Okay, good morning. We are gathered here today to discuss matters of the right ventricle. And pursuant to the session notes, we will discuss our disclosures, which are largely none. And please remember to evaluate us using the application on your phone. That said, we are gonna discuss first a non-invasive diagnosis and monitoring of RV failure. My name is Max. I am an intensivist from Washington, D.C. And I work predominantly in a CVICU. Oh, I have to be loud. Nobody in my life has asked me to be louder. It's the first time for everything. Yeah, this is good. Hawaii is a great fit for me. Okay, so when patients come to the ICU, they have many types of trespass. Whether it's an AKI, whether it is liver injury, whether they are just not acting quite right or more commonly than not, they have gotten an absurd, or I guess what some people would consider a reasonable amount of volume resuscitation, anywhere between 10 and 20 liters of isotonic crystalloid, which of course can result in RV dysfunction and failure. So there are a couple of ways that we can non-invasively go about figuring out who these patients are. And of course you can do physical exam. You can use an ECG. You can use echo and of course CT. So what do we see here? JVD, jugular venous dysfunction, absolutely. And there are many people that walk into a room and they can have this like sixth sense, this super normal inference of, ah, their CVP is at least 17 and a half. Okay, and you can argue that with the predictable passage of time and available of many different monitoring techniques and technologies, that the art of the physical exam has largely been lost in some populations. So the evidence to support the continued use of JVD is difficult. We know that patients that have JVD compared to those that don't have JVD probably have higher left heart filling pressures. This is a relatively blunt instrument and you lose a lot of important granularity when managing patients with right heart failure. So almost like a price of admission when you come into the hospital, you get one of these. You get an ECG and someone says that there's no STEMI and then they kind of hide the ECG never to be seen again in the chart. And when you are concerned for a patient with any type of right ventricular involvement in their presentation, there are a couple things that I want us to look at. The first is right axis deviation, where you have a downward deflection in lead one and AVF is largely isoelectric here. But more helpful is the RVH. And this is when you recall way back to when an attending, when you were a medical student, asked you very mean questions about R wave progression. And maybe this is largely autobiographical and I'm just telling my story here. So I don't want you to think about it as the right ventricle, I want you to think about it as the anterior ventricle. And this has lots of consequences when you think about echocardiography and electrocardiography. So you can see absolutely nothing because the mouse doesn't show up here, that the right vent, the laser. So here you see the right ventricle is closest to the sternum. And on yourself, I want you to find leads V1 and V2 on the chest. Please do not do this on your neighbor. So yeah, peristernal right and left, but between the third and fourth intercostal spaces. And so when your RV gets really big, and it's directs lots of electrical forces anteriorly, which will cause your leads V1 and V2 to have these massive R waves. You'll also see left atrial enlargement in lead two, these very, very peaked P waves, two and three here, which is not all that uncommon. Then of course we get to why we are all really here today is ultrasound. And every single modality of point of care ultrasound is readily applicable to patients with RV failure dysfunction. You can use the 2D or the normal phased array probe. You can use M mode Doppler, which of course comes in four flavors. There's color Doppler, there's pulsed wave Doppler, continuous wave Doppler, and tissue Doppler imaging. So the first view that everybody gets when they put a probe on the chest with a probe directed towards the patient's right shoulder is the peristernal long view. And one pitfall that some people will make is they will look at this and call this the RV. What is this really? This is the RVOT. So just like this is the LVOT right here, this is the RVOT right there. The reason that I draw the distinction is that the RVOT is not the most muscular part of the right ventricle. So be careful when you make sweeping generalizations about RV function just based on the RVOT. You can talk about RVOT size by looking at what's called the rule of thirds. And this is a gross estimate that the RVOT size, the LVOT size, and the LA size should be approximately the same. So it should be one third, one third, and one third. And so by contrast, what do we see here? Abject sadness. So what you see here is a large RVOT with something hanging out here in the RVOT. And you see the LV walls, which are relatively close together. You can see that the RVOT diameter is clearly bigger than the LVOT in the LA. We then go to our peristernal short view, which is, for me, the most exciting. So the peristernal short, outside of RV considerations, is unique because it is the only view where you have all three coronary artery distributions. So you can see the right and both systems of the left. And you can take a peristernal short view in three different cuts. So here you have the level of the papillary muscles, which looks like two boxing gloves. You have the mitral, which looks like a fish mouth. And then you have your basal view, which is similar, if you are TEE friendly, an RV inflow-outflow view. I find that when you talk to trainees or to friends, if you just talk about carbs, they are usually into it. This is not my slide. I found this on Twitter, or X, or whatever we were supposed to call it since we killed the bird, that when you do a peristernal short view, your LV should look like a donut and your RV should look like a croissant. And usually when you tell a trainee that, that sticks with them for life. So when you compare a RV that is volume overloaded to a normal RV, which is not, which is more concentric, when the RV dilates, it starts to push the septum closer to the left ventricle. And so the septum will start to appear flat. And of course, you'll see this most readily on a peristernal short view. One thing I caution you about is when you get a peristernal short view, you wanna make sure that you are cutting the LV at an orthogonal angle. You wanna be very sure that you see both papillary muscles when you are evaluating the septum. So when you see this echo here, you may be tempted into calling septal flattening right here. But notice you see like half a pap, half a mitral, and you don't really have a good idea of where you are in the LV. Now, when the image was corrected, you can see both papillary muscles. You can actually quite nicely tell that the septum is nice and rounded. So what do we see here? That's correct, more manifestations of abject right ventricular sadness. So you'll see what's called the D sign, where you have the septal flattening, a very small LV cavity, and a very, very large right ventricle. This gets to the idea of ventricular interdependence or interventricular interdependence. Don't think of the right ventricle and left ventricle as brothers and sisters. They're roommates fighting for space in a condo. The pericardium really only has so much room. And when one ventricle fills, it takes up space that the other ventricle could also use to fill. And when the RV starts to fill even more, it will exert pressure on the interventricular septum, which will push the septum towards the left ventricle. One way of quantitatively describing the output of the right ventricle is to use what's called RVOT, or right ventricular outflow tract, volume or velocity time integral. I won't go into the elegant derivation of calculus because it's early in the morning and people are probably still sleepy. The important thing to know here is that VTI is proportional to stroke volume. The reason this is important is because up until now, we've only talked about geometric changes in the right ventricle. The way that we see them of the amount of RV cavity that goes away with systole, or the amount of dilation that you see, these are all geometric changes. What we're inferring here is something about the amount of blood that the RV is ejecting. So RVOT VTIs, when measured, are usually lower than LVOT VTIs. So LVOT VTI makes a very similar assumption with a caveat. We assume that the LVOT is a cylinder. We know, based on a lot of imaging using MRCT and echo, that the RVOT is not actually cylindrical, that it's actually more ovoid in its appearance. The other piece of data that we can get from an RVOT VTI is something called the pulmonary valve acceleration time. So when the PA pressures are very high, you can imagine that it will take a short amount of time for the pressures between the RVOT and the PA to equilibrate. So the faster that those two pressures equilibrate, we will call it the faster the acceleration time. And so, while it's a little bit counterintuitive, the higher the acceleration time, the more time it will take for the pressures to equilibrate, and the likely more normal your PA pressures are. There are many factors that impact what's called your PVAT, or the pulmonary valve acceleration time. This is a very fair, quick, and dirty way of gaining inference into the presence or absence of pulmonary hypertension. Then, of course, we get to our apical shot here. And what do we see? We see a large right ventricle, and you also see the moderator band here, which houses the right bundle branch. And whenever you see a large right ventricle, you see this moderator band, and there's this space between the moderator band and the apex, which looks a little bit hyperkinetic, that's almost winking at you. What are we always looking for? What sign? McConnell's sign, absolutely. And so I was at a music festival, and I saw McConnell's sign, and I took a picture of this and sent it to a couple of my friends. I was like, I found McConnell's sign. Both of my friends were very unimpressed. So McConnell's sign should not create a monosynaptic reflex to pulmonary embolism. This has been described in pulmonary embolism, but it actually performs relatively poorly when talking about its presence and specificity and sensitivity for PE. What we don't do a good job of is looking at the whole picture. What you see here is a clot in transit. You see this somewhat worm-like, gross thing hanging out here in the right ventricle that is trying its best to get into the right ventricle. This should be a monosynaptic reflex to call for lytics, plus minus ECMO, plus minus an intervention. But what you also see here is stigmata of chronic pulmonary hypertension. The shot here is a little bit posterior, and what you see is a dilated coronary sinus. And for patients with pulmonary hypertension of chronicity, you can almost universally expect to see some degree of coronary sinus dilation. So when we move on to M-mode, you can see that the tricuspid annulus is very bouncy. And so this is a local measurement where you put the M-mode cursor over the tricuspid valve insertion into the lateral free wall here, and you can see that it goes up and down, up and down, up and down. I caution people to not make overarching statements about RV function based on a local measurement. So a global function should not be determined from a local measurement. And this is true whether you're using M-mode or any types of Doppler. If you're going to do TAPSE, there are a couple of things that we want to make sure that you're doing correctly. When the tricuspid annulus moves, it moves towards the apex. So you should expect in a normal four-chamber view to see the tricuspid annulus move towards the apex, not off to the side near the side of the screen. The other piece of information that you can get from an apical four-chamber is the presence of tricuspid regurge. I want to be clear. A lack of tricuspid regurge does not mean everything is fine with the right ventricle. In fact, what it could mean is that the pressures have equilibrated and you have no RV output at all, which is a very dangerous place to be in. The reason that you care about TR is that using the modified Bernoulli's equation, 4V squared plus right atrial pressure, you can gain some inference to your PA pressures. So your RV systolic pressure equals your PA systolic pressure. This is likely underestimated in patients with chronic pulmonary hypertension. And so here, you want to make sure that you use what's called the chin and not the beard. So you see that your continuous wave doppler has this kind of like almost ragged looking kind of disgusting things hanging off the edge here. You want to make sure that you get the very tip of the parabola and none of the trash underneath it. No information is always better than wrong information. So make sure that when you are, regardless of the measurement that you're doing, whether it is a tricuspid valve gradient, whether it's an RVOT VTI, that your measurements have reproducibility. The last part of the echo that you care about is tissue doppler. And the tissue doppler is a relatively old school way of just looking at how bouncy the myocardium is. It's really not all that sophisticated of a technology, but the number I want you to remember is 10. You put the tissue doppler gate similar to where you would place the M mode for your TAPSY. And you expect that the tissue doppler would move closer towards the apex like we discussed. And I want you to remember the number 10. Usually 10 is a normal value for your tissue doppler. And I wouldn't be living up to my training as an emergency medicine doctor without talking about a CAT scan. It's okay, you can laugh. It's fine. I have friends that are ER doctors. No, I'm just kidding. So there are a couple of great studies that look at the utility of CT in patients with RV dysfunction and failure. And the really obvious ones are to look at flattening of the interventricular septum, though I caution people here because these are averaged images. These are dynamic things that you are getting just a narrow slice in time. The other thing that you can look at is IVC reflux. This is graded one through four. Four is bad, zero is none. And you can compare RV to LV ratios. And of course you can use volumetry, which is not available routinely on every single scan. So with combinations of the physical exam, your ECG, echo, and our friend and colleague, CT, you can start to manage your patients with RV dysfunction. Next I want to introduce Dr. Tonelli to take us through one of my favorite subjects, hemodynamic trends in right heart failure. Maybe. Well, it's gonna be hard to follow that act, but I'll do my best to keep it up. So I'm gonna talk about hemodynamics in right heart failure. No real conflicts of interest with this presentation. We're gonna show some of the typical RV characteristics. Some common errors in the measurement of cardiac output, which is essential to assess right ventricular dysfunction. Some tests that'll challenge the cardiopulmonary circulation. And then I'll show you a little bit about pressure volume loops, which is the gold standard to assess the coupling of the RV with the pulmonary artery. In the definition of right ventricular failure, we have two important concepts. One is the dysfunction, which is just the RV not working well. And the other one is the right ventricular failure when you have a clinical diagnosis of right heart failure in association with the RV dysfunction. So you could be compensated and not have failure, but just the dysfunction. It's important to know that the RV is coupled with the pulmonary artery has low impedance. It's very distensible. And then the systolic function of the ventricle depends on a bunch of things. And that hopefully with hemodynamics we can assess one would be the contractility, the afterload, the preload, and other factors that may affect the function, the rhythm, the synchronicity of the contraction, the interdependence, whether you have TR or shunts. The pulmonary artery catheterization allows you to measure a bunch of things, basic stuff, initially right atrial pressure, mean pulmonary pressure, which in cardiac index and mixed venous oxygenation. And with that, you can calculate PVR. You can also do a nitric oxide challenge test to assess pulmonary vasopressor activity. And you can do some more advanced interrogations such as exercise or the vitamin challenges that we'll show you in a minute. These are the key hemodynamic determinations. The mean pulmonary pressure, the wedge, and the cardiac output. And based on that, then you can place patients in different categories that we just recently updated. They're going down, the mean pressure went down from 25 to 20 for pulmonary hypertension, and the PVR for pre-capillary pH from three to two. And hopefully at some point in the future, the wedge will also go down from 15 to 12, which is the upper limit of normal. This is the only one that yet has not been adjusted by the upper limit of normal. It's important to know that as you start getting sicker, the RV dysfunction progresses over time, the radical pressure will go up, the cardiac output will go down, the mixed venous oxygenation will go down, and the mean pulmonary pressure, it's important, will go up initially, but then it will go down as the cardiac output goes down. So that relationship is important because if you have just one picture instead of the whole movie, you don't know exactly in what part of that spectrum you are. And also it's important, the hemodynamic evaluation, because at some point in time, you will not know how is the RV preload. Maybe it's too much, maybe it's adequate, or maybe it's not enough. If the preload is low, then the RV will lose some of that contractility. But if it is too much, then by the interdependence that we just recently described, the LV will be smaller with decrease in filling and decrease in the cardiac output. In that case, you will want a diuresis. But if your diuresis is a patient that's compensated, then you will lower the preload and then the contractility of the RV will go down. So you have to be very careful in the ICU when you give fluids or diuretics to these patients. Cardiac output, you can measure by different ways. Thermal elution, which is the normal way we do in the ICU, where you want three measurements with less than 10% difference. Then you could potentially do indirect FIC, but indirect FIC, you can see that it has a bunch of parameters here that are very hard to estimate, particularly in a patient that's sick in the ICU. One of those is the oxygen consumption. I mean, 125 times body surface area for everyone appears to be a very general calculation. And then the mix, the arterial and the venous oxygen content also has hemoglobin, but the saturation arterial and venous, and certainly you need an ABG for here because obviously the pulse ox is not good. So indirect FIC, not recommended. And ideally you want to do direct FIC where you will have 15 minutes of metabolic heart attached to the patient with no leaks and then you get an arterial and a mixed venous gas. And that's important because we've previously shown that in 75 patients where we did both direct FIC and thermal dilution, that although the average difference is not significant, zero, there is a lot of, the limit of agreement is significant, up to a liter for cardiac index, which is a lot, particularly if you are on the range of 2.5, which would be kind of the cutoff from normal to low. And one thing you can do, certainly in the ICU, is to measure the mixed venous O2. We have seen before that it differentiates pretty good the survival, better than the cardiac index. And there's a lot of overlap between the mixed venous O2 and the cardiac index. So there's maybe patients that have a cardiac index above 2.5, like in this one, with the mixed venous O2 less than 60, so this group. So ideally, mixed venous will provide more than just the cardiac index since it also reflects how good the oxygenation to the tissue is. And as it gets worse, obviously the tissue will extract more oxygen and the mixed venous will be low, even when the cardiac output index appears to be appropriate. Another way to challenge the right ventricle is by doing exercise. Obviously you will not do it in the ICU, but patients that come and they have symptoms of shortness of breath and you're suspecting that some of that is related to RV dysfunction, you can check with these the contractility reserve. So with exercise, the cardiac output goes up and you need to have an appropriate response. You can calculate cardiac output percentage of predicted for every patient. New guidelines on pulmonary hypertension, for example, they use results of the CPED, and if you have oxygen consumption less than 11, you are what we call high risk. 15 to 11, this is milliliters per minute per kilogram, then you're intermediate, and more than 15, you're normal. And this has a direct relationship with the right ventricular function. You can also give the vitamin, and if you see a normal response here on the right, whereas you are giving the vitamin, this is a large increase in cardiac output with minimal increase in mean pulmonary pressure, but if you were to have, for example, pulmonary hypertension, you have a minimal increase in cardiac output with more significant increase in the mean pulmonary artery pressure, and you can calculate this right ventricular contractility reserve that's diminished in patients with pulmonary hypertension or RV dysfunction. Another thing, the gold standard, is the pressure-volume loops, and there's more and more literature coming up on this topic to assess right ventricle, since this is the gold standard. It has been used in all these different conditions, including pulmonary hypertension. This pressure-volume loops measures the pressure and the volume. There is a catheter that I'll show you in a minute that will allow you to get these two measurements. As you're measuring, the volume will go up in diastole. The pressure will increase until you are here at the end of diastole, and then there's contraction of the heart. Pressure goes up. The volume doesn't change. Then you eject. Volume obviously lowers, and the pressure is sustained, and then you have the relaxation where the pressure goes down, and then the feeling goes back again. This goes counterclockwise, and that will be important because that tells you when the catheter is well-placed. You have that. With that, you can calculate if you have several loops, what's called this multi-beat method, even by doing valsalva, abdominal compression, or an inflation on inferior vena cava balloon. You will have several of these loops, and with that you will be able to calculate this encystolic pulmonary vascular relationship called EES, encystolic elastance, which is a measurement of the RV function. The better the RV function is, the steeper this curve will be, the larger the angle. Then you can assess the afterload by this other line. That will be a measurement similar to a PVR. The better the contractility of the RV and the lower your afterload, then the better will be the coupling. The coupling is from 1.5 to 2, and that is important since this is the best way to assess early RV dysfunction. I recommend you this paper, which is a summary of all what I'm mentioning here. This will be an example of a normal patient here in blue, a compensated patient with pulmonary hypertension in orange, and a decompensated patient in green. As you can see, the decompensated patient has a less steeper slope here and a similar artery compliance. The index is 1.2, where normal value, as I mentioned, is 1.5 to 2. This is a compensated one, the same as a normal individual. That's important to know. This catheter is the one that does that for you. It measures the pressure here in this sensor. It has a bunch of rings that have electricity that runs through them, and the higher the volume that you have, the lower is the drop in voltage here between these rings. It measures volume at different parts of the heart. This is how the catheter is placed. This patient has a pacemaker too, but you put this in the tip of the RV. It comes in 7 and 4 French. Then it will measure the volumes here at different parts of the RV. Then we'll integrate the volumes with the pressures that you are also measuring, and then you get the pressure-volume loops. Using the pressure-volume loops, then you can assess the coupling. Here is 0.93. When we're giving this patient, for example, nitric oxide, it did improve. It didn't improve by increasing the contractility of the heart because you can see that the EES, the end-systolic elastance, is similar, but it decreased the afterload from 0.8 to 0.68, so then the ratio improved, so the coupling improved by giving nitric oxide to this patient, and you see the relationships there. This is kind of a more sophisticated tool. The tool is not reimbursed by insurance, so unfortunately it has very specific centers that do this, but it's kind of the gold standard if you wanted to prove a concept without people criticizing it. So for hemodynamic evaluation, it's essential to identify the mechanisms of right ventricular failure, whether you want to give fluids, you want to give diuretics, an endotropic agent that Matt will discuss in a minute. And then wedge and cardiac output are essential to be adequately measured because you're making decisions based on this, and then there are different methodologies that you could potentially use to get a more deeper insight of what's going on. And with that, I finish. So next is a man that needs no introduction, a true champion of the right heart, Dr. Shuba himself. Thank you, Max. Thanks, everyone, for being here. This is super exciting to see this many people packed into a room to talk about the right ventricle. I could not be more thrilled. And the other thrilling thing for me is I just truly admire and love everyone that I'm speaking with today, so it's great that this session was able to come together. So now let's get into the meat of it. Let's start busting some myths about how we take care of the right ventricle. As stated, I'm Matt Shuba. I'm an intensivist at the Cleveland Clinic in Ohio. So the thesis, the only thing you really need to take away from this whole presentation, is that physiology-guided critical care and excellent RV-centric care are usually indistinguishable. That's the pretense of this whole talk. This is a talk that's physiology-rich and evidence-sparse, and you'll find out why. That's because nobody cares about this poor ventricle. All right, so the objectives are to just understand when we're expecting to see the right ventricular dysfunction and outline some physiologic principles to help us decide how to treat it, and then we'll talk about a therapeutic framework for how we might work through these problems. So who is at risk? Patients with ARDS and septic shock, who most of you take care of, about a quarter to as many as half of them are going to be affected by right ventricular dysfunction, and it might increase their mortality by 50%. Pulmonary embolism is the obvious case. I'm not going to dwell on that too much. Another sort of orphaned group here is patients with decompensation or preexisting PAH. We have no data on how to take care of these patients, but we know that they develop right ventricular dysfunction, and it's sometimes a common pathway towards death. Primary cardiac dysfunction in most of the units that we work in, like RVMI, is going to be less common, and we'll talk about why that's important coming up later. So now we'll talk about the RV is challenged and how it must rise to that challenge. Every RV talk features some version of this chart, so it's there. You can put it in your phone. I'm not going to walk through it. The most important thing that we need to talk about is these pressure-volume relationships that Adriana alluded to, and we'll get into that in a second. The first thing to start with there is let's talk about the RV being preload-dependent. It's everybody's favorite thing to say about the RV. It's preload-dependent. That must mean it needs fluid. Preload dependence, my friends, is life. We should all be preload-dependent. That would be a desirable circumstance to be on a part of the Starling curve where if I augment your end-diastolic volume, your cardiac output goes up. That's beautiful. But the sick RV is usually volume-overloaded and requires preload optimization, which often means removal. However, the primary problem I will contend to you in most of the patients you take care of in the ICU is going to be excessive afterload. This is a condition of acute pulmonary hypertension in the vast majority of cases. Now I get to move into pressure-volume loops, which you just heard about, but gosh, how could we not talk about them? The most important things here to understand are this stroke volume, which you see represented as the distance across the X axis between those bounds, is bounded by that contractility of the ventricle and the diastolic elastance. So it's stuck in this box between these two areas. And the stroke volume cannot rise outside of those bounds. So that's really important to know. So the only way you can grow that area is to improve the contractility or to improve the diastolic function, which if you're going to do that in the ICU, good luck. But the other important bounding factor here, which Adriano alluded to, is the arterial elastance. This is more a reflection of pulmonary afterload. Just like the EES curve, the steeper that is, the better the contractility is. The steeper the EA curve is, the higher the pulmonary vascular resistance. And so as you can imagine, as you pull that curve up towards the right, the bounds of that stroke volume are going to contract a little bit. So let's revisit this issue using this beautiful framework. Let's revisit this issue of what happens when you raise the end diastolic volume. So in Panel A we have a patient with a left ventricle, which has a beautiful end systolic elastance of 3. That's a high normal. And you see for each time each of those boxes, successive boxes, is raising the end diastolic volume from one-fold to two-fold to three-fold. And you can see the stroke volume rises nicely and the pressure rises. In a normal RV, you very quickly become limited by those bounds that I talked about. So even in a normal circumstance, if you increase that end diastolic volume by just a little bit, you'll quickly rise the pressures because you're bounded by the diastolic elastance. So the diastolic function is going to do what's called limit. It becomes volume limited. So it's taken all the volume it can take, and it cannot improve its output above that. Even worse, when you have an RV with decreased function, let's say the systolic function is decreased, as in Panel C. So now my end systolic elastance or my contractility is cut in half. That bounding occurs even faster. This would be a typical case you would see in somebody with a pulmonary embolism whose contractility has fallen, and they can't even raise their RV systolic pressure above 60. That's why that 60-60 sign comes into play when we're talking about trying to assess hemodynamically significant pulmonary embolism with echo. So what's a better strategy? Because obviously increasing preload here had minimal effects. Changing the arterial elastance can actually have a huge impact on this. So in Panel A here, we have a normal contractility, and we go from the stroke volume the farthest to the right is 50 mLs. And as we decrease the pulmonary afterload, we really dramatically increase the stroke volume. We can get it down to 110. Even in the case on Panel B here when you have impaired contractility, rather than rising the contractility, you get more bang for your buck by decreasing the afterload. So what about the preload? Because everyone likes to talk about it. You usually have to decongest these patients. If you decide that for some reason that this patient needs fluid, and some of them might, if the CVP is rising, the cardiac output must rise, otherwise you've congested this patient. If you're not sure what to do, it's kind of an intermediate situation, just save the preload for last. It ain't the most important thing, I promise you that. So fact one to bust the myth one. Afterload and contractility are the dominant factors in RV performance. So preload dependency is something we need to just take out of our minds and put on the side because it's really not the most important thing about this issue. If you're going to focus on it, though, you need to try to decongest the heart to the point where you improve the geometry of the heart. So Adriano and Max both talked about intraventricular dependence. You should try to reverse that. Stroke volume, remember, is bounded by contractility, diastolic elastance, and afterload. You have to manage these first, but really, really focus on the afterload because that's going to be the most modifiable. Let's take myth two. The RV hates peep. Everybody says this. It depends. So if your lungs look like this, and I put you on zero peep or five of peep, your lung volumes may fall and the extra alveolar vessels may collapse and your PVR might rise. Similarly, if I overdescend your lungs, the same problem can happen by compression of intraalveolar vessels. So it really depends on how far you are from FRC. FRC should be your goal in most patients on a ventilator, but especially in someone who you're trying to minimize their PVR. You really have to pay attention to the ventilator prescription you set on these patients because with rising tidal volume, your PVR will rise. With rising driving pressure, your PVR will definitely rise. The other things that we often think about in these cases are the gas exchange issues because if you induce hypoxemia, hypercapnia, or acidemia, those all have kind of a synergistic effect on raising the PVR, and it's reversible. This is a mouse model. What happens in people? These are healthy people who have pressure volume loop catheters placed and are exposed to progressive hypoxemia. So you can see at FiO2 of 0.21 on the left panel, this is kind of like a normal-looking pressure volume loop, but you see it's not as pretty as the diagrams I showed because this is in real people. As that FiO2 lowers, your end-systolic volumes are rising, which is telling you that your stroke volume is worsening and your RV function is worsening and your PA pressures are rising. So even in a normal subject with no infection, no ARDS, hypoxemia could be a problem. So if I'm managing a patient in the ICU with RV dysfunction and they're on a ventilator, I'd like to have an advanced respiratory monitoring toolkit, and these are some components of things that I think would be helpful. I think volumetric capnography is probably essential for two reasons. One, to minimize dead space, and second, it's a surrogate for cardiac output. I think if you're going to manage a patient with severe RV dysfunction in the ICU on a ventilator, you should probably be measuring cardiac output some way, and I'll leave that up to you. My choice would be the pulmonary artery catheter, but that's what I have. But it doesn't mean you can't learn more information about the loading conditions by looking at the echo parameters that Max described. And then finally, I like esophageal balloons in these patients because I really want to make sure that I'm not over-descending the lung, and I want to make sure that my PEEP is optimized. So you have a patient that's very, very obese with RV dysfunction, and you set their PEEP at 8, same problem. We're going to raise the PVR by dropping the lung volumes below FRC. A couple of words about intubation because I don't have time to talk about all of it. First of all, one of my fellows is going to present on this in the hall downstairs at 1015 about how to intubate the patient with pulmonary hypertension in the experienced chest area, so go listen to Dr. Monick talk about that. But the first thing about intubation, maybe don't do it. This is a really dangerous situation. Easy to say, right, but this is a time where you really have to have the most aggressive early goal-directed palliation conversation you've ever had in your life because if it doesn't make sense for this person to go on a ventilator, it's going to get bad real fast. You should already probably be resuscitating your patients before you intubate them as it is, but you really need to be proactive about management of the blood pressure before you put these patients on because remember that you need to have some sort of gradient between your systemic systolic pressure and your RV systolic pressure to make sure you protect coronary perfusion. Consider awake fiber optic approaches if you have the skills and the tools to do that. And then really importantly, make sure you have an exit strategy. So if this is a patient who you think might be a transplant candidate or an ECMO candidate, maybe you put some introducers in ahead of time so if they crash you can quickly put them on ECMO. Or like I said in the first place, maybe don't do it. If this is an end-of-life situation, putting them on a vent is not going to make it any better. So to summarize, lung volumes and pressures are an important determinant of the effect of positive pressures on RV afterload. Careful intubation strategy by your best operator is the key. And utilize an advanced toolkit for respiratory monitoring when you have these patients on a ventilator. Now let's go into the last myth. All failing right ventricles should receive whatever medicine. Everyone's like, oh, they do great with the butamine, milrinone, nitric, EPO, levosimendan. I don't have that, but maybe you do. Epi, vaso, they all have the perfect things. And then they just put the medicine on and they walk away and they go see the next patient. This is what I call the Ronco School of Physiology of set it and forget it. It doesn't make any sense. So we looked at this question because we were really curious. It was like, what actually works for the RV? And we decided to focus on a group of patients with ARDS. And as it so happens, two of my co-presenters and I wrote this paper together, and it was headed by one of our excellent residents who will hopefully become one of our excellent fellows, Simran Gananurwal. So in this study, we did a scoping review of all studies that assess right ventricular function changes with different treatments across time. We only found 51 studies. And only 30% of those were actually directly trying to modify the RV function. And only three of these were randomized control trials. As you can see, most of them are non-randomized experimental studies. Some of them are retrospective. The data quality is not very good. So you might ask me, Matt, what's the best medicine to manage a patient with right ventricular dysfunction? I don't know what to tell you, man. So let's talk about some general principles quickly. It's really important to manage the ventilator prescription well. If the patient has ARDS, there is some suggestion that prone positioning may be RV protective by improving the distending pressures and maybe the gas exchange. So that's something you should think about earlier. Maybe even if they don't meet traditional criteria for proning, but they have a bad RV is something to think about. You can trial inhaled pulmonary vasodilators. But please remember, again, it's not set it and forget it. You should actually see if it helps. Because if it's not helping, then take it off. You're exposing somebody to a medicine that could potentially be harmful. And you should be thoughtful about your vasopressor selection. We can talk all about vasopressin. Maybe the fact that there's no V1 receptors in the pulmonary circulation. Maybe you won't have pulmonary vasoconstriction. Some people think there's pulmonary vasodilation. But you just have to be thoughtful about it, whatever you're trying to achieve. And it's not just blood pressure. The real principles of managing RV geometry by preload optimization is key. You should optimize the systemic milieu as best you can, acid-base and systemic pressures. We really don't know what the best inotrope is. And all of them come with risks. But remember, this is predominantly an afterload problem. So you should really think about afterload before you think about contractility. So what this comes down to is RV therapeutics are actually very poorly understood. But what I ask of you is please consider that if you're going to apply a treatment to a patient, you must reassess it in some sort of objective way. So you have to say this is the model that we ask our fellows to follow when they're treating patients with hemodynamic failure, is to say I'm going to assess the patient, I'm going to create a hypothesis, I'm going to test it. And then you have to reassess. This is a constant loop. And until the patient gets to a place that you feel better about them, you should be careful. And don't just assume that putting on a certain medicine is going to make things go away. So hopefully by now I've convinced you that physiology-guided critical care and good RV-centric care are often indistinguishable. But what if we did all this and we still didn't get to the place we want to go? Is mechanical circulatory support an option? And which modality might be an option? And I have the brilliant Dr. Gage to talk about that. Good morning. Thank you to the CHESS for hosting this session. It's great to see how much love there is for the right ventricle. So I'm going to speak about mechanical circulatory support and right ventricular failure. How many of you in this audience have used mechanical circulatory support for RV failure before? Okay, good. So a good amount of familiarity in the audience. So my name is Anne Gage. I'm an interventional cardiologist as well as a cardiac critical care physician. I live in Nashville, Tennessee, and I do have these disclosures. So as I just alluded to, Dr. Hochstein, Tonelli, and Shuba have beautifully described the diagnosis, the hemodynamics, and options for medical therapy for right ventricular failure. But as Dr. Shuba noted, sometimes we have right ventricles that are just refractory to medical management. Over the past decade, we really have had an evolution and maturity in the options for mechanical circulatory support for RV failure, and I think that that's why I've been invited here to discuss these things with you today, and why in your ICUs you're gonna see your patients more frequently undergoing mechanical circulatory support when all else fails. So my objectives are to describe the hemodynamics of RV support devices. I'm gonna touch on the currently available MCS devices to manage our patients. I'm gonna talk about how we match patients and RV MCS devices. We're gonna review the data on RV mechanical circulatory support devices, which as alluded to already, is SCANT, and then ultimately I'm gonna walk you through the protocol for how I decide what MCS device I offer a patient. So let me begin by making a case for RV mechanical circulatory support. We know that the reported survival after acute RV failure is 24 to 43%. This is not good. RV failure post-acute myocardial infarction, so in the world that I live in frequently, is associated with an eight-fold increase in mortality. However, we know that actually maybe 50% or so of patients with acute RV failure may recover sufficient function to allow for explantation of mechanical circulatory support. We also know that while there's a lack of randomized controlled trial data in this space, that we have numerous studies that have shown that RV assist devices are feasible, that they're safe, and that they are associated with acute improvement in RV hemodynamics. So the goal of RV mechanical circulatory support is actually quite simple. It's to bypass a failing right ventricle. So in most of these systems, what you'll see is that blood is withdrawn from the right atrium, and then it's reinserted into the heart above the level of the pulmonic valve in the pulmonary artery. So for the remainder of my talk, I'm gonna focus on percutaneously placed mechanical circulatory support, but I do wanna take a moment to tell you that there are obviously, for those of you who work in the CVICU, there are surgically placed options. These are normally cannulas that are directly inserted into the SVC or the right atrium, and then the return cannula is directly inserted into the pulmonary artery. These are usually for patients who are post-cardiotomy, so your post-CABG patients, your LVAD patients, and your transplant patients. I'm not gonna talk about that. That's an entirely separate lecture, the surgical realm, but I wanted to at least give it a moment's discussion. So this is what this looks like, whether percutaneously or surgically placed, normally something from the RA reinstilling blood into the pulmonary artery. So why do we use right ventricular mechanical circulatory support? Well, the problem is alluded to already is that progressive RV failure fails to fill the LV, so you have decreased LV preload, and ultimately this leads to decreased LV stroke volume and cardiac output. In a very simplistic form, the beneficial hemodynamics effects of RV mechanical circulatory support is to unload the RA and the RV, and ultimately to preserve LV filling, which preserves cardiac output. So how do we do this? Well, these devices actually directly reduce right-sided filling pressures. They suck blood out of the right side of the heart. This can improve LV filling in two ways. One, as we discussed already, when you put the RV back on an appropriate Starling curve, you may improve contractility simply from removing blood. You also then, in a system where there is ventricular interdependence, if you restore more appropriate geometry to the right side of the heart, you're not encroaching on the left side of the heart as much, and you can optimize your LV performance that way also. Then we have to say that this device is actually directly maintaining cardiac output by taking blood and putting it to the pulmonary artery. As you do this, you're able to maintain your RV output while reducing your RV stroke work. This decreases your RV oxygen demand, and frequently, in many situations, this will allow for RV recovery. We've seen that the RV is exquisitely sensitive to ischemia in some of the prior talks, and so if you can unload the RV, reduce the amount of work that it needs to do, frequently this is enough to allow for RV recovery. Shown here are the four commonly used types of percutaneous mechanical circulatory support. These devices are usually placed in the cath lab by an interventional cardiologist or by surgeons. These devices are the Impella RP, the Impella RP Flex, ProTek Duo, or VA ECMO. So I'm gonna begin with a general overview of these devices and then speak about each of them individually. So RV mechanical circulatory support comes in a variety of flavors. We refer to these as either direct RV bypass devices or indirect RV bypass devices. The Impella RP, the Impella RP Flex, and the ProTek Duo directly bypass the RV. They pull blood from the right atrium, they travel through the right ventricle, and then they unload the blood above the pulmonic valve. The VA ECMO is an indirect system, right? This removes blood externally from either the SVC, the IVC, or the right atrium, depending where your drainage cannula is placed, and then you instill blood into the descending aorta. So really you're just bypassing the entire heart, not only the RV. The Impella system of devices rely on axial flow. So this is a principle of Archimedes screw that's housed within the device itself, and that's how we generate forward flow within the Impella devices. The ProTek Duo and ECMO both rely on extracorporeal centrifugal flow, so a pump external to the system. So to walk through some of these. The Impella RP, this is a device that I think is falling out of favor. It has many issues. I have not personally used an Impella RP in about five years, but I had two delivered to my doorstep last week from outside hospitals. So the Impella RP is a 23 French peel-away sheath that's placed through the right femoral vein. This is a 22 French impeller that is loaded onto an 11 French catheter. It, as noted, takes blood from the RA, delivers it into the pulmonary artery. It can get flows of about four liters a minute, flows through this axial pump, and it does not have the ability to oxygenate blood. My personal feelings about the Impella RP are that this is a historic device that we won't be using much longer. It is very hard to maintain its position within the right side of the heart, and obviously you have to cannulate the femoral vein so these patients don't have the ability to get up and to mobilize. And then as the device itself warms up, the geometry of it within the right heart changes over time, and displacement is a real problem. So AbioMed has corrected some of this with the Impella RP Flex. This has not had a full market release yet, but is available in multiple institutions. This is still a 23 French sheath, but now it's placed through the right internal jugular vein. Similar sizes, ultimately, with the device. Works almost exactly the same. May give you a little bit more flow. Again, you cannot oxygenate blood with this. The advantage here is that it's trying to be the competitor to the Protect Duo, which I'll speak about next. But these patients, now it's all upper extremity cannulation and so these people are much better as far as positioning and mobility within your ICU. So the Protect Duo is my personal favorite of these devices, I'll tell you. But it comes in two, it's a dual lumen cannula. It has a venous drainage cannula and a return cannula. These are more similar to the Avalon or Crescent cannulas that you guys, I think, will have familiarity with from VV ECMO experience. This comes in a 29 French or a 31 French cannula, and this is actually determined based on the patient's height. So one lumen is your drainage and that's from the right atrium. You then return blood via a multi-fenestrated distal tip that delivers blood above the main pulmonary artery. These can actually get you very high flows, greater than five liters per minute of flow. And you have the option to add an oxygenator or not. So this is an advantage over the Impella system of products. This flows via the extracorporeal centripetal pump. And ultimately looks like these kind of pictures here on the right side. This is a patient that I put a Protec in recently. It's kind of hard, it is always hard to see. There are kind of three triangular, or three dots here that will make a triangle that sit in the right atrium. They just need to be above the tricuspid valve. And then the outflow here is above the pulmonic valve, ideally shooting straight up into the main PA. You do not want this device shooting to the right main PA or the left because then your flows are going there and you end up in a lot of trouble. So VA ECMO, again, direct RV bypass. Deoxygenated blood is pulled from the venous system, passes into an oxygenator where gas exchange occurs. Blood returns to the arterial circulation via another large bore cannula, frequently a 19 or 21 French cannula. Peripherally cannulated VA ECMO, so what most of us will be seeing unless you work in the CVICU, uses a femoral artery and a femoral vein. Again, you can flow greater than five liters per minute and this has an oxygenator on it. So what do the hemodynamics look like for these devices? Well, right atrial pressure across the board is decreased. These devices all remove blood from the right heart, which decreases your right atrial pressure. So with the Impella system and ProTec Duo, your mean PA pressure is increased. They increase the afterload that the RV is seeing. They are putting a bolus of blood above the pulmonary artery. VA ECMO actually, so long as you have a functioning, a normal functioning left ventricle, normally does not significantly change your mean PA pressures. In all of the direct bypass systems, these improve flow to the left ventricle, which means that you increase your wedge or your LVEDP. VA ECMO, that is not the case. It normally decreases your wedge. And then in all of the direct bypasses, your cardiac output should be increased. As far as VA ECMO, this is dependent on many things, your intrinsic LV function, competency of your aortic valve. So you may see cardiac output actually decrease with VA ECMO or remain unchanged. And so since I can't stand up here and not use a pressure volume loop, what do these things look like? So if you're using a direct system, the Impella system or ProTec Duo, this is going to, I think as we've seen here, well, maybe. So in both of these, either whether you have a volume overloaded ventricle or a pressure overloaded RV, you decrease your RV end diastolic pressure and your end diastolic volume. However, you increase your afterload as we discussed earlier. And then RA to AO. So this is a system of ECMO. And here you're able to, this also shows that you decrease your end diastolic pressure and volume. Afterload is largely unchanged. So in vivo, what do these hemodynamics look like? So this is an Impella console. Some of you may have seen this before. But so this is before a patient goes on support. Central venous pressure, RA pressure 17. Mean PA pressure reported here at 25. And a PAPI, which we use quite frequently when we're talking about which mechanical circulatory support device to use. This is your RV systolic pressure, or your PA systolic pressure minus your PA diastolic pressure divided by your CVP. Anything less than one is a problem and signifies RV failure. So PAPI here of 0.4. This patient is in trouble. This patient goes on to support. Within a few minutes, you can see that your mean pulmonary artery pressure is higher. This is what we talked about, right? You've increased your afterload, but your RA pressure has decreased. You can see that with this support, the PAPI has increased, which signifies that we do not have as bad of RV dysfunction. Again, another way of looking at this, in the aortic side of things also, is that if you look down here, we're looking at arterial pressures, pulmonary pressures, and right atrial pressures. I don't know, there's a mess going on here, right? All of these numbers should not be overlaid. But you put in an impella, so RV support device. Three minutes later, you see that now your aortic pressure, way higher. This is the goal of all this, right? Fill the LV, improve your cardiac output. Hopefully your vascular resistance is appropriate and your aortic pressure rises. You also see that your right atrial pressure, that sort of started up in this mess, has now decreased. And then your mean PA pressure has also risen as you've increased the flow into your pulmonary artery. So there's not a lot of data here, but, oh, I have to move fast. We're gonna, okay, I'm gonna touch on this very quickly. I wanna talk about variables affecting these flows. So device flow, you plug in an RPM. But these devices are exquisitely sensitive to afterload as your PA pressure and RA as your preload. So what you can see is that when you have situations where you have elevated PVR, so your PA pressure, let's put it here, it's in the denominator. If this is rising, your device flow will decrease. So afterload decreases your device flow for a set number of RPMs. If, similarly, so what this means is that in pulmonary hypertension, where you have elevated PVR, you should not expect a high device flow. But in a situation of acute RV failure, where your PA pressure isn't that high, and your RA pressure is the one that's elevated, you actually can have a much higher device flow because there's not as much afterload, and there's lots of preload. So just know that these devices, you're not gonna get the same flow out of each of them. It really is afterload and preload dependent. So basically, that's the thing. Acute RV failure, such as ischemia or pulmonary embolus, for a fixed rotation, your device flow will be high. And for chronic right heart failure, you very well may have decreased flow for a given number of RPMs. The data, it's scant. I will not stand up here at a national meeting and tell you to do anything based on 18 to 180 patients. So how do we walk through this? So very quickly, this is kind of what's going on in my mind, the mental construct that I use when I approach a patient with medically refractory RV failure. So I think what's going on? What is the etiology of this? Is it acute? Is it chronic? And do I expect recovery? I think as you've heard from all discussions on mechanical circulatory support, these are devices that are abridged to something. Notably, with the RV, we don't have durable support options such as with the left ventricle. And so in this situation, you really need to know where you're planning on going with these patients. Is it recovery or is it going to be transplant? So I think about non-invasive, or about the etiology, this may be through a CT chest. Do you have parenchymal lung disease? CTPE, is there a pulmonary embolus? Chest x-ray, is this an ARDS patient? And then in my world, also, is this due to ischemia? We look at the echo, as already described. Invasive hemodynamics. I think that there are lots of ways to assess hemodynamics, but when you're really talking about making a decision about mechanical circulatory support, we fully characterize this. And I think that it's imperative to do that via a pulmonary arterial catheter. And then last, there's a big dichotomy between oxygenator and not oxygenator. This impacts your decision for a device. And so do you need to add, is hypoxemia an issue in your patient? So rapidly. Suspicion for RV failure. We go through these things I just discussed about. We talk about then medical management of RV failure, as Dr. Shuba described. And then if, despite medical management of RV failure, you have worsening hypotension, worsening lactate, or worsening end organ dysfunction, for me, this necessitates a heart team consultation. These are the protocols that I use at my institution. So I just wanna note that you have to characterize and make sure that you do not have biventricular failure. That would be a big problem here to miss that. But for this talk, RV failure. This means that on my invasive hemodynamics, I want a CVP greater than 15, a wedge that is low, and a PAPI that's less than one. And then really, this is how I make all decisions. The question is, is it a hemodynamic emergency? If it is a hemodynamic emergency, the most rapidly deployable support system is ECMO. And so all roads lead to ECMO for me in this situation. If it's time sensitive, I can have someone, hopefully on ECMO in five minutes or so. All things considered. If it is not a hemodynamic emergency, my question becomes, does this patient, are they hypoxic or not? If they are hypoxic, I need one of the devices that I can splice in an oxygenator. And that means that I'm gonna put them on a Protech Duo with an oxygenator, or that they're gonna go on VA ECMO. If they aren't hypoxemic, then they get a RVAD in the form of a Protech Duo without an oxygenator, an Impella RP, or the Impella RP Flex. These are my quick cases, but so hands up here in a moment. 56-year-old male with past medical history significant for a ICH four months prior to presentation and a hypertension, who now presents with acute onset of shortness of breath. He, hard to monitor his heart rate, he's on Carvedilol, blood pressure low, respiratory rate high, and he's hypoxemic. He has a CTPE that shows a large saddle PE. His echo, as you can see here, severe RV enlargement, severe RV dysfunction, there is septal flattening and diastole and systole, LV function is normal. Hands up. Are we going to go down the VA ECMO route here? All right. All right, he's shaking his head, so that's normally a sign that that's the right choice. Oxy-RVAD, or a RVAD without an oxygenator. That would be a bad choice here. All right, so for me, this is a hemodynamic emergency. Normally, I would say that you can make an argument here for giving systemic lytics, but this man has a contraindication because of the ICH, so I would put this person on VA ECMO. I have two quick cases here. 46-year-old, progressive ARDS and progressive hypotension. Lactate 6, LFTs are right through the roof. Creatinine has quadrupled. We've put them on a reasonable ventilator prescription. Let's say this PEEP is optimal for their FRC. Hemodynamics are that their heart rate is mildly elevated, blood pressure tolerable, oxygenation is 90%. The right atrial pressure is 22, mean PA 23, wedge. You can see these. Ultimately, you have a PAPI of .45. This patient we know has ARDS by their CT, and then the echo, same echo. The RV is in trouble here. So what would you do in this situation? VA ECMO? All right. OxyRVAD? Okay, or just a percutaneous RVAD without oxygenator? Oh, sorry, did I mess that up? So for me, I think that this is not a hemodynamic emergency. They've been sitting in the ICU for a little while. We can take a few minutes to gather ourselves, and for me, I would put them on a ProTec Duo plus an oxygenator. I can have them up and moving right after that. And then lastly, I have a 62-year-old with an acute inferior wall MI due to RCA occlusion who now has undergone PCI to the RCA. Despite volume optimization, initiation of an inotrope, the patient remains hypotensive. 12 hours after revascularization, her lactate and her LFTs are continuing to rise. She's tachycardic, more so than in the SECO. Blood pressure 98 over 62. She's oxygenating well. The things to note here are that her CVP is very high, her wedge is normal, and her PAPI is 0.42. We know that the etiology of this was ischemic. That means that we really very much hope that over time, this is going to improve in the next 24 to 48 hours. And so in this situation, ECMO, oxy-RVAD, or just a percutaneous RVAD? All right, I agree. So here, I would put this patient on any RA to PA support device. The goal is just to decrease the myocardial oxygen demand for the right ventricle and hope that we can support it through this period of time to recovery and resolution of end-organ dysfunction. Thank you.

RV failure

RV function

diagnosis

management

fluid resuscitation

Doppler imaging

mechanical circulatory support

Impella RP

Protek Duo

VA ECMO