Aloha and good afternoon, everyone, and welcome to our session on acute right ventricular failure. I'm Aniket Raleigh from Vanderbilt University, and I'm an advanced heart failure and transplant physician up there, also trained in critical care medicine. And it's my distinct pleasure to introduce this session to you on acute right-sided heart failure. As you can see from the name of our session, Different Trainings, Different Pathways, across two different training pathways and several different experts from United States and abroad, we are going to be discussing the two most critical aspects of acute right failure. One, what is the best way to diagnose it? And second, what do you do once you do diagnose that somebody is in acute heart failure from right-sided failure? So without further ado, I would like to introduce our first speaker. That's going to be Dr. Bindu Akanti. She comes to us from Houston at University of Tennessee, where she serves as the director of heart and vascular critical care medicine. Dr. Akanti. I won't take offense to the Tennessee comment. Houston isn't Texas. Good afternoon, everyone. I know this is after lunch, but I hope if nothing wakes you up like right ventricle, then I don't know what will. And especially you're dealing with four ECMO intensivists and heart failure intensivists in the room speaking to you about it. I have disclosures, nothing pertaining to this. So I think, I guess, we do have a couple of ARS questions embedded into the talk. If you could use your QR codes. Question one, what is your preferred initial method of diagnosing right ventricular failure in a cardiogenic shock patient? Assuming you're at the center where both options are readily available. Okay, I think I speak for all of the people on the panel that we're humbled by your presence here. The second question, once right ventricular failure has been diagnosed as a cause of cardiogenic shock, what is your preferred initial treatment modality? Okay, thank you. So here we are. I think it goes without saying, regardless of the ideology of right ventricular failure, if you take all comers, the mortality is worse in patients that have RV failure versus that they don't, right? Naturally speaking, we're 2023, 20 years from now, I'm sure AI will take over and just kind of blurb outside the room, RV failure, RV failure, right? Until then, we lowly humans have to kind of succumb to our understanding of pathophysiology and how do you put this together? Right ventricular failure is quite complex, whether you understand it from the preloads perspective, from the squeeze perspective, or the afterload perspective, the end result is the same. It is deathly spiral towards death, right? So if you start with a massive PE patient, increased PBR, or an inferior STEMI patient with RV ischemia, or our straightforward sepsis, GI bleed, metabolic acidosis patients that lead to RV failure, and of course, any kind of issues with RV preload. What do we have to diagnose multi-morally in terms of RV failure? I think again, at this point, we're in the cusp of revolution in terms of the use of CMR, the use of nuclear scans, and other imaging modalities. But today, I've been given the task of, is echocardiography the right modality to evaluate right ventricular dysfunction? And in the next nine minutes or so, I hope I can talk to you all about what are some simple tools you can use that are readily available in the ICU to kind of predict, hey, this patient is probably not going to do well and it's, you know, his RV is down. But to start with talking about the right ventricle, we really need to go back to our anatomy lessons. The right ventricle has circumferential fibers as seen in panel A, and it has longitudinal fibers. To think of the RV as just a pump that's going up and down as we typically think about it is a gross misunderstanding, because geographically, it is not quite similar to just a sphere. It is kind of spread out. So you need to recognize that the contraction of the longitudinal fibers pull the annulus up, as you see in panel C, towards the apex, while the movement of the free wall is done towards the septum. And the traction on the free wall on panel 4 now are the points of the attachments to the LV. Now, that aspect is very crucial to understanding the pericardial constraint and the RV-LV interdependence that the RV depends upon. So what are the determinants? We talk about it. Can we just divide it up? You have preload, you have squeeze, and afterload. I call it the PSA method, but we have pericardial constraint. And this really complex RV-LV interactions that play a role, and do not forget the rhythm. I think in the mismanagement of the patient, sometimes we forget that the heart rate is barely 60, and the rhythm is gone, right? So let's talk about the preload, squeeze, and afterload, and if an echocardiography can help us understand it, before Eric comes and tells you otherwise with his right heart cath section. Now, assessing the preload with echocardiogram, and I think pretty much everybody in this room has had an opportunity to do that. So the diameter is measured perpendicular to the long axis of the IVC at end expiration. That's on the left. And then the inspiration, just proximal to the junction of the hepatic veins, 1 to 3 centimeters to the IVC right atrial junction. The reason this is important is, as we assess the patients and come to a conclusion, you want to have an objective way, and the same way, whether it is 3 AM in the morning, or 10 PM at night, or 7 AM on a Monday morning. But how do you take that and assess if the preload is high or low? So normally, the IVC diameter, like right there, about, you know, you look at the 2.1 versus 2.1 versus more than 2.1, and then high in terms of pressures, and if it collapses with the SNF test. These are widely available publicized tables that you can assess the right atrial pressure in. Now, in the right panels, I'm showing you assessment of the RV diameter in the four-chamber view. This fractional area change can also give you an understanding, hey, is this patient In combination with the IVC, how does this look? Because you don't want to look at it as a single method, right? You want to combine each method. How do you then determine the squeeze? If you don't remember anything else from this talk, I would like you to remember TAPSY. Tricuspid annular plane systolic excursion. The normal range is about 24 plus or minus 3.5. Anything less than 17 millimeters is abnormal. So in an M mode, you can see normal excursion on the top is 28 versus bottom is 6. Simple, effective, yes, it has its limitations, but it's a good start. So I showed you the anatomical figure, right? I showed you how there is the longitudinal contraction and that circular fibers. TAPSY does not look at the septum. TAPSY is blind to the septum. TAPSY is just looking at where that point that you're looking at it is. So while it's great to say TAPSY is low, so there's RV dysfunction, you are being again agnostic to that septum. In patients with cardiac surgery, in these patients, you will mislead yourself into thinking there's RV dysfunction when it's just a matter of somebody touched the heart and that's normal, but the septum is working fine, so the patient is likely fine, okay? Next is the squeeze in terms of assessing at the S prime, the tissue Doppler. So the normal range for this is about 14.1 and the abnormal threshold is less than 9.5. Similar to TAPSY, you're really looking at what's happening at that lateral pre-wall, easy and fast, reproducible, and it has an established prognostic value. Again, the limitation, same as TAPSY, again, you have the longitudinal function of the basal lateral. It neglects the contribution of the septum and the RVOT, and these are dependent on the angle and how you do it and whether it's load or load dependent. When it's abnormal, whether it is TAPSY or S prime, you really, really want to compare it with other methods. The third one is the fractional area change. The normal range in terms of diastole and systole, you want to get it about 49% of the squeeze and the abnormal threshold in steady after steady, you can say about 35%. Easy, widely available. These points that you see, it's basically cutting it into planes because you can't look at it just as a sphere, but if you look at it as a volume, then this enables you to do that. It reflects both longitudinal and radial contraction. Now this is the first time you're taking the radial contraction. Now you see why you want to combine one or the two from the previous to this to really get an assessment and an understanding. It has established prognostic view. It's image quality and view. How many of you can tell me that you got this beautiful right atrial and the right ventricular view in your ICU on a regular basis? It's poor reproducibility. And remember, you always have to keep in touch. What is the fuel I am giving to get this? Who is the dude on epi 10? What else is going on? So I just urge you to keep things in context and combine. Should be used in addition to other parameters. Now we have like REMP. This is really nice to talk about, which is basically right ventricular index of myocardial performance and the global RV performance. And this is taking a stab at Eric's talk about the only way to do it is right heart cap. I'm a pulmonary hypertension physician, so of course, right heart cap is important. But I urge you all to also keep in mind, echo has moved significantly in terms of the level of sophistication. So when these values are available, let's at least understand them. You may or may not use them. So what does this do? It's literally taking the relationship between the ejection and the non-ejection time of the heart. So what is the efficiency? Is it taking longer to squeeze or relax and it's having a little difficulty to squeeze? Of course, that is oversimplification. But when you look at it, the normal range is about 0.38. So once you get into the more than 0.5, it's taking its time for the systolic to happen. So it reflects a global right ventricular function. It's less dependent on the acoustic windows. Single best acquisition is what is taken in. And it's limited use in a normal RV, but it can be unreliable in the RA pressure, so really large. Again, it could be used as part of this global approach we're going to do. Then that's great. What about that squeeze and preload? What about the afterload? Easy. I'm not even putting it. You all know about the tricuspid regurgitant jet. Four times velocity times velocity, 4V squared. It gives you right RV systolic pressure, and then you add it to right atrial pressure, and you get an estimated PA systolic pressure. But what else can you use? RV to LV, your diameter at the basal. It's bigger than the LV. Eyeballing is what most physicians actually use. Should they use it? They did a global study in terms of people across the globe. Yes, all of them use it, eyeball test. RV bigger than LV? That looks big. Do you agree? Yes, I agree. Okay, the patient is sick. Okay? What about the acceleration time? This becomes very key in people, patients that have PE or PAH or chronic RV overload. The main thing that you want to take away from this is, is the acceleration time less than 105 milliseconds, and is it seeing that resistance in the mid-systolic notching? The right atrial area more than 18, and the septal flattening. This is called the left ventricular eccentricity index. How big is the septum in diameter compared to this? If it is being squeezed and the longitudinal is being squeezed, you know that the RV septal is so under so much pressure that it is being squeezed. So that ratio of more than 1.1, bad. And when you look at the pulmonic valve and you look at the diastolic velocities, if it's more than 2.2, and of course, we already went over that IVC, the 2.1. So can we put this in context with diseases? So we talked about PSA, preload, squeeze, afterload. Let's talk about three simple diseases, and then we'll talk about the right hard cap with my colleague. PAH, TAPC, less than 18, bad. Fractional area change, less than 35, bad. This is the RV global longitudinal strain, which is this fancy, nice imaging that you can see in the sophisticated echocardiogram. Basically, even like one standard deviation worsened, the hazard ratio is 1.54. If you put the TAPC and the estimated PA systolic hazard ratio, TAPC divided by PA systolic, more than 0.32 is good survival in patients with PAH, but less than 1.9 is a really significant high mortality. The RV to LV ratio, I already told you, it's been proven in trials. So it's not just your eyeball test. This is bad. What about heart failure? TAPC, less than 14, has been validated. Fractional area change, less than 35, is a hazard ratio of 2.2. Global longitudinal strain absolutely predicts RV failure in our LVAD patients. And then that ratio, less than 0.45. Aortic stenosis, I think a lot of programs we do TAVR, a lot of pulmonary critical care physicians are called to see, to pre-op optimization. How do you predict RV failure? Less than 14 for TAPC, less than 35 for fractional area change. This S prime of less than 9.5, and the TAPC ratio again. I'm not giving you a list. I'm trying to say that these values do matter. These values have been validated. For us to be agnostic to these values is being blind if you're just reading the report, right? We want to put it in context with the patient. What about, is there like actual head-to-head trial looking at this? Not quite trials, but in terms of the estimated right atrial pressure based on the IVC and the confidence index versus actually an invasive right atrial pressure with the catheter in the RV, pretty correlatory. But then remember, remember where we can use it and where we cannot use it. So with that understanding, with the focus next to you, with like all these sophisticated ultrasounds, I have to believe that echocardiogram is the best way to assess right ventricle. And we'll see if Dr. Osborne will convince you otherwise. Thank you for your attention. Thank you. Thank you very much, Dr. Akanti. And you guys were so welcoming in Houston during my time up there that it still feels like home, which is Tennessee. Yeah, and you called it Tennessee. Our next speaker is going to be Dr. Eric Osborne. Dr. Osborne is the chair of Temporary MCS and ECMO Domain for CHESS. And he's a world-renowned ECMO educator and a great mentor to several early career faculty members like myself. So Dr. Osborne. Thank you, Dr. Raleigh. I'm Eric Osborne. Thank you for all coming here. I don't know if I'm a world-renowned expert. I wouldn't call myself that. I would say my patients survive, which is probably better. Dr. Akanti, outstanding talk. She was correct. Her slides were beautiful, were amazing. And it's an honor to be here. I'm going to talk about what's the best or what's the most accurate way to diagnose RV failure. So the objectives, benefit of using the RV PA catheter, a limitation of echo, and two reasons why a PA catheter is superior to echo. So we're doing a thought experiment tonight, or this afternoon. If you had to choose between an echo and a PA catheter, that's the decision we're making tonight. In reality, you're going to be doing your echo while you're setting up your swamp, while you're setting up your swamp. But we have to assume that we're in a place that routinely places PA catheters. Like I said, in actual practice, you would be performing your echo as a screening exam, and then you would place your PA catheter. And then you would... So why do we care? RV dysfunction, as Dr. Akanti nicely showed, is a robust marker for mortality. Early recognition and accurate diagnosis followed by early treatment will improve outcomes. So the key here is we can diagnose it, but we also need to... We can recognize it. We also need to get the diagnosis right. We get the diagnosis right, we can get the treatment right. So as Dr. Akanti nicely said, RV contractility, these are some of the things that will cause problems. And then immediately, volume overload is transfusion, resuscitation. Pressure overload is our lung, our PE, ARDS, mechanical ventilation. We're all very familiar with that. Right ventricle is fire. Do you guys have teenagers? You know what fire means? So it's both. It's actually really cool, but it's also... I called a mentor of mine, a nationally known heart failure echo cardiac critical care expert last night. And I said, look, we're talking about getting ready for this talk and the RV is kind of a rabbit hole. And she said to me, I cannot quote it exactly, but the RV is effed up. And it's actually kind of true. The pictures that Dr. Akanti showed you, they're beautiful. They are. They're very beautiful. But how do you reproduce them? I don't know. It's really hard to do. When you look at those echo studies, they're giving you the idealized pictures. Getting your accurate windows on a structure that contracts in different ways and depending on where you put your cursor, it can look big, small, happy, sad. So in the old days, there was an RV problem, possible RV problem. The pulmonary said, oh, send it to cardiology, it's the heart. And we send it to cardiology and they said, well, send it to palm, it's the right heart. So as we all heard, as we go through our career, it's the forgotten stepchild, but it is fire. We now are understanding, thankfully, the importance of it. And thankfully, the PA catheter has made a resurgence. Here's the right ventricle. I will concede five minutes of my time to Dr. Akanti, because her slides were better than mine, but it's triangular and crescent-like. So the shape is weird. It's a geometric shape. It has both superficial, circular, and deeper longitudinal fibers. It contracts in three different ways. Her slide showed it better. But think about it. You've got inward motion of the RV free wall. You have the apex pulled towards the base of the heart. And then when the LV contracts, you have traction pulling on it. So you're trying to measure the function of something that doesn't, it's not a symmetrical contraction, it's geometrically challenged, to be nice about it, I guess. So the geometry, the 3D shape, and the complex movement, the retrosternal location, make the RV function really hard to measure. That means it's really hard to look at it consistently with an echo. We need to do an echo. I believe in echo. We have them. Do we have more of an echo than a stethoscope? Don't tell my pulmonology mentors that. But actually, I use ultrasound way more than my scope now. One thing I will point out is that the study that Dr. Akanti referenced comparing the accuracy of echo pressure measurements to SWAN measurements was done with 3D echo. How many people here do 3D echo every day on their ICU patient? We're not there yet. We might be, but we're not there yet. That's a research phenomenon. So what's the current optimal way to look at measure RV function? You get your pressure volume loop, and this is a conductance catheter placed in the RV, and it can most accurately measure its function. This is a research thing. Nobody does it. You're not going to do it on a sick patient in the ICU. Cardiac MRI, a little bit easier to do. We do this, but you're not going to take a critically ill ICU patient down for a cardiac MRI to really measure the function. So what this does is it shows the normal RV-PA coupling. What does that mean? That the RV, if afterload increases, then RV contractility should increase. And we have realized that this is the most accurate way to prognosticate and predict how the RV is going to do. You can look at this with SWAN. There's a study by Jake Jenser. Maybe he's here. He can correct me if I'm wrong, but he did a nice job showing that you can look at this with ECHO. Again, in an idealized setting where you're looking at the best pictures. This just shows the diagnosis, the nice review in the New England Journal of Medicine. You're going to look at your history and physical, and you're going to do your EKG. Then you're going to look at your serum biomarkers, and you're going to go to your ECHO and your PA cath. So the ECHO, it's accessible, it's fast, easy to do, non-invasive, but here's the million dollar question. We all love ECHO. Is it accurate? I don't know. Will ECHO help you continuously manage your patients and assess your interventions? It's a simple yes or no question. We have the, have you ever used the Imacore ECHO, the probe you can put in that gives you continuous ECHO? You had that, but you're not going to be looking at an ECHO every five minutes or every, even every hour on your ICU patients. So the problems with ECHO we talked about, the windows are hard to get. If you get them, they're hard to reproduce. There's access variability, meaning you're doing a two-dimensional cross-section of a three-dimensional structure that is contracting in a geometrically complex and aberrant way. And you're getting one snapshot. This changed really fast. Some of the ECHO limitations, this is just a partial list. So if the geometry, again, will make it harder for you to see the same views. Your Doppler tissue imaging is very sensitive to tissue, to your cursor alignment. The TAPSI is great. Also sensitive to tissue, your cursor, cursor alignment is your TAPSI. The TAPSI is only really measuring one small portion of the RV. Is it predictive? Sometimes, but it does not give you an estimate of why is the RV failing? What's going on? Doesn't show you segmental wall motion abnormality. 3D ECHO, we're not going to do that very often. 2D strain, also, you're talking about speckled stuff. That's more in research and you need special software to do that. Haven't seen that. Anybody have a speckled ECHO in their ICU that they use every day? Excellent. All right. That's awesome. One out of like 200. So the PA catheter, it's been around for 50 years, 1970. It's older than me. I'm old, but I'm not that old. So I remember in the 1990s, we went away from the PA catheter. There was a number of studies that says it does not improve mortality. Doesn't change outcomes. And there was a suggestion that it might cause harm. If you really look at those studies, it didn't really hurt people. Yeah, they had some arrhythmias. They go away. But it wasn't looking back in the 90s. So this is like over 30 years, about 30 years ago now, it didn't. Fast forward to the 2020s, thankful, grateful to our colleagues in cardiac critical care. They've gotten together. And like the cardiologists do, they do big numbers and big data. Sometimes it's actually true and it shows. So they have multiple studies now showing that there is improved mortality and shock CHF with the PA catheter. Well done studies. In 2023, we looked at the PA catheter in cardiac ICU use and it improves mortality. You looked at about 2,500 patients, starting off with about 13,000. And these are patients that are in cardiogenic shock. And it showed that there was a 6.6% survival, statistically significant survival benefit if you use a PA catheter in a cardiac ICU. This was well done and it's a well done study. You can look it up. What do they think were the top three drivers of this? So it led to the earlier initiation of mechanical support, which is not for everybody. But if you give it to the right patients early, it saves lives. I'm obviously completely biased because I'm an ECMO doctor, I'm an MCS doctor, but I believe in it. And that the headline about COVID not working for ECMO, that the headline about ECMO not working for COVID, that's not true. It works in the right patients. There was a headline that came out today, that's a side comment. But site related, there's a lot of site related variation in terms of PA catheter. The big thing was the diagnosis of heart failure here, and a lot of that was right heart failure. The earlier diagnosis of right heart failure using a PA catheter led to improved survival. The PAPI, Pulmonary Arterial Pulsatility Index, one of the best markers, initially done in MI and then done in BADS. Then there was a group at Hopkins that did a very elegant study. It's ASLAM. Anybody from Hopkins here? She's not here. They looked at tissue. They actually looked at tissue on hearts. So they did biopsies, and the PAPI was by far the best reflected the underlying defects in RV myofilament contractility. So if you wanna look at how the RV is functioning, the PAPI here, this is a tissue validated test. And to get a Pulmonary Arterial Pulsatility Index, you do need a SWAN. So like you said, the PAPI less than one indicates possible RV failure. Less than 1.8 is failure after RVAC. So the benefits of PA catheter use, you can directly measure the pressures in the RV. It's accurate and it's reproducible. It's continuous. It's easier to trend over time. You're not gonna be dependent on who the echo tech was that day or your own echo tech abilities. You can ability to monitor the effect of your interventions after you make your diagnosis. And it can be placed safely. Absolutely, it can be placed safely. You wanna place a lot of them, but we need to have a resurgence, a new push on the benefits of placing SWANs in the right patients. So PA catheter echo, echo absolutely has a role. It's good for screening. If echo is abnormal, then you're gonna place your PA catheter. The PA catheter is more reproducible and accurate than echo. I actually believe that, and Dr. Aconte in her heart of hearts believes that too. I know you believe that, she does, but she still is gonna completely win the debate. Those were great pictures. Those are great, great pictures of the RV. So if echo is beauty, we have nice pictures. It's also blunt, it's fickle, and it's inconsistent. So that's beautiful, but that flower is not gonna look like that forever. If the PA catheter is the brains, we're getting hard data. And this guy's not as beautiful, but it's precise, it's trustworthy, and it's consistent. So provided that the two are readily available and routinely used, if we're forced to make a choice, we all know you're gonna use both, but if you had to pick once, there's growing evidence that supports the use of a PA catheter over an echo. It's physiology versus blurry photos. And so your pictures were so much better, but this is more like the picture I'm gonna get. So the swan is back, the swan is definitely back. Thank you very much, we'll send questions at the end. If you have a chance, that's the Lonnie Conway Pillbox Hike, it's on the Windward side, some of the best views you'll see, go try to make it out there. Thank you very much, Dr. Osborne. Shifting gears a little bit, now that we have diagnosed acute RV failure, what do we do about it? So the next speaker will be Dr. Cara Egerstrand from Columbia University, where she serves as the medical director of ECMO. And she will be arguing that the best initial strategy in right ventricular failure is indeed medical therapy. All right, thank you so much for the introduction, I'm happy to be here today to discuss my favorite part of the heart, which is the right side. And the best strategy, my task, is medical management. I'm a simple pulmonologist, so the TAPCs and the PAPCs, and all these things we're talking about are so great and amazing to look at. And now let's think about what we actually do with these patients in the ICU. So this is really the beginning and the end of it. Medical management is the standard of care. The next slide shows you a list of all the studies that support the use of mechanical management over medical management. We'll keep it short and sweet. But since we've already made this point, let's think a little bit more about how we can contextualize and think about the RV failure we might see in our ICU patients. All right, so first, let's characterize the problem. What are we really talking about when we speak about right ventricular failure? Is it just RV dysfunction? Does that mean that we're not doing enough? Is it just the right ventricular failure? Is it just the right ventricular failure? And then we're going to look at the right ventricular failure and the right ventricular failure. Is it just RV dysfunction? Does that come with hemodynamic compromise? Think about the number of patients you have with ARDS who have moderate to severe RV dysfunction on echo. And it's like, well, what do I do with that? This is not causing me a problem, right? Or is it? You know, and does that lead to RV failure? Are there signs of systemic hyperperfusion, elevated lactate, et cetera? And could this progress to acute corpulmonary? Okay, and I think it's really important for us to remember that when you see that patient at the bedside and you say, oh my gosh, their urine output's down, their lactate's up, they're cool and clammy, you know, something bad has already happened, right? It has already happened. And we want to be able to catch this beforehand and try to prevent that exact scenario. So we want to think not only about where we are in that curve, but also what's the etiology of this constellation of dysfunction and also the chronicity of it. Here's just a whole list of all the things that can cause RV failure. So all types are not the same and they really can't be managed the same. So from structural heart disease to pH to medical conditions, we really have a whole host of problems that can lead to this one sort of downstream syndrome. So what's leading to this? There are gonna be three main elements as Dr. Arconti mentioned. So we're gonna have excessive preload, excessive afterload, and insufficient myocardial contractility. And these are all elements we want to consider when we're thinking about how to best optimize our patients. So excessive preload. This is very common in the patients we might see in a medical ICU especially or at a CCU, but these people come to us very volume overloaded, like right atrium stretch, RV distended, et cetera. And really the mainstay of treatment here is not gonna be MCS, but it might be a different kind of catheter, which is like a dialysis catheter. So fluid management is a mainstay of treatment in these patients when they come to us especially critically ill. MCS is not an alternative to diuresis. And also we really wanna think about not only just our attempts at diuresis, but our effectiveness of it. If we're not able to keep up with that negative two liters a day, you're now for whatever it is our goal is, then we need to think about early initiation of RRT where appropriate. And I do just wanna make a comment that as well we talk about excessive preload is a real common cause of RV failure in these patients. You must remember there are a subset of this group that have the acute RV failure due to low preload, right? Those who have maybe, who have had acute PE and have just real pressure overload or hypovolemia or whatnot. And in which case their management's quite different often with a small trial of IV fluid illness. The one last thing to say about excessive preload is just to remember as I think Dr. Osborne showed us the starling curve of that right ventricle, right? It's much flatter than that of the left-sided heart. So a lot of fluid removal may have to occur before we actually see changes in hemodynamics. We just should not give up prematurely. All right, let's move on to excessive afterload, okay? So what is this? So think about all these factors we have that are gonna increase the PVR in patients. And really excessive afterload is probably one of the most common and sort of universal elements of patients who have RV failure in our ICUs. So we really wanna take this, minimize the afterload as much as possible with reversible and adjustable elements. Some which may be possible, but a lot of these patients with fixed heart or lung disease, we may only be able to modify them to a degree. And once those things have been optimized, think about a judicious use of pulmonary vasodilators, okay? So factors that may increase the PVR that we can manipulate. Oxygenation, as simple as it is, right? We wanna optimize our PaO2. We wanna target an oxygen saturation of at least 92%. You can see here in this graph how at lower levels of alveolar PaO2, you're gonna see more increase in hypoxic vasoconstriction, okay? So we wanna optimize the O2 to really minimize that occurrence. We also wanna normalize the pH and the CO2 as we're able to do, right? Similarly, at all levels of oxygenation, but especially as we become more hypoxemic, at lower levels of pH, increased PVR. So acidosis is not your friend, okay? When it, really, when is it? But acidosis is certainly not your friend in patients with RV dysfunctions. We wanna normalize those things. And also, let's not forget about lung volumes, right? So high or long volumes can really worsen RV afterload. When the lung sits at RC, that's really when the PVR is lowest in general. So as a balance, so sort of at this intermediate level of RV to TLC, that's really where these kind of, the distension of the intrinsic versus extrinsic vessels are going to be matched, minimizing that PVR in these patients, okay? So we wanna minimize hyperinflation when we can, and really cautiously apply PEEP, okay? Be mindful of the impact that it may have on someone who already has a weakened right ventricle. Now, once you've optimized and modified the things that can be modified, let's think about pulmonary vasodilators. And I say you just use the pulmonary vasodilators because even they may not have the intended effect or the same effect in all patients. And we need to be aware of that potential as we treat them, okay? So starting off, something we probably, many of us are familiar with, using halometric oxide. It's a rapid onset, has a short half-life. If the intention is not what you want, you can quickly turn it off. Typically will improve VQ matching, but again, not always. So it's sort of a, you know, give it a shot, assess at the bedside. Also has been shown to improve RV ejection fraction, RVEDV, PAP, mixed venous, et cetera. Well, we know that there's no benefit long-term for mortality in ARDS with the initiation of INO, for example. Pulmonary pressures and PH, RV failure, we definitely can see substantial improvements. Other options for medical management, process cycle and derivatives, okay? Very similar in nature to INO. Rapid onset, short half-life. Again, typically improve VQ matching, though not always. So we need to be very cautious there. And we have some inotropic appendix as well. And albeit less commonly used in the acute critically ill setting, especially if someone has multiple reasons for their PH or RV dysfunction or is concurrently septic or whatnot, but the PDE5 inhibitors. So they can increase contractility, but again, very cautious in our ICU populations, okay? Finally, the third thing we need to think about in these patients as an etiology or cause of their RV dysfunction is going to be that insufficient or limited myocardial contractility. This can be for several things. So mechanical disadvantage to the increased stretch of that right ventricle, okay? Derangements in cellular metabolism. It adequates you to do the decreased coronary artery refusion, okay? And as Dr. Conti mentioned, we really want to remember the importance of maintaining normal sinus rhythm in these patients. They do not like being in AFib. And also that AV synchrony. These high degree AV blocks can be real problematic in someone who has underlying PH or RV dysfunction, okay? So as far as optimizing myocardial contractility, some tools we have, you know, vasopressors certainly. So our goal here is going to be to increase the MAP and RV contractility without increasing the PBR as much as possible. We know that different vasopressors have different mechanisms of action as far as the receptors on which they act and at varying levels. So typically one might consider norepinephrine with its mix of alpha and beta one properties to be a great first choice in this scenario. And we know that beta one effects can improve contractility. They can improve the PA and RV coupling in animal models and improve right-sided output. And we also know that can improve myocardial oxygen delivery in patients who are septic like many of our patients might be, okay? And then what about inotropes? So once we've optimized them as far as vasopressors are concerned, we also want to think about is an inotropic agent going to be a benefit? You know, certainly we have a couple options to choose from. Dopamine, which can act like three different medicines at different levels. Dobutamine and milrinone, you know, a favorite of the cardiologists and like my cardiology colleagues. But we know that dobutamine can improve that PA RV coupling as well. Also myocardial contractility and these PVR, okay? Certainly caution to be used with both milrinone and dobutamine in someone who's already hypotensive as they have these inodilator properties and may exacerbate existing hypotension. Now, beyond our kind of management and considerations characterization of RV failure, let's think about another reason why medical management should really be primary. Well, number one, it's the complications of MCS. Here's a list of all the complications you have of VA ECMO. Oh wait, and there's the hemorrhage ones and the brain death ones and the neural ones and then the ischemia and the compartment syndrome, the amputations and the pulmonary hemorrhage and oh my God, and the arrhythmias and everything else. So, and I say this as a ECMO enthusiast myself, but it is something to remember that this is not a benign technology. You know, MCS, while it can be very helpful in our patients, has its place and it's certainly not before the less invasive things, right? We know bleeding is the most common complication even in modern application of ECMO and can result in increased odds ratio mortality. Thrombosis can be quite common and problematic, particularly when it's extracted from someone's MCA artery, like in this case down here. And we also have to remember that MCS is resource intensive. This is a finite resource that we have in our ICUs and we really need to be good stewards of how it's used, at least in COVID-related ARDS, center capacity for ECMO in this case was related to survival. And we can see in a German study looking at patients on VA ECMO for acute PE, the greater access to ECMO that was had based on sort of the urban, suburban, rural locale also associated with improved mortality and improved survival benefit in over 2000 patients. So what's a rational approach to RV failure in our patients? Well, number one, we wanna have a high index of suspicion. If we're concerned about this, you know, this is not the time you order the echo and see if the tech comes tomorrow morning, right? If we're concerned, we're teetering on the edge of medical versus mechanical support, you wanna call the cardiology fellow overnight, we need to do this here at the bedside if you can't do it yourself and get that read so you can act. Immediate diagnostics, rapid intervention. Again, this is a 2 a.m. call to the surgeon or person cannulating if they require that or immediate action and prompt reassessment. So we start them on norepinephrine, a little dobutamine, we diurese them. And I'm not gonna wait eight hours for my next set of labs, we're gonna check them again one hour later. What's that lactate? What's that urine alpha? This is a constant reassessment because it's a very dynamic process once it gets to these levels of severity and 12 hours later, it can be too late for the patient. So in conclusion, MCS should be reserved for patients who are refractory to these things, the refractory to our basic medical management for acute or chronic RV dysfunction. And it has its wonderful place way down here in the corner after we've already characterized the problem and tried the interventions that we know to be effective and of minimal resources. Thank you very much. Thank you very much. Thank you, Dr. Eggerstrand. One of the joys of moderating a session is you get to go last. You learn from everybody's arguments before you make your own, right? I'm just getting my slides are pre-met and had to be submitted. So... All right, so I'm gonna argue that mechanical support is indeed the best initial strategy. And over the next nine minutes or so, I will convince you why it is so. So first we will talk about the mechanical problem that acute RV failure presents. And then we will talk about how a mechanical problem must be solved because of the mechanical solution. Second, not just that it requires a mechanical solution, but there's a narrow window in which we must act and not wait to see how certain therapies are working because that window may close on us. And ultimately, making the distinction of different pathophysiologic states in which you have to match the right pump to the pathology to be able to see the outcomes get better. We will get to those questions in just a second. But if you think about what happens when a ventricle fails. As you can see on this graph, this is a PV loop. And in that you can see that the slope that you see in the gray is your slope of myocardial contractility. Whether it is an acute setting or it is a chronic decompensation or an acute decompensation of a chronic state, in both of those your myocardial contractility reduces. Once the myocardial contractility reduces, it moves your PV loop to the right. And why is that important? It is important because we know that between the slope of myocardial contractility and myocardial relaxation, the ESPVR and the EDPVR lies what we call the pressure volume area. And we know from several modeling systems, including animal models, that the area under the PV loop, the PVA, actually corresponds directly to the amount of myocardial oxygen consumption by the myocardium. Now that we think about where is this oxygen going? You can see that a very small fragment of this oxygen is actually going to the basal metabolism. Most of it is going to the calcium cycling and the actin myosin uncoupling. In other words, a lion's share of the oxygen requirement by the myocardium is going towards mechanical work. And we just saw on the previous slide that the mechanical work, the PVA, the area under that loop actually increases both in the acute and acute on chronic situations. So now we talk about what should be our initial strategy and stuff. If you look at this graph, that shows what happens when you give somebody dubutamine. Yes, you can sit there and argue that as the dubutamine infusion increases, so does your coronary sinus flow, which is a surrogate marker of how much oxygenated blood is getting into the myocardium. But look what's happening in the graph in the bottom. You may be offsetting the myocardial supply of oxygen, but you are also increasing the amount of myocardial oxygen demand. There's a reason why in chronic heart failure, and when we take care of patients longitudinally, we call them palliative inotropes. It doesn't recover the ventricle. It doesn't make the patients live longer. It simply whips a dead horse so that you can get more juice out of it. Now, does that sound like something you want to do in a patient that is critically ill? Perhaps not. Contrary to that, what happens when you actually unload the ventricle with a temporary MCS device? Your ventricular volume, this pressure loop is from the left ventricle, but a similar phenomenon exists on the right side as well. So as your pressure volume goes down and your LV volume and pressure, both of them come down, the graph again, the PV loop again shifts to the left. And as you saw on the previous slide, once it comes down to the left, the area under the PV area, it goes down and so does your myocardial contraction, myocardial oxygen demand. So overall what it is doing with this temporary MCS, it's allowing you to actually provide cardiac rest while you are enabling the patient to have circulatory support. It is an important distinction to make. What is cardiac support versus what is circulatory support? Temporary MCS allows you to deliver the circulatory support without jeopardizing the ailing myocardium. This is similar to the slide that we saw in Dr. Akanti's slideshow as well, that eventually what happens is that you start off with it being a hemodynamic problem, but as you go down the spiral of death, it becomes a hemometabolic problem. In other words, if you are gonna propose a solution, that solution has to come early so that you are tackling the hemodynamic problem before it becomes a hemometabolic problem because a lot of things that you may do for that patient once it's become a hemometabolic problem may be less effective. All the more reason why your temporary MCS should be the initial therapy in patients that present in a critical situation. That brings us to this concept of the golden hours that I like to think about. This is generally the progression of what happens in cardiogenic shock, whether it's coming from the left ventricle as the primary etiology or the right ventricle. You have a narrow window of golden hours where it's starting to kind of project the end organ injury and your multi-organ dysfunction syndrome is starting to creep in. This is where it is still a hemodynamic problem, a mechanical problem that can be rescued using mechanical solutions. But then over a period of a few hours to days, it goes into the silver days where you still may be able to salvage the situation, but beyond that, it's too late. This is where the SERS has kicked in, the irreversible multi-organ dysfunction has kicked in, the acidosis is progressively getting worse, and if you wait too long to see what plan A, B, C, and D will do, you will be in sky stage E, and that's the end game. That's how it ends. So it's important not just to put patients on mechanical support for the mechanical problem that we called acute RV failure, but it is also important to identify which of the devices that are available to us is gonna deliver the exact solution to the problem that we have inherited. And as we are all aware, there are several different devices available. Obviously, the best device is the one available at your center, but for the sake of discussion, you have devices that directly bypass the RV, as is the case with a right-sided Impella, a tandem RVAT, or a Protecvio, and then there is indirect bypass of the RV, as is the case with VA ECMO. It is important to recognize that every single one of the pumps, the continuous flow pumps, works on a principle called HQ curve. What this means is that the flow across the device is dependent on what is the pressure gradient against which it has to push blood forward. In other words, if your RV pressure is very low and your PA pressure is very high, the pressure head is gonna be very high. So at any given RPMs that you set, the machine's not gonna be able to flow as much blood across it because it's more resistance that it has to meet. This is why identifying the etiology of your RV failure is critical, because if you have a patient that has pulmonary hypertension, where the RV is failing and the RV systolic pressure may be low, but the pulmonary systolic pressure is high, that puts you in this end of the graph where your pressure head is high, and so at the same given RPMs on a machine, you will not be able to flow as much. On the other hand, if somebody's presenting with an acute RV infarct, where your PA pressures are perhaps not high, but your right-centered pressures are very high, the sicker the ventricle, the better this device works. And in that sense, you would fall in the graph where your device flow would be closer to six liters because the pressure head is lower. So in conclusion, it is a mechanical problem that we are dealing with that requires mechanical solution. It is important to make the distinction between what provides circulatory support and what actually provides cardiac support. Early comprehensive support is the key to halting the death spiral. You're gonna get one shot, if you're lucky, maybe two at saving that patient's life. And third, it is critical to match correct prompt to the pathology. And with that, I rest my case. And you guys may recall that we asked you two questions at the start of this session. We will go back to the exact same questions and then we'll share with you what your answers were. So the first question again, is identical to where we started the session, which is what is your preferred initial method of diagnosing RV failure in a cardiogenic shock patient? Assuming you're at a center where both options are readily available. We'll give it a couple more seconds for any last-minute votes. I think we started the session at 170, so some people have been thoroughly confused. They just don't want to hurt some of us, that's all. They're staying neutral. All right, we will move on to the next question. Actually, it's going to show us the answer, so let's see. For the first question, what is your preferred initial method of diagnosing? We had pre-test 76% said that they would choose echocardiography, but after the debates, only 54% said that they would use it. Go Eric. So Dr. Osborne, that... It's because I said that Dr. Akanti would choose a PA catheter, and she would. Which I probably would. Probably, you totally would. It's together, together always. I'm not good enough to do the P-value, but that seems statistically significant to change. Yeah, I think so, I think so. All right, we'll go to the next question, and then we'll open the floor for any questions and stuff. The second question, once RV failure has been diagnosed as the cause of cardiogenic shock, what would be the preferred initial treatment modality, assuming that you are at a center where both medical and temporary MCS options are readily available? All right, we'll give it a couple more seconds, and then view the results. All right, so it sounds like. There's been a few. Go pulmonary. That's right, that's right. I am a chest after all, not at ACC. So it looks like 81% chose inotropes as the initial choice before. We're able to move the needle a little bit, probably trended towards significance, but not significant. And with that, we'll open the floor to any questions that you guys may have. And thank you very much for being a part of this session. Thank you guys.

acute right ventricular failure

echocardiography

pulmonary artery catheterization

early intervention

mechanical support

medical therapy

diuresis

vasopressors

inotropes