to suspect an acute coronary syndrome or a coronary disease is the trigger, yeah, I bring those patients to the cath lab. And if they have none of these factors but they're awake, I might let the dust settle, do further evaluation, and then consider whether they may need a delayed coronary angiogram. On the other hand, if they're comatose, I try and do some sort of assessment of the depth of their coma. And if they have a mild coma, meaning maybe they have some motor response, maybe they localize or have spontaneous movements or at least respond to pain, and then they don't have a lot of these adverse prognostic signs, I would consider bringing them to the cath lab if they had VTVF arrest or suspected acute coronary syndrome. Doesn't mean you have to because the COAC data would imply that you don't have to, but I would certainly at least consider it in the right patient. Otherwise, you could defer until they wake up. On the other hand, if they have a deep coma where you're seeing multiple adverse prognostic signs, I would not bring that patient to the cath lab. I would wait. I would cool them, let the dust settle. And then if they awaken, then sure. Then you're going to evaluate them for coronary angiography at that point in time. So I'm going to finish with one sort of semi-related slide. Now, eCPR, it's its own talk. But it is important because it emphasizes the role of the cath lab in cardiac arrest extends beyond just looking at the coronaries. So what is crucial to understand is that this is a bundle. Trying to just do one component of this bundle is not good enough. You have to get people into the cath lab quickly, which means that you may have to transport them before you get return of circulation, in essence, by definition. And the way to do that is mechanical CPR. So you start within the field. If they have VF and you can't get them back after, say, three shocks and a dose of drug, then you put on the mechanical CPR, bring them to the cath lab with lights and sirens as fast as you can. Then cannulate for ECMO. Start the ECMO once you have circulation restored in that way. Then you do a coronary angiogram. And after that, you cool them. And this is the way they do it at the University of Minnesota. And they are the leaders in this. And they're phenomenal. But you need to remember that they have been practicing for years to get the EMS crews to collaborate and to get the best system of care possible. And they were doing that for years before they even started the ECPR program there. So if you want to do this in your own shop, you need to have a really good multidisciplinary system involving all the links in the chain of survival, particularly your EMS crews. And you need to make sure to avoid any delays because every minute delay is brain cells you're losing. Importantly, if you're starting up an ECMO program, this is the hardest one to do. And these patients have the worst outcomes. If you actually look at patients who can't be resuscitated but are put on ECMO and you compare their outcomes to patients who are resuscitated but then have severe shock or recurrent events, they do worse. So this is, I think, the way of the future. I know these guys are doing a randomized trial, which will demonstrate if this is as effective as we think. So in summary, coronary disease is the most common cause of out-of-hospital cardiac arrest. Early coronary angiography may reduce mortality in appropriately selected out-of-hospital cardiac arrest patients, particularly those with ST-elevation myocardial infarction or those who are awake. Revascularization drives the benefit of coronary angiography, and so identifying patients who need revascularization is one of the things you want to think about. And brain injury mitigates the benefit. So patients who have a bad brain injury are probably not the ones you're going to want to bring to the cath lab. And I, at this point, am doubtful that all stable out-of-hospital arrest patients who are comatose, who don't have STEMI, need to be brought immediately to the cath lab. I think there's a subgroup that does, and I don't think that we yet know exactly how to identify those patients. Thank you so much. All righty. So we actually have some patient cases. These are real patients. And I'm hoping that the other speakers and moderator can come join me. And we're hoping to have this be as interactive as possible. We have some images. We have EKGs, cath films, echoes, things like that. And so please, there's a big room. I see a lot of people are sitting in the back. If you're able to come up front, you'll be able to talk to us. And we'll be able to talk to you. And we'll be able to talk to you. are sitting in the back. If you're able to come up front, you'll be able to see some of these images better just for your own benefit. And it might make it a little more interactive. So you're welcome to join us up front. All righty, so without further ado, I'll get us started here. So the first patient vignette I wanted to tell you about is a patient who I took care of when I was a fellow, an 86 year old gentleman with a VF out-of-hospital cardiac arrest. So he, we didn't know much about his history. There was something on his chart about coronary disease, had some risk factors, and a right bundle branch block. He was doing yard works. This is a pretty robust guy, and he had a VF arrest that was witnessed. He got bystander CPR, a couple shocks by EMS, and was intubated in the field. I think overall he got maybe 12 minutes of CPR or something like that. The medics found him after resuscitation to be hypotensive and bradycardic. They actually started him on norepinephrine as well as transcutaneous pacing and transported him. In the emergency room, he was comatose, had adequate blood pressure, but was needing the pacing and the norepi. Lactate was a little bit, a little bit elevated, but not too bad. CTA was done. It was negative for pulmonary embolism, and his first troponin I was mildly elevated, you know, a couple times the upper limit in normal. So the first EKG, I hope you guys would, again, I wish this projected a little better, other than the lack of reading and lead V1. What you can see here is that it's a sinus, it's a sinus tachycardia as the underlying rhythm, but he has a significant heart block. And so you can see that it, you know, you might call it a four to one or something along those lines. And they repeated the EKG, and it looked quite a bit better. Now, if you actually look at this real closely, you can see that he actually is still in two to one AV block. But let's see, two to one is twice as good as four to one, so at least there's that. But as a cardiologist, I don't really see any ST elevation here. I don't see much in the way of ischemic changes either. So we did a, we did an echocardiogram down there in the ER, and there's a parasternal short axis view. And as I hope you can see, the anterior wall, and really extending out beyond that, is akinetic. There's significant alvetis function. I'd say, you know, basically this part of the heart doesn't do much, and this part's better, but not great. So this brings up the question, would you take this guy to the cath lab? Now, of course, you know, I just gave you this long lecture about how you should take people to cath lab, and this guy kind of maybe falls in between some of the different, falls in between some of the different criteria. So I'm gonna ask my panelists what they think, and then maybe get a show of hands. I hope that's okay. I would ask if he has a living will, for starters. He's 86, right? Yeah, no, he doesn't have any living will or no code or anything like that. He was otherwise healthy. So any particular question you have for me? Well, what do you think? You know, if you were in the ER, would you push for him to go to the cath lab? Yeah, so I'd call a cardiologist down and see what they want to do. So first of all, I mean, the guy's 86, but he's doing yard work, so I throw out that kind of criteria, you know, that in this particular situation, and so on. And just as an interesting thing is that over, in over half the cases of cardiac arrest cases that we resuscitated over the years, like when I was in Seattle and Houston, we found no evidence of heart muscle damage whatsoever. It was a primary electrical event, you know, ischemic area. But it doesn't, but the thing is, it could be worthwhile looking at it in this case because they may have not had enough time to have heart muscle damage under these circumstances, and you got your anterior wall out. So I don't know. I'd ask them to do it. I'd be looking into doing it. So, all right. So I'd ask their opinion. Luckily, you're sitting next to a cardiologist, so we'll see what he says. Yes, indeed. So I, you know, I'm voting yes here, too. I've got an 86-year-old guy doing yard work, so he's functional this morning. He's got a wall motion abnormality on his ECG. The rest of it pumps okay. It might be worth saying that I care not at all what his neurologic status is right now. It's early, and you really don't know a neurologic prognosis. So this guy is quite likely to have a lesion that is worth doing, and I think I'd take him to the lab. Should we take a vote? I have one extra commentary on that. The other extra commentary is that, you know, the EKG is evolving to better, but it was slowly coming back to a kind of a more normal EKG, which tells me that there is something still there probably causing a problem. So that's why. How about a show of hands? Who would take this nice gentleman to the cath lab right then and there? Well, good. It sounds like I'm going to skip the rest of my slides. All right. So I did a little pro-con here, which I'm going to do for several of the cases. So this is a VFRS, and I already told you that, you know, it makes you a little more suspicious. The AV block itself may not necessarily be a sign of coronary occlusion, but you might choose to put in a pacing wire, a temporary pacemaker, which would send him to the cath lab anyways. Might as well get a coronary angiogram while you're there. He does have some shock, and he is requiring vasopressors. And so that, you know, he's hemodynamically unstable. And of course, he has those impressive regional wall motion abnormalities. Now that being said, if you're not a true believer in cath, he doesn't have any ischemic EKG changes. His first troponin I was quite unimpressive. He is 86, and even though he's a good 86, he's certainly not 66, and you don't know much about his neurologic status. But it sounds like we all are in agreement that we were going to bring him to the cath lab, which is what we did. And he had horrible coronary disease. So again, not all of you are very familiar with coronary angiograms. We call this a spider view. You're looking basically through the heart right up at the left main. This is the coronary sitting in the left main. You have your LAD and your circumflex, which are your two major branches. And if you look at this part right here, where they all join together, you can see very, very severe narrowing of that branch point. And so this is an incredibly high-risk coronary lesion. Actually, in this case, it turns out that because of some of the uncertainty, what they did is they put in a balloon pump, and they actually waited to do PCI, but they eventually did PCI. And I'm not saying that the balloon pump is or is not the right answer here, but just, you know, full disclosure, that's what happened. So in the end, he actually woke up, was neurologically intact, and he had, you know, 86-year-old patient in the ICU, as you know, often develop some complications. He had this aspiration pneumonia, etc. But he survived to leave the hospital. And so I think we agreed that, you know, this was a good outcome, and I think we were all... But the irony is is that it's hard to know exactly how much brain of the cath lab influenced things, because he didn't actually get revascularization immediately. He had a delayed revascularization, but it seems like it was the right thing to do. All right. So I'm gonna take this opportunity to point out that we've got a microphone here and a microphone over there, and we'd love if somebody would come up and render an opinion, ask a question, otherwise, just tell us who you are and where you come from. Yeah, please. William Bailey. I'm from Pensacola. You know, the only thing that I saw here that made Cath not seem favorable to me wasn't his age. He's active. He's out in the yard. But you have no idea of his neurologic status. If he had a bleed, you're gonna be on dual antiplatelet therapies. If you would have found an LAD lesion, you would have stinted it in a second with a drug-eluting stint, and then possibly complicated his recovery. It's a very important question. I know that there's a lot of controversy and differences of opinion about whether patients should all have head CTs before they go to the cath lab. I think that there are people who believe that, people who strongly don't believe that, and you know, I think there's some... But it's an important question, and I can certainly say I've been burned by that before. It's a point, I'll give you freestanding bias, which is that the incidence of a substantial head bleed without a focal neurologic exam is very low. So if you have a focal neurologic exam, then you got to worry in this and that. And if you don't, I guess I don't personally believe that everybody has to go to the cath lab just because the possibility they might have a bleed. But your mileage may vary, and there are certainly cases where you wonder, they do have a bleed, you wonder whether you missed something on neurologic exam, or whether it's just one of those things. There are a number of ways for it to go bad in an 86-year-old. We're agreed on that. And for what it's worth, there actually is some data that patients who go to the cath lab early and urgently do have a higher risk of cath-related complications. So it's safer to go later if you are safe to wait. Well, you think you've been standing longer? Please. So that last case illustrated a beautiful point, which is the power of echo or point-of-care ultrasound. Was any of that covered in the trials or talked about in the trials you mentioned in terms of how we stratify which ones are actually actively ischemic? It's certainly a tool we've been using more of. Cardiology colleagues seem to find it very helpful, and I think it might be heavily influential in how we decide who's going and who's not. It's a really good question. I don't believe it was used in any of the trials, and in fact, the last time I looked at the literature, which I want to, I have to admit, wasn't this year, I saw very few, if any, decent studies looking at whether or not the echo was predictive. And the real problem is echo can rarely, if ever, tell you if something's new or old. And we know that chronic cardiomyopathy is one of the leading causes of cardiac arrest. We also know that there's post-arrest stunning of various forms. And so it's really, I personally think it's valuable, and I think that, you know, Dr. Hollenberg clearly, you know, thought that that was an important component of his decision-making. But you can be burned on either way. Right, I agree completely and also specific but not necessarily sensitive. So if you see it, you know it's there, but if you don't see it, you're not so sure it isn't there. And so I think it's a useful adjunct to answer the straightforward answer to your question. Is there any study of this? No. Thank you. All right, please. Conor and Myler from Penn State. My question was, I may have missed it. I didn't understand the reason for the delay for the PCI in the stents. Was it because they were thinking about doing a cabbage in this 86-year-old guy? No, I think it was a neurologic thing. You know, he was, at the time, he had stabilized with the balloon pump and they felt that with the uncertain neurologic status, they wanted to wait a little bit because it also wasn't going to be an easy approach. It wasn't necessarily the kind of thing you wanted to do at 3 in the morning if you didn't have to. But that is a tough lesion. That's a left main lesion. You know, Jake told me about this case. This one was a Y technique with a crushed stent. This is a big lift for an interventional. So it wouldn't be entirely unreasonable to stabilize and to get a surgical opinion in this setting. How to stabilize with a balloon pump is the right way to do that is a story for another day. Let's do one last question or comment and then maybe we'll do the next. Yeah, the key thing was the neuro thing. And I really looked at this. There's a lot of people who really just give up on people right away. And particularly in this case, I don't know if we got the cooling done or not, et cetera, which I still do. Sometimes we don't know. But you can pretty much tell in the first few hours if you're not cooling. And I don't think it was done in this case. You did? All right. Never mind. But I was going to say, I can predict your pupils will start reacting within an hour or two. They should. And you'll see a progressive improvement neurologically. If they don't, they make some improvement in the first 24 hours. It's a really good sign. If they don't make any in the first 24 hours, that's a really bad sign. So, but with cooling, that changes the game a little bit. Thanks again for your talk, Gary, from Duke. And we've talked a lot about out of hospital cardiac arrest. I was wondering, as someone who responds to rapid response calls, and some of these are code blues and they're not all PEs. You know, just, it's a very common source of anxiety for me in which of these patients who don't have, they have nonspecific ST changes on their EKG. All their troponins, you know, the troponins are going to be elevated. We're using the high sensitivity now, so they're all elevated. And it's just really, you know, kind of a stress provoking area. And if you could comment on that kind of a scenario, I'd appreciate it. So, that's unfortunately, the question that I'm hearing is use of coronary angiography for in-hospital cardiac arrest. So, it's an area that, as far as I know, hasn't received much, if any, attention in the literature. It's certainly important. I would say that if a person is admitted with a cardiac problem or has other evidence going on that suggests that they're, you know, truly having a coronary event, again, a VF, for example, then I think I'd be much more likely to do it. I think, you know, as you know, it can be very hard to pin down the cause of the in-hospital arrest, but many times it has to do with respiratory things and aspiration, et cetera. And so, I think you have to use your judgment. You can use the same kind of an algorithm. You know, do they have ST elevation? Do they have, you know, was it a VF? You know, are they in cardiogenic shock? You know, those are, I think, going to be good no matter what type of arrest you have. But I think that the, and certainly if you're on one of the cardiology wards, you know, you may have a bias there. Another question? Yeah, I mean, I would agree with that. I think the thing about it's not well studied. To my mind, I have a bias toward going to the cath lab because you can get there very fast compared to, right? You know you had your in-hospital cardiac arrest. You can get that artery open quickly if you need to, but you know why they were there. So, if there's something that point, you know, about comorbidities, at least hopefully you can figure that out relatively quickly. So, unless there's some reason, you know, unless they're 115 and have four forms of cancer and this and that, if it came out of nowhere and they were just sitting around, and it is in the PE, and, and, and, and, actually a pretty good setting for a point of care ultrasound test. My bias would be to go more often than then because you know you don't have a big, long downtime. Please. Yeah, it's Pedro Salinas from Milwaukee. I'm just curious. I know this is a long, you know, topic, but I'm just curious to know, like, at your institutions, are you doing 33 or 36? Very tricky question. So, I think, I think we're actually participating in the TTM2 study, but otherwise our bias is usually 36, although sometimes I decide to get funny and I say whatever temperature they came in at, let's leave them there. I have no idea if that's good or bad, but, you know, and when I was there, they were doing 36 mostly. We do. For cardiac arrest, it's 36. For some other populations, we often go a little deeper. So, I'm in a post-op heart unit, so we use 36 as well, mostly because, sort of two reasons, bleeding risk and bleeding risk in the notion that you're about to do dual antiplatelet therapy plus minus mechanical circulatory support with the need for anticoagulation. So, the notion that there's a little more bleeding at 33 than 36 tends to tip the balance, but your mileage may vary depending on where you are and what your biases are. So, my bias is based on knowing a lot of the systems that did the different trials. And in some cities, you're not going to see any difference because the response is so good, a lot of bystander CPR, that you'll get, you'll say that, oh, we didn't see any difference between 34 and 36. I think in other areas, other settings where they had more profound injury is that, and I tend in those populations maybe to go a little deeper, even 34 or whatever, and actually extend it for a longer period of time than, say, 24 hours, et cetera. So, it depends. It's my answer. Okay? All right. I hope it's okay if we go to the- But I agree with yours about what you were saying about the coagulopatase. I'm sorry. Yeah. I hope it's okay if we go to the next case. Very different kind of case. Yeah. So, this is a young patient, 37, had a non-shockable out-of-hospital arrest. He's got, you know, all over his chart is this, you know, substance abuse concerns and issues like that. Basically, his girlfriend, you know, came back from the bathroom and found him, you know, apneic and pulseless, did not perform bystander CPR. Medics found him in asystole. They gave him epinephrine, naloxone, got ROSC, had a pretty prolonged downtime in the field and was intubated. In the emergency room, he had another arrest. This was a PEA arrest this time. Again, no shockable rhythms during this. And then this time, he had return of circulation after more epi and some calcium and was in shock, needing epinephrine infusion at a fairly stiff dose, as I recall. Ponicare ultrasound ruled out tamponade as the cause and he was quite comatose. Now, his initial blood gas, as you can see, is quite deranged. pH 6.88, PCO2 72. This is the bicarb was 13, base excess negative 20. And his lactate was almost 13. Potassium was up. His first troponin was quite elevated. So for those of you who aren't using the high sensitivity troponins yet, normal is six. So this was 100 and some odd times the upper limit of normal. Now, his first EKG, as you can see here, is grossly abnormal. So he's bradycardic. You're not really seeing P waves. This is kind of a junctional rhythm with this really impressive STT abnormalities here. If you like to look at lead AVR, which I suggest you do, you get the impression that there could be some elevation there and maybe V1. So this is clearly a grossly abnormal EKG. Well, what do you do next? You're there in the ER. You got this guy. He's sick. How many people here would say these are bad enough EKG changes? You take him straight to the cath lab. Do not pass go. Do not collect $200. Anyone? Any takers? Okay. Who would take this guy to the CAT scan or as your next step? You know, he's comatose. He had this weird event. You're not sure what's going on. Any takers for a CAT scan? Okay. All right. Many more. Well, he's bradycardic and on epi and all this stuff. Who would, you know, maybe do some more medical treatment, give him some atropine and try some temporary pacing to see if that improves his shock severity? Okay. All right. So people think that's another reasonable option. And how many people don't like any of those options, but maybe try something different? Any other, any takers? Okay. So, we'll get there. We'll get there. I promise. And so, so in this case, again, several of these options are probably reasonable. I think that my personal bias is that I would have done something else. And this was actually not my case. So I feel, I feel fairly justified in criticizing it in front of a wide audience. So, all right. So we gave him some bicarb, right? The guy's got this horrible acidosis, a bunch of crazy electrolyte stuff. And then lo and behold, his EKG does not return to normal, but clearly changes in a dramatic way. The ST stuff goes away. The bradycardia goes away. You're now seeing P waves. And so, I just want to emphasize, I want to stop to emphasize that the first post-resuscitation EKG often looks really gross. You guys have all seen it. And that's in the setting of, you know, the person just gotten pounded with all sorts of horrible things, and they have this metabolic disarray. And the metabolic disarray itself can make the EKG look really bad. Usually not ST elevation, but almost anything else. Okay. So now the question is, he had these horrible-looking EKG changes. He has this unexplained arrest, and you're not sure what's going on. How many, how many, I'm going to ask my colleagues here if any of them have an opinion. They chose not to render an opinion last time. But who would bring this guy to the cath lab? Let's just do a show of hands, including my panel here. Any takers for intracoronary iodine deficiency and treating it directly? A little bit of, a little bit of x-ray added on? No takers. Okay. Okay. Well, I could see, I could see kind of both sides of this. And like I said, this wasn't my patient. So, I feel perfectly justified in criticizing them widely. So, he had these really marked EKG abnormalities. Just very ugly looking. He was in shock. You know, the guy's really sick. He did have recurrent arrests. And his troponin is real high. I told you it was 700 and some odd, which is very high. Again, this wasn't a VF arrest. So, it's a different kind of beast maybe. We think maybe he's, there's a drug overdose or something. We're kind of suspicious. And then all this metabolic stuff is going on, which kind of makes your EKG a little bit less accurate. And you're pretty worried this guy's not going to do well. He had a long arrest, multiple events, et cetera, et cetera. And he's deeply comatose. So, that being said, he went to the cath lab. And probably didn't help him too much. As you expect for a 37-year-old guy, normal coronaries. And unfortunately, had they listened to you guys and done that head CT first, they would have seen severe anoxic injury, which is, you actually don't see it very often. It's only maybe 20% of patients truly have brain edema, loss of gray-white differentiation, But when they have it, it's a really bad prognostic sign. And it was in this patient's case. I don't know if he actually progressed to brain death, but he certainly was close. And he unfortunately didn't make it. And this is a reason why not everyone needs a cath, is that if you die of brain injury, cath won't help. I have comments already. Please, sir. Not on this one. So, if you'd like to finish up, that's fine. Oh, that's OK. OK. Well, I'm Nano Salgado from Wichita, Kansas. And just like you have these in-between cases, that you're not really sure what to do. The same thing for hypothermia. I mean, we get a lot of calls. And it's like, well, from what they describe, it could have been a respiratory arrest. And then when they get there, they find them in V-fib. Or first rhythm is a systole. Then they go into V-fib. Or patient is, you know, got intubated. And so they sedated and paralyzed because he was starting to fight. Now you can't do a neuro exam. How strict are your protocols for sticking to the indications for hypothermia, if that makes sense? So, I was trained at University of Pittsburgh. And the way that it was explained to me by Cliff Calloway, as well as many excellent colleagues, was if you're going to provide critical care for the patient, adding hypothermia to the rest of critical care isn't a big deal. And it might be beneficial. And as long as you can do it safely, you might as well do it. And so that's kind of the way that I practice. And so that's why I will still cool a lot of patients with non-chockable rhythms. There's a new trial which says that's probably justified anyways. And I'll cool in-hospital arrests, again, if they're candidates for ongoing critical care. So I try not to quibble about it too much. Because best case scenario, the patient wakes up in the middle of cooling. You stop, and then everyone's happy. It's not like anyone's going to be sad if the patient wakes up and you have to abort cooling. That's kind of my bias. I don't know what my panel thinks. I would say same. Generally, therapeutic hypothermia, just be careful. You need to do a lot of monitoring. But it's very safe and probably efficacious. But it's not going to hurt somebody as long as you keep an eye on things like labs and coagulation and rhythms. So yeah, I mean, I'm fairly permissive, too. The downside is that it prolongs the time to an accurate neurologic prognosis. Because you've got to do it for 24 hours. Then you have to wake them up. And then it's not even entirely certain that at 72 hours, you can make an accurate neurologic prognosis. So it does prolong things. But that said, if otherwise doesn't seem unreasonable, we tend to be permissive trial eligibility notwithstanding. Thank you. All right. Super. All right. Well, I have another case that I think has a little bit different spin, hopefully. So I have a 50-minute question. Wait for a question. Go for it. Oh, please. I wasn't sure if you were just joining us at the front. My name is Esther. I'm from Robert Wood in New Jersey. So just going back to the TTM portion of it, what does your institution do in terms of pharmacological management of shivering? Because our institution, we do continuous infusion of paralytics. I'm just curious if you guys did pushes. That's one question. Second question is, in terms of patient going on ECMO post-cardiac arrest, and then we then decide to cool them, we use pads for cooling because adding another line in there when you're on ECMO is kind of traumatic to the patient's body. But how do you guys manage rewarming? Because most of the time, the ECMO circuit is on a heater-cooler type of thing. So just those are my two questions. The second question, I guess, is easier than the first. My understanding is the best way to cool and rewarm a patient is ECMO. In fact, there are studies of using ECMO for treatment of near-fatal hypothermia. You put them on ECMO, and you warm them up. So I actually am not aware of a lot of places that even need the cooling pads. Everyone's different. Part of the ECMO circuit is the temperature management system. Put some ice in the water bath. Rewarming is very specific. You've got to do it slow. So how do you manage that on the heater-cooler? Because then you have to manually dial it up. Literally what you do is you press the buttons. I don't mean to make light of it, but unfortunately, that's probably the simplest way is just to increase the degrees by whatever it is. As far as the first one, there's a lot of controversy about the best way to manage shivering. And I think what is the good recommendation that I can give is each hospital should talk about what they think is the best protocol and then follow a protocol. Almost any sedative medicine that you use can work well. I know there's some data that, again, the guys at Pitt did that show that dexamethamidine can actually work very well for shivering, but opioids, benzos, propofol all work. There is some older data that suggests that people who get pharmacologic neuromuscular blockade have better outcomes. Unfortunately, it's a little bit of a murky area. I personally have a low threshold to use neuromuscular blockade, but I always make sure that I've adequately sedated and tried all the other stuff first. There's some adjuncts people use, like BuSpar and stuff. I don't even know if that works, but a lot of protocols include it. We use it. I would argue against a routine neuromuscular blockade. If you want to do neuromuscular blockade because you can't control shivering with other measures, that's one thing. But the idea that everybody has to have neuromuscular blockade means that you then have to sedate everybody heavily enough to make sure that you are confident that they are not feeling, et cetera, et cetera. And now that stuff in hypothermia is going to take a long time to wash out. And so now, three days later, in addition to not being sure about the timing for prognosis after hypothermia, now you've got to be sure that this stuff isn't washing out, shock liver, et cetera, et cetera. So you do it when you have to. But I would argue against trying a protocol that does it routinely. The only thing I would add to that, because I pretty much agree with you, I'm an old nurse. And when we first started doing therapeutic hypothermia, one of the things we used to do that is still used often by nurses at the bedside is just try to warm the hands and the feet, the most peripheral point. And sometimes that will soothe the shivering. So it's a good first line, which means you don't have to use any drugs. So I think that it's sort of distal surface warming, but sometimes that can really calm the shivers too. All right. Good recommendation. All right. So another case here is a young gentleman, 51, with a VF out of hospital arrest, previously healthy or at least no prior doctor visits. He unfortunately had a witness out of hospital arrest during intercourse, had bystander CPR by his wife, was found to be in VF by EMS, was shocked, and initially was transported to the ED. And again, as I recall, I think they actually transported him with CPR in progress and did not get ROSC until he got to the ED, or at least they didn't know whether he had ROSC or not. Maybe he did, and they just didn't find out. So then unfortunately in the ED, things didn't go well. He had a series of recurrent arrests. So he had some stability, and they were able to get sort of a neuro exam, and they were able to get an EKG, but then he had more arrests. And overall, the CPR duration was starting to push towards 40 plus minutes, needing quite a bit of support in the ventilator. The EKG that they got, I wish I had it here, but it got lost in the shuffle. It was massive anterior ST elevation, like 8, 10 millimeters, something that a medical student wouldn't miss. So the question is, this guy is now arrested again in the ED. What do you do now? And so we have a couple of potential options. One is just keep doing manual CPR. You know, if it ain't broke, don't fix it. Send him to the cath lab. Well, maybe we shouldn't be doing manual CPR. We should do mechanical CPR and send him to the cath lab. Maybe we don't even have time to bring him to the cath lab. We just need to put him on ECMO in the ED. You know, we don't want to lose any more time. Or after this kind of bad story, you know, multiple arrests, prolonged downtime, et cetera, et cetera, maybe this is futile. Maybe we should actually stop. So let's go. What do you think about manual CPR in cath lab? Who's any takers for that? All right. How about mechanical CPR in the cath lab? A few more for that. How about just straight up ECMO in the ED? Don't mess around. Do not pass. Okay. All right. And who thinks this guy is cooked and they don't think that deploying advanced therapies is warranted? Okay. So we obviously have a multitude of opinions. So one of the questions, of course, is do you cath a guy like this? You know, I think a lot of things are pointing towards being in favor of cath. He's got VFRS, ST elevation, cardiogenic shock, he's young to comorbidities. I think that kind of held the day. But then again, there was a number of reasons to suspect this guy might not make it even with a cath. He had all these, you know, multiple arrests, prolonged downtime, et cetera. You know, certainly you don't know anything about his neurologic status, but it's probably not good. He was needing some, I think I left off the fact that he was needing pressers, but he was on high dose pressers, you know, epi drip at 0.3 per kilo or something. He was a big guy. And again, had pretty severe respiratory failure. And so in the end, they actually did mechanical CPR and brought him to the cath lab. And part of the reason was, you know, he was in and out. So it wasn't like he, you know, he sort of had some, you know, recurrent arrests, recurrent frosk. And so they did that and they brought him to the cath lab rather than doing ECMO. Honestly, probably more because he was stable enough to bring to the cath lab and they knew they could do it in the cath lab if they had to. All right. So this was kind of an interesting case. So he's got bad coronary disease. This is a different view. And I apologize if you can't see it that well, but I want to just emphasize these are ratty looking coronary vessels. This is circumflex down here. It's just kind of ratty. And then the LED should come down here. You see sort of the beginning of it, but it doesn't, it should go all the way down there. And you really see that it's, it's missing. And they tried it this for a while thinking, well, gosh, ST elevation is probably a fresh MI. Of course, that's what's going on here. Turned out that it probably was more of a chronic occlusion. And so he, it may have actually been that he had ST elevation from demand, which you don't see every day, but can happen. If you have an occluded vessel and a high level of demand, then you can get transmural ischemia from the demand. And that is what I think happened here. And so, so that's, so they weren't able to actually revascularize him. But, well, they haven't done anything useful for him yet and he's still in bad shock. So now what do you do? Do we just stick with the drugs he's on? I mean, he had an okay blood pressure on a bunch of catecholamines. Any, anyone who just would stick with medical therapy? It's never been proven to be beaten yet. Anyone, medical therapy? Okay. What about a balloon pump? I mean, we've been doing those for years. That's easy. I mean, so easy I could probably almost do it. Anybody? Not so much. Okay. How about an impella? I mean, if you're going to spend as much money on a medical device as you do on your car, why not have it be an impella, right? Okay. All right. We got a couple people do that. And now, okay, for those of you who didn't already want to put him on ECMO, who wants to put him on ECMO now? All right. So we got some takers. All right. So I think that we consulted our ECMO team and they felt that with the unknown neurologic status and the downtime and this and that, that they did not feel that he was a candidate for ECMO. And we actually placed an impella. So this is the impella CP, which is the one that goes from the, which is usually placed from the femoral artery. You can see it coming up from the bottom of the, of the view. And so for those of you who haven't seen a whole bunch of fluoros here, you see that this is the, this little pigtail keeps the device in the left ventricle, which is right here, keeps it from bouncing against the walls too much. This is a blood inlet port. Then the blood gets drawn here into this device in, from the ventricle. It gets sucked through this catheter housing and it gets pumped out here in the aorta. And here's the motor. And so that's, so the impella is a continuous flow pump and it really just brings blood across the aortic valve. Now for what it's worth, he got quite a bit better hemodynamically after the impella. So I think we could have argued that maybe he didn't need the ECMO anyways, cause he did okay with the impella. The pro, and so he, you know, his shock stabilized. I think he maybe needed a little bit of dobutamine or something, but really much better. Eventually got the impella out. Unfortunately, he didn't wake up and ended up having a bad anoxic brain injury and didn't make it. You know, I think this case, this is a tough case, as you can imagine, you know, we're all fighting for this young, you know, otherwise healthy guy. But it, you know, it's one of those examples of you can, you know, try and do all the right stuff, but sometimes people don't make it. And if you actually look at the randomized literature for the use of the impella, what you'll find is that there actually isn't a difference in mortality with an impella device like this versus a balloon pump. And there's not a difference in mortality with a balloon pump versus nothing. And that doesn't necessarily mean that the devices don't do anything. But what it means is that if you have populations that have lots of cardiac arrest patients in them, which those studies did, you may have the mortality effect overwhelmed by the brain injury. And so that's an important thing to keep in mind when you're interpreting clinical trials and cardiogenic shock in particular. Granted that this gentleman's die was cast before he made it to the hospital, probably. Part of the reason for my insistence with the ECMO is not just the hemodynamics. I mean, he was on 100% with 15 apiete. I don't know, it's like, try to hit both sides at the same time. I actually don't disagree at all. And so on most of these cases, I'm telling them exactly how they happened. This one was a little bit different because he went to an outside emergency room where they were at a smaller community hospital and couldn't offer ECMO. So the most expeditious thing we could actually do was just take him by helicopter straight to the cath lab. And so then by the time he was in the cath lab, he had pulses and was stabilized enough. And I think his oxygenation had improved a little bit. Once we got some blood flowing, I think his venous sac got up. And so the point about the respiratory failure and the fact that Impella does nothing for that is well taken and accurate. I think I've got an impression my colleagues here had some thoughts or comments. But it isn't unreasonable to wait a little bit and see if hemodynamic optimization helps your oxygenation. You know, you're thinking guys in pulmonary edema. So if you can get them out of pulmonary edema, maybe you don't. Maybe a ventilator isn't enough to support the guy. So I may take the point that the ECMO should be considered, but it doesn't necessarily have to be mandated. All right. Another question up there? Well, yeah. My first reaction during this whole thing was it said he was in significant respiratory failure. So I did want to know, is it an aspiration? I just wanted to know what that was about, because that's a big confounder here for the reason that you all brought up, that knocking out his cardiac output and all that. So. Another question? Yeah. I think he had all of those things. Oh, OK. Yeah. Victor Koba from Henry Ford Detroit. Can you describe what are the resources you have in your cath lab? So do you have anesthesia there? Who's monitoring your drips? Who's monitoring your ventilator? How are you doing that with these complicated cases? Yeah. So for cases like this, we do have anesthesia there for anyone who's intubated, pressers, drips, et cetera. And quite frankly, I show up as the cardiac intensivist to help, because I'm going to take the patient anyways. So I figure, get as much knowledge of the case. All right. So I do have. So we got another question here. But anesthesia will come and intubate. But if you're putting in an impella CP, anesthesia will come and intubate with respiratory. If you're doing ECMO now, you're talking about the whole crew, perfusionist, specialized nursing, anesthesia, et cetera. But generally, you're summoning them. I have a question with this. Joe Pachkowski from Palmetto down in Miami. For this last case where we're trying to resuscitate someone who's in electrical storm, do you have any opinions on double sequential defibrillation or adding beta blockers to the cardiac arrest management? So that's a tough one. I think there, I'm not sure if I have a good answer, because I think that the, my understanding is the data is kind of murky. And there's certainly some data that suggests that, you know, using beta blockers, you know, can potentially increase, you know, shock success. I think this issue, you know, the problem was, is I think that he was ischemic. And so he kept having recurrent events, mostly because of the ischemia, if I had to guess. I don't, Dr. Pepe, you probably know a lot more about this than I do. Some of the issues related to that question, asking about, you know, double sequential defibrillation and refractory fusion and stuff like that. So it's interesting because, first of all, when I see refractory ventricular defibrillation, meaning whether it's persistent or persistently recurring, it's always means to be LAD, lesion left main or something like that. So I'm tending to go after it if there's other reasons to, young and healthy, all that. Now, as far as using the various other approaches, there's, there's just limited data. It works sort of anecdotally to use, you know, all this thing, but there it can screw up the machines, number one. And number two, one person who's got a lot of experience was Dr. John Ju in Portland. He's the medical director there. One of the things he found was that the people who seem to survive and do well had non-coronary artery disease stuff that was going on. It was something else. So just, it's kind of interesting from that point of view. So I tend to be with refractory guys, just sort of get them on a machine, get them in, get them to ECMO or whatever, get them to the cath lab. Those are how I tend to do versus mess around with the various energies. And, and, and, you know, and, and sort of story for another day, if you've really got a lot of arrhythmias, mechanical support to help the circulation, despite the rhythm is often a useful thing in the right setting, right? You get your impella going, that goes whether you're in VF or not, and et cetera. And just one other thing along those lines right now, both the Minneapolis and other places where I'm working, where we're doing some of the things that I mentioned today, we're actually using the ITD, the whatever, the HEDA. We're getting people, they're profusely so well that they're waking up in VFEB and we have to sedate them. It's kind of a whole different deal. So that's, that's why I'm biased that way. That's good. Another question, please. Thank you. Alex Bastillas from Texas State University. Thanks for this great lecture. Just one question, because we know like subclinical seizures can be frequent after cardiac arrest. I mean, you have like, like a routine EEG monitoring after cardiac arrest. So what is your protocol in your institutions and your practice? So at Mayo, we do less EEG than we did at Pitt. So at Pitt, basically everybody who was comatose after cardiac arrest got an EEG. And I think that's, I assume that's still the case. At Mayo, we do it if they've had abnormal movements during cooling, or once they're being rewarmed, then we do it. Is that, I don't know if you guys do that? Yeah, I, it's, we now have the availability of video EEGs with remote reading, and that's a little easier. You don't have to, you know, you can send it out and, sorry, if you will, tele-EEG reading. So we've done it a little bit more. People who aren't waking up, et cetera, et cetera. Don't know whether it needs to be routine, but certainly something you should think about. All righty, so I suspect we only have time for one more case. I actually have three more, but two of them are really just show-and-tell anyways. So this is a little bit more complicated even than the last one. So this is a guy, he's 66. He has end-stage renal disease on dialysis. He's got all sorts of coronary disease. In fact, he's actually had a prior VF arrest in the setting of an MI since his bypass. He went to dialysis, he was doing okay, but then he had a VF arrest. Initially, got initial return of circulation, got a couple shocks, got those 3 epi's and bicarb intubated, brought to the ED comatose. And then in the ED, the story continues. Another VF arrest was even longer this time, as I recall. And again, sort of a bad case here. And he was needing rocket fuel to keep going. And then his SATs were bad despite being on high ventilator settings. EKG didn't show any ST elevation. So the question comes up, is this a guy you take to the cath lab? And I'd be interested in seeing a show of hands. Who thinks this guy needs to go to the cath lab in the sense that it's likely to be a life-saving intervention for them? Yeah. How long ago is the cabbage? Oh, I have no idea. I forget. But he's had stents and MIs since his cabbage. I mean, he's got a lot. Let's go with more than a year. Yeah, let's go with several years ago. Not last week, more than a year. Yeah, yeah, yeah. When was the biggest cardiac problem? I think his EF was maybe in the 40s. So not terrible, but not normal either. So do you call the cardiologist from the ED here? We're here? No, no. No, in this case, are you going to make this call, or are you going to call a cardiologist to make the call? Probably, again, make the cardiologist. If they have to do it, they have to be the ones to make the decisions, as far as I'm concerned. We can recommend it, or strongly put it, or I'll call your boss, or whatever, that kind of thing. But I mean, you could argue that if you don't really think that it'll help this guy, you shouldn't even bother to call him at all. Would you let them make that decision regardless? Who, the cardiologist? Yeah, right. In this case, this guy. I mean, you call him. Yeah, you call him. They call us. I got it. That's your job. I'm trying to provoke him. That's hard to give. Yeah. There was one person who provoked me. Let's see. She's still at home. Did I survive the cardiac arrest? So I think you guys have picked up on the meat of this case. So yeah, it's a recurrent VF arrest. That's an indication. Cardiogenic shock, that's an indication. This guy's got known coronary disease. He had a VF arrest the last time he had a STEMI. But he's got end-stage renal disease at baseline. That's not a good prognostic sign. He's got refractory hypoxemia, and he's got terrible metabolic disarray, which I probably left out. But trust me, he has that. And then, of course, he had a prolonged downtime. Now, this was another case where it wasn't my case, and so I, well, it wasn't my decision, so I can criticize it. But they did bring him to the cath lab. And I think that I probably wouldn't have. But they did. And they found that, predictably so, he had diffuse coronary disease. I'm not going to show you all his graphs and this and that. But he definitely, there wasn't a fixable acute lesion here. But now the question is, so what about ECMO for this guy? I mean, he's got like seven indications for ECMO, right? He's got refractory hypoxemia. He's got refractory cardiogenic shock, recurrent cardiac arrest, et cetera, et cetera. At your institution, would they offer a guy like this ECMO? Anyone who, their institution, they feel would consider this gentleman to be a potential candidate for ECMO? My institution agrees with you all. What about cooling it? I mean, we're not done with him. You know, we took him back to the ICU. We didn't just give up on him in the cath lab. What do you guys think? Do you think this guy is someone who needs to be cooled? Do you think he's too sick to cool? Who would cool him? Yeah. So it's geographic. Most of that side, most of this side, OK. So yeah, I mean, as I said before, I think if you're going to do critical care, it's reasonable to cool them. I will say that in the guidelines, though, one of the few contraindications to cooling is refractory shock. We do know that cooling can adversely affect the hemodynamics, although that's a very complicated story for a different day. But you could make an argument this guy's got too much shock and everything to bother cooling him. As I recall, he was cold already. So I think it's sort of an irrelevant argument. A distinction without a difference. So unfortunately, he was also, again, not an ECMO candidate, not really a candidate for anything. And he had persistent refractory hypoxemia, bad respiratory failure, and had progressively escalating vasopressor requirements that he could not be kept alive. And we eventually made him comfortable. And of course, this case is actually even worse than it sounds, because he was transported. Because we do a lot of transport stuff. We have a lot of hospitals in our system. And so he actually was transported with a SAT of 80 for a long time. So very difficult case, unfortunately. The last couple are really a question. Just so you know, the last couple are kind of cool cases, show and tell, nothing too in-depth. Please, sir. Hi, I'm Emilio Mazza from Virtual Health in New Jersey. So I think one of the things that I think this case, before I even went down the pathway, is having a conversation with the family. This guy's got probably terrible quality of life, right? Bad coronary disease, been to the hospital, end-stage renal disease. I don't even think it should have gotten him that far. I think the conversation I had up front, which we have all the time with families, is that, all right, what's the trajectory here? And I think it's the important thing, and it's not getting addressed here, is that I think it's very important to have that conversation. I couldn't agree more. Unfortunately, as I said, I became involved at the time that he hit the cath lab, which put me at a disadvantage as far as the things that actually really mattered, such as avoiding heroic measures for someone who was not likely to benefit. Yeah, I'd give Jake a little credit. That's part of the reason we presented this case. Not so much to defend what they did, but to have somebody get up and say what you said. Why are you doing this, Wyandchasset family, before you start down the pathway? I do family members, plural, not somebody that may have whatever reason. Supposed to be the caretaker and is tired of it, whatever, so. Because then someone else comes after you later on and said, why'd you do that, right? Just something that's a practical thing to think about. Hi, I'm Karthick Joe, the intensivist in Nashville, Tennessee. Does the public reporting of cath lab mortalities, is that, are you seeing that as an issue impacting these cases going to the cath lab? I came in late, so I don't know if you covered this already. So that is a whole lecture all of its own, very important question. So for those of you who aren't aware, just like surgeons, cath doctors actually get, can get graded on their mortality related to their PCI. And so for elective PCI, the mortality should be 0.0. For MI mortality, it should also be quite low, maybe not 0.0, but certainly only a couple percent. But if you do a couple of these cardiac arrest patients, about a third of them die, right? So that means if you do three of them, you have a mortality on your numbers statistically. And so there's actually some evidence that says that in states where there's public reporting, they have decreased utilization of cath in critically ill patients, and their critically ill patients do worse. I'm fortunate to work someplace where we try and do what we think is best for the patient, and my interventionalists aren't held to the fire about that, but you may come across interventionalists in practice who say, nope, if they can't shake my hand and say that I want a cath, they're not doing it. I personally don't agree with that approach, but I certainly would understand if you were under that level of scrutiny. Yeah, I second that. It's a complicated issue, but it's a real consideration. And it depends quite a lot on the volume of your cath lab. So if you're doing a lot of cases, and you take a couple that don't turn out well, it doesn't really make that much of a dent in your statistics, and maybe your average is better than the rest of the state. Eric Peterson at Duke will tell you that if you actually look at this, the high volume, the people that do this don't have worse statistics, again, in part because maybe they're really good at doing everything else. But if you're asking somebody to do one of his or her 14 cases on one of these, they do not get risk assessment. And there is currently, there's somebody from New Jersey, there is currently an effort in New Jersey to try to throw these cases out of the state reporting for precisely that reason. Whether that succeeds on the political level is still up in the air. One more question. I have two quick questions for you guys. First of all, I know you guys also let you cool to 36, so hopefully this will apply to you. What do you do when patients come in colder than 36? I know you kind of made reference to, I just kind of leave them where they're at. The reason being, you probably don't want to rewarm them to 36 too quickly. And then my second question is, at what point do you prognosticate? Because I know there's been a lot of more recent research that's come out that's saying the whole 72 hour thing maybe isn't the best approach. A lot of people wake up at day five, day six, day seven. I'll answer the second one first and then I'll pass on to my colleagues. So I don't prognosticate before 72 hours. I may start getting the tests together. So I may start doing SSEPs on day two and stuff like that. And we get the NSEs, which I think are basically a waste of money, but we get them anyways. But I think it's important to think of prognostication as a process, not an end point. And I think it's important to set realistic expectations. You also have to think about the drugs you've given them. So if you have given them 170 milligrams of Versed, gosh, that might take some time to go away. On the other hand, if they've been not getting very much, a little bit of Propofol or something, that's a different story. And then as far as the most important thing is that don't actively rewarm them. So if they come in at 33 and you want to do 36, let them passively rewarm, but don't heat them up. I think that's what happens most places. They don't actively rewarm, but don't also let them go higher than 36. Yeah, so it's a good question about the neuroprognostication. I guess my answer is it depends, which is a little bit of a dodge. But I'd certainly at least 72 after rewarming regardless. But I think it depends on sort of two things, underlying comorbidities, young and otherwise okay before this, or old and not otherwise okay with this and that. And it depends a little bit on exactly what the neurologic status is. If they're really doing nothing at 72 hours, I'm a little more confident in being, maybe not fully confident, but if they're doing a little bit and it's 72 hours, and again, as long as that trajectory isn't coming up, again, in the right setting, it could be a long time before you get there. But if they're really doing nothing, it's time to at least have a prognostication that opens up the possibility that it might not get better than this. All right, well, thank you. You guys have stuck around to the bitter end. Appreciate your patience and time. That being said, if you're, I can quickly go through two cases just for fun, if you want, because you've already been here this long. And so I'm gonna go through these very quickly, and I'm just gonna close my eyes, and if you leave, I won't notice. So I wanted to show you two cases. These are recent cases that I saw that I thought were really cool. So I had a 19-year-old kid VF out of hospital arrest. So his dad was driving him to urgent care for an upper respiratory infection when the kid's in the backseat, and the dad sees him pass out and have some weird movements, so he pulls the car over. And he realizes that the kid's not breathing, and the kid's pulseless. So he calls EMS, and they're like, oh, start CPR, we'll send a crew. And he's like, no, no, I'm just gonna drive him to the hospital. Fortunately, they talked him out of that. So he started bystander CPR. EMS found him in VF and got him back single shock. In the ER, he had a bunch of weird stuff go on, and they thought he was having a seizure, and maybe he was, and they treated him, and his extremity was very febrile. He was pretty much unresponsive, but moved his extremity spontaneously. He got a pretty extensive workup. They did an LP, had CT, all that stuff looked good. Needed a little bit of norepi, but pretty stable. And his first troponin was 2,700, which is, if you have a STEMI, it could be that high. If you have almost anything else, it's not that high, except for a couple things, and this is one of them. So initially, KG, real tacky. Do you want to say there's some ST elevation here? It's a little hard to say. They repeat an EKG once he's kind of been sedated, and it may be, but probably not. Certainly not progressive, and I probably wouldn't call it. Echo looked kind of messed up. This is a parapsyndromal short axis view. It's a little bit off, a little bit substandard view, but you can see that he's got LV dysfunction. It's kind of a little bit of strange contraction there. So the question becomes, do you cath him? And so he's got these weird EKG changes. His troponin's through the roof, VFRS, LV dysfunction, but he's 19, seriously. He's pretty much hemodynamically stable. He has more of a global LV dysfunction picture, and in fact, they'd already done a chest CT, and you can look for coronary calcium, and you can look at his coronary origins, because you want to think about, well, what would make a 19-year-old kid have coronary disease? And the answer is a congenital coronary anomaly, which he did not have. So we actually didn't cath him at the time, but in the end, we did cath him eventually, and he had normal coronaries, just like anyone would suspect. So I was going to ask some questions, and I'm just going to skip that. So we cooled him, but he actually woke up during cooling, which is, you know, we all were, like, literally slapping high-five in the middle, because you can't let a 19-year-old, you know what I mean, like, you can't let a 19-year-old kid have a bad outcome, and he was neurologically intact, a little bit scrambled, but was fine, and he ended up having a pretty rip-roaring myocarditis, which I thought was an interesting case. You just don't see it every day, but it's sort of a perfect presentation of it, myocarditis causing VF arrest, and that's one of the only times in myocarditis that you actually do a heart biopsy, if your institution even does them, because not everyone does, but his was negative, and he did fine, and it was, you know, the biggest save I've had in quite a while. And last case, again, just another... You're looking for giant cell myocarditis in that biopsy, right? Just to be clear. With arrhythmias, you're looking for giant cell myocarditis, which would respond to immunosuppression. Right, so just, you know, with most myocarditis, you really don't do anything, but with the specific giant cell disease, which is autoimmune, it's terrible, and you pound on them with high-grade immunosuppression, and if you don't do that, they don't make it, so that's the reason. Sometimes you just empirically treat, actually, because it's so severe. Another young patient, 38, and I thought this was a fun case. So the story is this lady has migraines, so she goes to Mexico to buy Imitrex on the cheap, because that's a good plan. So then she took some of that, and the next day she started having this chest pain, so she goes to the ER, and in the ER waiting room, she arrests. They gave her a couple shocks, got her back. When you look at the rhythm strips, it looks kind of like a polymorphic VT. She had a bunch of PVCs after return of circulation, but she was awake and neurologically intact in the ED, because they got her back immediately. They gave her some procainamide, because apparently they wanted to do that, and then she really didn't, she felt better. Apparently the cardiac arrest cured her chest pain, or she was afraid of complaining about it at that point, and her first troponin was normal, but then it went up after that. EKG, normal-ish. Echo, normal-ish. So do you cath this lady? Well, I hinged it all on these things. So I said she had a brief VF arrest, she had chest pain prior, she's awake, and the troponin, whatever, I don't care about the troponin. All this stuff against cath is nonsense. Don't listen to it. So we cath her. And so she actually had spontaneous coronary artery dissection. Now, angiographically, this is not the most impressive case, but spontaneous coronary artery dissection is a disease that we're recognizing more and more frequently, predominantly in young women who are typically healthy, and it can present with a lot of different things. It can present with recurrent chest pain, it can present with STEMI, and obviously cardiac arrest. What it is is it's a tear, and then bleeding into the lining of one of the coronaries. So like, instead of an aortic dissection, it's a coronary dissection. And like I said, this is not the most impressive, but just so that you're, to orient you here, LAD goes down the front. It looks normal, except it's kind of squiggly, and a lot of these spontaneous coronary dissection patients have these little squiggly vessels. We think that somehow they have a vessel abnormality that we don't quite understand. This is the circumflex coming down. It's a very big circumflex, and this is a branch of the circumflex. And you see how it just kind of abruptly kind of tapers here, and then is more normal downstream? Just take my word for it that this appearance is not the normal appearance for atherosclerotic coronary disease, nor do you expect it in a 38-year-old woman who's otherwise healthy and doesn't have the diabetes. So this is just, I thought, a really interesting case just to talk about the fact that just because you don't think the person has atherosclerosis doesn't mean that they don't have something going on in the coronaries. And just to sort of increase awareness of this disease, because a lot of folks aren't aware of it, and I think the more we find it, the more we look for it, the more we find it. And this lady, as you, luckily did well and behaved herself. Yeah, it's interesting because I've seen a couple of these cases, too, just like this with the dissection. I was not expecting it. We did see some EKG changes, though. So I just want to ask you, because I probably need to be looking into this more, like who's at risk? Is there underlying risk outside of, like you said, diabetes or something like that? But is there a way to guess? The fact that she was younger, you might think, let's go catheter anyways, but is there a way to predict this thing? Yeah, so it's always hard to predict rare things. I will say that some of the people who I work with are very, very expert, and I don't know all their nuances, but interestingly, migraine seems to kind of go with that. So migraine can go with coronary spasm or can go with spontaneous coronary dissection, which are sort of the two non-atherosclerotic causes that can cause cardiac arrest in young, otherwise healthy people. SCAD is usually young, healthy women, and a lot of times they don't have any risk factors at all, except bad luck. They commonly have fibromuscular dysplasia, so they may, which you often find after the fact, but certainly if you have a person who you know has fibromuscular dysplasia, renal artery stenosis or something in that spectrum, gosh, you could raise your suspicion there a little bit. And pregnancy. Yep. Pregnancy. So pregnant women who come with chest pain. So just as a quick sidelight, there is a registry now of SCAD, and that registry was, someone named Jacqueline Saw runs that registry. It's a very impressive set of data, and that was motivated by patient groups. There were some patients who had this and said to Dr. Saw, does anybody know about this? And she said, no. And they said, okay, let's make a registry. And the national registry got together. So it was patient-driven. Yeah, they do a lot of research on this at Mayo, and so we take cases from all over. So if you have a patient and you think about us, because I have six partners that are experts in this, and it's like, where do you have six experts in a rare disease at one place? All righty. Thank you so much. I hope you guys enjoyed the cases. Very good. Thank you for staying around. Thank you.

cardiac arrests

coronary angiography

abnormal EKG changes

metabolic disarray

severe brain injury

resuscitated multiple times

anoxic brain injury

end-stage renal disease

cath procedure

acute lesions

patient's overall condition

contraindications

decision making

cardiac arrest management

patient outcomes