 So our next speaker is Dr. Felipe Turan. He's an emergency physician and investigator at Wheel Cornell Medicine in New York City. He completed a fellowship in emergency ultrasoundography at Mount Sinai Hospital, a master of science in clinical epidemiology at the University of Pennsylvania. And he's a test member of the National Board of Ecocardiography, Critical Care Ecogardiography Examination. As a translational research scientist and resuscitation scientist, his research aims to investigate novel resuscitation strategies in both laboratory and clinical environments with a primary interest in novel strategies to improve cardiopulmonary resuscitation, including the use of transesophageal echocardiography. He's the founder of the Resuscitative TEE Project, a principal investigator of the multi-center TEE Collaborative Registry, aimed to accelerate the development of outcome-oriented research and knowledge translation on the use of TEE in emergency critical care settings. Without further ado, Dr. Felipe Turan. Hello, I am Felipe Turan. I'm an emergency physician and researcher in the Department of Emergency Medicine at Royal Cornell Medicine in New York City. It is my honor to join the Congress and present on the topic of resuscitative TEE during cardiac arrest. I am a founder and course director for the Resuscitative TEE Workshop, and I'm also a consultant for Fujifilm's Sonoside. When we talk about resuscitative TEE in emergency medicine or in critical care, there are a number of other related concepts that are often used that more or less aim at describing the same thing. So rescue TEEs, more commonly, I think the term used in the anesthesia literature, focus TEE or point of care TEE, are other terms that are also used to describe this modality and the scope of this modality in emergency and critical care settings. But regardless of what term we use, fundamentally what we're describing here is the application of transesophageal echo at the point of care in order to obtain real-time data that will impact decision making at the bedside. It is always emergent or urgent, and for the most part, is going to be performed in intubated patients. So this is different from comprehensive, perioperative transesophageal echo or comprehensive consultative transesophageal echo performed by our cardiology colleagues. So this is in the hands of either emergency physicians or intensivists or cardiologists or anybody with the right level of training to apply this modality, but specifically what I'm going to describe today is the application of TEE in cardiac arrest. And so it is really not about the number of views when we refer to resuscitative or rescue or focus TEE. It could be four view protocol, six view protocol, it could be 12 views. It is really about the questions that we're asking and the clinical information that we can obtain and that we can impact. This is, from my perspective, the three groups of applications that today we can see in this landscape of resuscitative TEE. And this is, as you can see on the right hand, is really across the acute care environment. So no matter whether it's in the emergency department in the OR, ICU, CCU, it is going to be the same patient that can have any of these clinical conditions. And it's in these conditions where, whether because trans thoracic is not able to provide the information that we need or because simply trans esophageal echo represents a better tool for that job. That is why we're going to be using TEE for these different clinical applications. And cardiac arrest is the one that I've been studying for the past several years. And it is a unique application in that TEE represents really a number of new opportunities in terms of understanding the disease, in terms of understanding CPR physiology and also potentially intervening, optimizing, improving doing CPR specifically. So this is an example, this is a picture of our team expecting a patient with out-of-hospital cardiac arrest. Everything is set up as you can see at the foot of the bed. We have a clinician already gowned up, ready to help with procedures. We have our nurses. We have a physician at the head of the bed here, ready to intubate, to confirm airwhip, advanced airwhip placement. And that physician is also going to perform the intra-arrest trans esophageal echo. So before I tell you more specifically, what is it that TEE can help us with in cardiac arrest today, I wanna take you through a very brief history of how we got here. What is this modality? Where was this modality used and how? And it actually goes back to 1993 where this modality was first described actually by a group of cardiologists, Dr. Reidberg, at the time believe at University of St. UCSF in San Francisco. With her colleagues did the study evaluating the use of TEE as a mean as a tool to understand CPR physiology and specifically direction of blood flow. So it was this study actually, along with another couple of similar studies performed in the 90s, that actually provided us with the current understanding we have of CPR physiology and specifically the cardiac pump theory. That is how CPR actually works, how close chest CPR actually works. Documenting what the valves were doing, doing this compression, doing the compression and decompression phase. The mitral valve being closed during the compression phase and the aortic valve being open represented the key findings that define this theory that establishes that the way that we generate forward flow during chest compressions is by directly compressing the left ventricle ejecting a flood into the aorta. So fast forward, it was in 2019 that our group following the work of others in the years prior performed the first study actually evaluating systematically cardiac arrest patients without a hospital cardiac arrest as a diagnostic tool, but also as a tool to evaluate CPR physiology and identify what later has become to be a common phenomenon in cardiac arrest, which is specifically the abstraction of the left ventricle attract doing CPR. So I wanna describe why is it that this can be helpful? Why to perform what should we consider performing resuscitative or focused in cardiac arrest? Well, I think the first argument here is that transcephagealic was simply the right tool for the job. It is the best tool we have to evaluate the patient's heart in real time, unlike trans thoracic, we don't have to rely on interrupting chest compressions in order to evaluate the patient's heart's function, characterize the type of cardiac arrest that we have, the rhythm, and identify if we have a reversible cause. But really what makes transcephagealic or unique is its ability to perform not just a snapshot of information doing the resuscitation, but rather continuous imaging. So serial reassessments in the case of cardiac arrest continues imaging during the resuscitation. And a reason why this has become so relevant in the context of CPR specifically is because we have learned that the ability to look at the heart while we are delivering CPR is an ideal opportunity for us to actually appreciate in real time whether what we're doing, what we're intending to do that is compressing the left ventricle in order to eject blow of blood in generate for flow, whether that is actually happening or not in accordance with the cardiac pump theory. So this is for instance, an example of a patient in the early phase of the resuscitation of an out of hospital cardiac arrest, you can see here a midisophageal long axis view and there's ongoing chest compressions with a mechanical compression device. As you can see, while the compressions are happening, you see a little bit of activity here of compression of shortening of the diameter of that left ventricle, but it's very, very minimal. And there's very minimal opening of the aortic valve with also very obviously low velocities. You can see smoke sign is essentially blood really not really moving much in that left ventricle or out of it. So in accordance with that, the entitles CO2 at that point was 11. So this is in case that somebody might not be aware, entitles CO2 represents the best surrogate that we have during cardiac arrest of cardiac output. It's an indirect parameter, of course, but it's non-invasive readily available and it has been established as a parameter that can inform us about the effectiveness of chest compressions. In this case, in agreement with this echocardiographic finding of inadequate chest compression depth, essentially, that we're appreciating here is that left ventricle is not really adequately squeezed even though we're compressing with a mechanical device that is not generating adequate flow and that's reflecting that entitles CO2 at the time of 11. So what we do here is we try to switch out of that device and switch to manual compressions. As you can see, it's clear that this is manual compressions because there's a lot of more bouncing, it's a lot more irregular than compressions delivered by a mechanical device. And as soon as we do that, entitles CO2 in the minute that follows improves to 24. We're able to actually tailor the depth of the chest compressions, in this case while delivering manual CPR to optimally compress that left ventricle to a point that we were not able to reach in the sort of fixed compression depth that we have established by a mechanical device in this case. And as we continue to do this, optimizing the depth in this case of the compressions, the entitles CO2 kept going up as you can appreciate here is visually better quality of those compressions defined by better and greater shortening of the diameter of that left ventricle. And eventually we achieve Rosk. And so this is kind of a real time assessment of the quality of CPR that leads to an intervention, that intervention being switching from mechanical to mental CPR and optimizing the compression depth. So deviating from the one size fits all sort of recommendation from the guideline where all we have is chest compression rate and a sort of fixed rate that is sort of population based. And obviously in this individual case was not the most adequate. So in this case, you can see now the image on the left is the initial CPR and the image on the right is the final sort of optimized CPR with manual compression. So really easy to understand, I think the impact in this case of this intervention that follow the finding that was made with transesophageal echo in real time. And in addition to being able to identify cases where perhaps the compression depth is not enough, we have the ability to actually identify cases where what we are hoping to do, which is to have blood eject out of the left ventricle during the compression phase is actually not happening. And it's not happening in many cases because the area of maximal compression, the area that we're compressing the most with CPR is actually obstructing the alpha tract. This is an example of a midisophageal long axis image where compressions are obstructing the alpha tract. There's an example of an image on the left where we have obstruction of the left intercalphal tract and image on the right after having optimized, having changed the position of the hands in order to not obstruct the alpha tract and try to optimize the squeeze of the left ventricle. There'll be the before and after. This is a similar case where we were compressing the alpha tract and you can appreciate in a transgastric image here that the left ventricle actually is not changing its diameter, not changing really its volume, which means that we're not generating a change in pressure. In this case, the next question is, well, is there any data sort of supporting this mechanism? And the short answer is yes. There's been at least two well-conducted animal trials demonstrating essentially that when we compress the left ventricle, we obtain higher coronary perfusion pressures in that when we randomize swine to receive chest compressions over the LV, we get ross and when we do standard chest compressions in this case, abstracting the alpha tract in most cases in this trial, we simply cannot get ross. This was confirmed by a more recent study that also evaluated Cerebola blood flow as a measure of obviously cerebral perfusion in a similar swine model, confirming the previous findings in this hypothesis that obstruction of the left ventricle alpha tract actually leads to worse hemodynamics by means of lower chest coronary perfusion pressures, lower probability of ross. A study back in 2009 actually had identified in an observational study the finding of compression of the left ventricle alpha tract happening in around 40 patients without a hospital cardiac arrest in that study. The authors also correlated the actual precise location of that area of maximal compression with the stroke volume, the estimated stroke volume in those patients depending on the position, the distance of the area of maximal compression from the aortic valve. And so the farther of that area of maximal compression into the left ventricle, farther away from the left ventricle, the better stroke volume that we obtain. So how common is this problem? According to data from our group from 2019, this is actually quite common. We found 53% of patients that had obstruction of the left ventricle alpha tract or aortic root when evaluated with TE doing a cardiac arrest. And the same year a study out of Italy confirmed that for the first time there was actually a link between that finding, the finding of an open LVOT with higher probability of survival at 24 hours. So this is obviously very early data. In this case, this was retrospective, but this supports the theory that when identified this phenomenon of abstraction of the alpha tract, we can intervene and potentially improve outcomes. Our group in a collaboration through the resuscitivity collaborative registry with over 30 centers published last year at the resuscitation symposium of AUJ, the first study, multi-center study demonstrating the link between the area of maximal compression is specifically obstruction of the alpha tract with the lower probability of Rosk. There is a study currently under way to confirm these findings and whether we can not only improve or whether this finding is associated with lower probability of Rosk, but whether that actually also carries and is associated with lower survival to hospital discharge. Obviously, that's what we care about. Ultimately, we're currently working to evaluate that. For anybody who is interested in this topic and a more comprehensive review of it, I recommend this sort of state-of-the-art review published in Jack a couple of years ago by our group and similarly in collaboration with our cardiac anesthesiology colleagues, Andrew Dineult and Dr. Bilook. We have published this in the Canadian Journal of Cardiology, another comprehensive review of the application of T specifically in cardiac arrest. Anybody who is interested in joining this registry, this is an ongoing effort multi-center study at this point with 35 centers, we presented the first analysis last year and this year we'll be presented additional data of the American Heart Association Resuscitation Symposium. If anybody's interested in joining this ongoing work, I highly recommend to check out the website in retail to join. This is the work of many individuals around the country in the US, Canada and internationally that have collaborated, that have made this possible and I want to acknowledge them because it is only with the help of everybody who is performing T's in cardiac arrest that we can produce knowledge to learn more about the impact of this modality. With that, I thank you for your attention. This is my email and I appreciate the invitation to the symposium. Thank you. Great lecture from Dr. Tran and T is always the first thing we call for whenever there's an intraoperative arrest, mostly for diagnostic reasons, but it would be great to be able to also use it to evaluate the efficacy of compressions and the resuscitative efforts in order to optimize those things as well.