 And our session will close with case presentation. It will be again, Dr. Deno. Andref, Laura is yours. Hello, this is Andriy Deno. I'm back. Let's complete this session with some case studies. My disclosures are shown here. And I'm supported by the Montreal Heart Institute Foundation. 61-year-old woman, liver transplant. And she's five days post-operatively. And we're called at the bedside because she's hemodynamically unstable and also hypoxic. So that's her chest x-ray. And on the chest x-ray, you see some pulmonary edema, some mathedictosis. However, we do not understand why she's unstable. And because of her obesity, we do not have a good answer using surface ultrasound, which is always the first step in examining those patients. So we perform a transalphagelicocardiography. And what we see in this patient is very hyperdynamic heart with bloodventricular alfotrack obstruction. And you can see that the mitral regurgitation in this patient could contribute to the pulmonary edema. In fact, when you look at the right lung, you can see there is some atelectasis on the right side. And you can also see these B lines, which are present on the left side corresponding to the pulmonary edema. The real question is, why is this patient suddenly changing, developing this complication, which was absent the day before? And this is when you perform transgastric abdominal ultrasound. So one of the complications that can happen after liver transplantation is at the level of the inferior vena cava anastomosis. So we go right away at the anastomosis and surprise we see this obstruction, this high velocity signal at the level of the anastomosis of the inferior vena cava. When and then as you put Doppler, you see there is a continuous abnormal signal. As I mentioned in the first presentation, if you have normally a positile signal and it becomes continuous, that's abnormal. And this is an abnormal hepatic venous Doppler signal. We then took back our transgastric probe and tried to analyze a bit in more detail this process. And then you can see there was both a thrombus and there was also a stenosis just at the entrance of the hepatic vein using surface ultrasound. So the patient was brought in the angiosuite and this is the stenosis just before and the stenosis after and using a fluoroscopy and then there is a positile signal back into the hepatic vein and then you can see also there's no more turbulence in the inferior vena cava. So this case is a nice illustration of why when you have an hyperdynamic heart or a levid glout for track obstruction, you should just not say, OK, we'll just slow down the heart rate, give fluid, but try to figure out why is this happening. And in this case, that was a secondary to the inferior vena cava stenosis, which was reducing the cardiac filling. And the solution here was not to give more fluid, was to resolve the problem of the inferior vena cava stenosis. So the second case is a 74-year-old woman post-op day four after arctic and mitral valve replacement. This was a patient who had already biventricular dysfunction to some extent before, but mostly after the operation. She had chronic renal failure. She was also having vascular disease. And in the operating room was documented that she had severe atterometers and grade 5 atterometers disease. And on the fourth day after she came in the ICU, she was very unstable at 2 in the morning with very high lactate. So this is the T exam that I extract from the database. And you can see there was some left intercalary dysfunction and also some right intercalary dysfunction in this transgastric view after a cardiopulmonary bypass. And also in the operating room, the documented, there was some plaque. We see part of this over here. There's a small plaque in the aorta. So at 2 in the morning, we came back, put a T probe because there was no good acoustic windows in her patient. And then you could confirm that there was significant left intercalary dysfunction on this transgastric view. Four chamber view was difficult to obtain, but you can appreciate there was no tracheuspid endotrim motion and most likely also right ventricular dysfunction in this patient. The aorta doesn't project well, but there is almost spontaneous contrast. And you can see this was a Doppler velocity into the aorta, which was minimal. So basically, we were having someone in a very low cardiac output state. And in fact, the personnel noted that exactly at 2 in the morning, suddenly, she had a major reduction in her brain saturation, which correlated with her hemodynamic deterioration. So the question is, what was happening? Why was she suddenly deteriorating at that time? And so when it happens, we look at EKG. There was no change. There was no change in pulse oximetry and blood gases. There was no change also in the process EEG. So we examine the heart. We saw the ventricular dysfunction, but there was no good explanation. So we moved down to perform transgastric abdominal ultrasound. The IVC was dilated. But as we got closer to the IVC, we start to see some air bubble in the hepatic vein. And also, there was some suggestion that there could be some air also in the portal vein. But when you look closely to the liver, now what you see is all these white areas all over the liver, which suggests air into the portal vessel. And in fact, this patient was developing mesenteric ischemia, which was explaining why her lactate were very elevated. And the autopsy confirmed the diagnosis. In fact, what she developed was what we called an acute cardinal intestinal syndrome with myocardial depression. This is some paper we reported this patient just to explain the situation. And this was done by Stephanie Jari, who's one of my PhD students. Basically, this concept of cardinal intestinal syndrome was described by Sundaram in circulation in 2016. So the pathophysiology of the cardiotestinal syndrome is the following. Heart failure will be associated with gut edema, but also gut hypoperfusion. The hypoperfusion is related to not only a reduction in arterial pressure, but an increase in venous pressure. Therefore, the pressure gradient for the gut will be reduced. The consequence will be increased gut permeability and mesenteric ischemia. However, before you get to this point, what will happen is that you'll have a bacterial or LPS translocation activation of your monocytes and macrophage and release of the cytokines. Cytokines will create the vasoplegia that we observe in septic shock, but also will depress cardiac function, as we saw in our patient, both right and left. And also what we have observed also in those patients is that you'll have also encephalopathy and brain dysfunction. And this is an example of a patient who's dying from right heart failure. This is the bowel, and you can again see the bowel edema in this patient just prior to his death, unfortunately. So the gut edema is clearly related to venous congestion and RV dysfunction. And that could explain why those conditions have a poor prognosis. So this is something we've been interested now for more than 10 years. And William Bourbier-Souligny started his PhD at the Montreal Heart Institute and started to do research on this aspect. And just to give you an example, we've noticed again this congestion, which is not only affecting the portal, but also the renal circulation. And this is just an example of a patient who arrived in the ICU who had significant portal possibility. And when we remove fluid in this patient, in this case, we remove six liters over about six to seven days. And you can see the significant reduction in creatinine that we observe in this patient. The techno research program was a result of some of the observations we made in the intensive care unit in the operating room. So far, more than 1,200 patients have been recruited in this project. And the most important one that we've done is a multi-center international study in which we look at portal possibility before and after bypass. And as was mentioned by Dr. Lalanset, what we observe is that if you have portal possibility before bypass, well, and you resolve it after bypass, then your risk of major complication is the same as if you didn't have it before bypass. However, if you develop portal possibility after bypass and you didn't have it before, then your risk of major complication is almost double. It goes up to 40%. And the way we think about portal possibility is a bit like one of my colleagues, George de Jardin, mentioned. It really indicates that there's a fluid overload. And if there's a fluid overload, clearly to give more fluid is really not the solution and will not really improve your patient condition. This was illustrated in a study we published this year in plus one, my Loé Cantard, where we shown that if you look at the probability of prolonged pharmacological support after cardiac surgery and the intraoperative fluid balance, you notice that the best fluid balance is almost zero fluid balance. But as you get more fluid or if you remove too much fluid, then your probability will increase. And this was relatively independent of the Euro score too. So in conclusion, if you insert a T-probe for hypoxia or idemodernamic instability, always consider to perform telus or Tegas if there's no clear answer just by looking at the heart. And finally, venous congestion is highly prognostic in cardiac surgery and probably in other medical conditions that we encounter in the intensive care unit and should be identified as soon as possible before inappropriate fluid resuscitation. Thank you for your attention. Thank you, André, for this great cases. I think it will lead us to start discussion. We have one question from participants, a couple of questions from panelists. And while I was listening to your lectures, I noted 10 of questions from myself. Perhaps I should start with a question from the floor. How often do you see poor perfusion of splanchnic organs in patients who are having intraortic balloon pumping? And how do you quickly evaluate splanchnic vessels? So that's something that we've been aware since we saw this publication in circulation. And what we've seen in the intensive care unit is some patients in whom they have an interarctic balloon pump, which was inserted sometime because they have a left main disease. And they arrive in the ICU and the lactates start to rise. And then now people are very well aware of this condition. So you remove the interarctic balloon pump and the lactate just normalize. So we're not able always to quantify the severity of, say, the actronc or supermysanteric artery signals. But I would say, because this is not that common, but I would say when you have someone with an interarctic balloon pump in the operating room, first make sure that your tip is not too far away from the subclavian artery. And we all know how to do this. But then I would encourage you just move down and find the celiac trunk. And you'll see many, many times you'll see the interarctic balloon pump just close to the celiac trunk. And then if you have a good signal on the celiac trunk and you see that your dastoidic increase and you see your velocity, that means that probably there is no compromise. But maybe in some patients, the signals might not be that clear. And I would say just to be careful. Just to be careful. Keep in mind that that can be an issue. In the paper I mentioned in circulation, one of the conclusion was that the rule of using the length of the interarctic balloon pump, depending on the size of the patient, to determine how far you should go, it doesn't work. Doesn't work. Doesn't always work. And so I think it's important to individualize the position. And if there is any increase in lactate, I think you have to be very suspicious that that could be a compromise of your celiac, your misenteric, or even as we saw one third of the time, the renal artery can also be compromised. So I think it's important. And if you have, you can have good Doppler signals and the signals are clean. And you can see the diastolic. Maybe that could say, well, maybe you could still wait. But I would say I would just be very careful in this condition. Dr. Lalanset, as a cardiologist, what would you think about this? I agree, too, Dr. Dono. And there's mainly three sizes of Arctic balloon pump for the main company. And often for the smaller patients, they don't always use the smallest one first. So that's a big risk to cover the celiac trunk and the visceral arteries. And even we had a case recently. I think you were there at the Montreal Art Institute. And like the ECMO went well, and all the sign of hyperperfusion went down except lactates. And we did a TEE at the bedside. Even if we pull up the balloon just next to the left subplavian artery, it was still covering the celiac trunk. So it's not a rule of thumb that if you use the good IIBP, it will be the good side for the patient. So I think it's always to have a good suspicion, especially if the lactates are high, or if you have a small patient. Then if all like you, if you have a pulmonary artery catheter, or all the perfusion sign goes better, but the lactate still goes up. I think it's a good thing to verify. Perfect. We have follow-up question regarding this topic from Dr. Katalin Efremescu. Do you believe that TEE gas should be a part of rescue TEE then? Oh, absolutely, absolutely. Especially, and that's really what we think, especially if you have an unstable patient, was a normal heart, or hyprodynamic heart, or alpha-trach obstruction. That means the problem is not cardiac. It's extracardia. So definitively, and we've seen cases in which patient weren't stable from a hemotorax. So you just go 90 degree, and you turn to the left and the right and you have your diagnosis. So if you have an unstable patient, make sure it's not coming from the chest. And in the chest, what you can diagnose as immediate complications are hemotorax, but also in some case, you'll see pneumonia. And you can see bronchograms as described with long ultrasound. And then if it's normal in the chest, then move to the abdomen. And as we saw, there's some situation where you can diagnose blood in the stomach. You can see fluid in the abdomen. So these are critical conditions, but also you have to remember that one of the most insidious complication is when you have resistance to venous return. And this you can see in any situation like Dr. Alana said was mentioning where the IVC can be compromised. We saw this in liver transplant and heart transplantation. And then what will happen is that you'll see a non-stable patient with an empty heart with a big IVC. And that should really raise suspicion that there's something in between that is obstructing the venous, normal venous return. Because the treatment of this is not medical, it's surgical. You have to do an intervention. And it's very important to identify this condition. So for sure, it should be part eventually of rescue TEE. And in fact, when you have TEE, there's no reason why you shouldn't look at the IVC as we do with trans-surveysic echo in those patients. Dr. Alana, any comments? I agree with you, Dr. Dono. And in the critical care, we do the same thing. Like take a look at the heart. And after on surface echo graphite, take a look at the lungs, take a look at the abdomen. I think if you have a TEE probe in for an unstable patient and you don't have good view or you are in a perioperative setting, you already have the TEE probe in. So why not take a look at everything, especially when the heart is normal? We have, thank you for your answers. We have next question from Annette. Looking at so many vascular structures, venous structures when you do TEE gas, are flows affected by heart rate disturbances, AFIP, pacing, et cetera? Yeah. So for sure, pacing does affect the hepatic vein. And we did some studies initially when we start looking at the hepatic vein. We saw, well, that's a great way to assess RV dastolic function. And the first study we did, we found that in fact, if you have a normal hepatic venous flow, that was associated with difficult suppression from bypass. But from that study, what we found was that the pulmonary hypertension was more prognostic than the hepatic venous Doppler signal. And then subsequently, we did other studies where we find, in fact, that the right ventricle was more right in spirit dysfunction, was more predictive than the pulmonary hypertension. Because as you know, if you develop RV dysfunction, your peer pressure will go down. So if you just use the absolute value, that won't work. So RV dysfunction. But what we found over the years is that despite the fact that you have arrhythmia, spacing, the possibility of the right tissue should not be transmitted to the liver through the portal vein. So if ever you end up in a situation where you have portal positivity, that really means that the right atrial pressure is significantly elevated. And definitively, in an acute context, this is, this will, this can lead physically to a cardiointestinal syndrome. So you have to be very careful of this. And this will be relatively independent of the pacing. Because the pacing can be done, can have pacing on a patient with normal or elevated right atrial pressure. But so far, I haven't seen any patients in which we remove the pacing and the portal positivity normalized. So we have not seen this. Maybe the only situation which could happen is that if this patient has a better cardiac output when they have their own sinus rhythm, then maybe that could improve your flow. But definitively, portal positivity, if it's present, that's a very bad sign. It means that the filling pressure are very elevated and it's transmitted beyond the apathetic capillaries. So that's a bad sign. And that's what we were about to show in the multi-center trial. So Jasmo, any comments on this? No, I agree with you. And I think the other thing is with chronic fever, RV failure. So those signs might be present even if the patient is stable. So that's why I think you need to interrogate the Doppler before and after and to see if there's any change. And just to keep in mind that some patients, even at baseline, may be deeply abnormal in the critical care in the operative setting. So especially chronic fever or RV failure or chronic fever or TR. I think that's a very, very important point you mentioned, Jasmo, because we had one of our colleagues who was a cardiologist who studied patient with heart failure and portal postillity is extremely common and compensated and even decompensated a patient. So what, and that's why it's so important to obtain a baseline because if it's abnormal before, then you might expect it might stay like this after. But if it was normal before, as we show then and it becomes abnormal, this is significant. So really the change in portal postillity is very important. And that has, I think that's more prognostic that just looking at portal postillity and said, oh, I'm gonna try to remove this abnormal portal signs. I always tell you don't treat ultrasound, you treat a patient, okay? You don't treat an ultrasound sign, you treat a patient. And you have to integrate all the information you have the modanemic cardiac output, the portal postillity. And then you try to take the best decision for your patient. So from what you are saying, is it safe to assume that cardiointestinal syndrome is more common with RV dysfunctions and LV dysfunction or you see it in both entities? Yeah, it's a good question often, LV dysfunction from my experience, when you just have LV dysfunction but your RV is preserved, often this patient will do well after cardiac surgery. And that's probably the experience of everyone. If you have a bad LV, but the RV is fine. But when you have a poor LV and then the RV start to fail or if you have pure LV this is really when we get complications. And there's many studies showing the prognostic value of RV dysfunction. Dr. Laila Sosmo, what do you think about RV and LV issues? Yeah, I would say the same. I'm another art fellow specialist by the way I've seen in my training and in art fellow clinics that patient with bad LV but preserved RV, no pulmonary hypertension are doing pretty well. And the patient that with the same LV function develop RV failure, pulmonary hypertension that's the one that will do well, will develop mostly cardiac cirrhosis, more acute kidney injury. And that's the one that will worry about them and they will refer to advanced therapy sooner than later. We have another question from the floor. If you see air in portal vein and liver do you directly proceed to OR for laparotomy or laparoscopy or you will still confirm your findings with CT? I think if we see air in the portal vein we would typically go for CT scan to confirm this because there are some false positive. Like for instance, we've seen air in the portal vein in patient with due to in adjuvant tubes and the mechanism is not there but it's possible that with the feeding or the pressure some air might get in the portal vein so this patient will might have air in the portal vein doesn't mean that they have a cardiac intestinal syndrome but definitively what's happening, what we see in the ICU is that when you have high lactate people will look at the portal and if there's air the suspicion might be so hard that maybe they won't even go the CT scan is gonna go in the operating room for laparotomy because that's very suspicious especially when you have high lactate. So the combination of high lactate, portal air that's very, I would say very suggestive of Mizzateri-Kiskinia, if you just have portal air normal lactate, probably it's not the same significance. So again, putting all the elements together and again, I would repeat this never treat an ultrasound image in the patient and put all the things together and then take the decision. Perfect, we still have 15 minutes. I still encourage our participants to write questions in Q and A. I will take liberty to ask a couple of questions from my list. I must say, when I follow your lecture, read your chapters and when I try to get all this vascular structures which you describe from a trans-gastric view it's not always that easy. What are the tricks in education? How do you make it easy? And the second question is when you start teaching your fellows who are predominantly coming to learn cardiac ultrasound in first place, are you introducing a concept of T-Gas from the beginning or this is second stage of their education? Well, I will let Dr. Lalancet, who is a fellow answer this question, tell him how we proceed how we taught him how to do this just more. Yeah, so I was already performing cardiac T-E but I've never done T-Gas or anything before. And what are we working on in Montreal with Dr. Leno is to start with simulation. I think what can help a lot at the beginning is to view with the simulator and the 3D views where the structures are and when you're moving the probe down, left, right, left with the end degrees to see exactly where are the structure, where are the vessels. And so you can place them around in the 3D vision. And when you have maybe a day of training with that and after you go to the operating room, I didn't have any permission with that. And with Dr. Leno, rapidly I was able to do the basic Doppler vein, sorry, a hepatic vein, a portal vein, a splenic vein, celiac trunk. It's not that hard when you practice a bit with the simulator at the beginning. And I think it's to have seen some of the standard views. Sometimes it's harder for the celiac trunk and mesoteric arteries there. Like if the anatomy is not perfect, it might be a bit far. But for the hepatic views, it's always giving a good acoustic window. So for the hepatic vein and the portal vein, it's pretty easy, especially if you did a bit of simulation before with the 3D visualization. So it's not that hard. And after just practicing, you will have some case that will be harder because of the acoustic window. But most of the time, it's easy to obtain a good Doppler of the hepatic vein, the arterial, the hepatic arteries, the splenic vein, and the celiac trunk. So basically, Marcin, we're using simulation. So the simulators allow us to simulate all the abdominal vessels, abdominal anatomy. That's how I should use some of the videos. And really what's really helped us a lot is we're using holographic ultrasound. We have HoloLens. And we can see it in three-dimension. So you can hold the liver in your hand. And you can turn it around. You can see where the portal vein is. So that really, as Justin always mentioned, gives you really a 3D perspective of the anatomy. And it's much more, it really helps. And when we teach TE, the morning is cardiac. The afternoon is extra cardiac. That's how we do it. So for every fetus, for the critical care training fetus, and also for the anesthesia resident, the R3. So the morning, we teach them cardiac TE. In the afternoon, we teach them extra cardiac TE. So that's part of our standard training now. And when they are in the OR, the anesthesia resident, they spend three months with us. So the first month is just doing TE. And the second, the two other months, is doing cardiac anesthesia. So basically, they have three months of whole training. So before they come in the OR, they have a day of training in transapageal echo. And now with the new simulation center was recently officially, it's going to be officially recognized this week, but it's been open for almost a year. So what we're trying to do is to have the fellow to be able to perform the TE exam on the simulator before they go in the OR. So then they are much more faster. And they can also learn to do the measurements. So that's something we try to incorporate into our practice. And that really helps. But the simulation is the key, is the key. Because once you see it in three-dimension, and when you see how it moves, it really helps to understand where to do it. The last generation of simulator also has 3D echocardiography. So we're even able to get the biplane views, which would really help for the anatomy of the abdomen also. And the 3D NPR reconstruction also, which helps you to understand the anatomy. But you know the heart is much more complex than looking at a liver. I can't tell you that. But this is very important information. And there is a significant body of literature showing that if you start training with simulators, then it goes much faster and much more smoothly in the operating room and critical care. Another question from Annette. Once you see a pulsative flow in splenic vein or a portal vein, how does it change your management? I guess partially already answered, you try to improve our refunction and look for other causes, but anything to add? Yeah, in fact, and that's really part of the research we're doing. So we use a lot of in-ail basal dilators. And we did quite a few studies. And we're able to demonstrate that when you use a combination of in-ail basal dilators, and typically we would use epoplastinol and metronome, the combination is much better than when you use them alone. And there's probably 80% of those fictional responders. And what we were able to document is that if you're a responder, you're going to do much better postoperatively than if you are a non-responder. And that, I think, and John Smith could comment on this, because it goes with the literature and pulmonary hypertension. Like if you're responding or not responding, it really will affect your outcome. And what we've seen in the operating room is that if you have a patient, you start with RV dysfunction, pulmonary hypertension, portal postoperatively, we really want to bring that portal pressure down, the right-itral pressure down, because the more higher it will be, the more dispassion. Not only will it develop complication, but it will bleed. Because most of your bleeding is not arterial, it's venous. So if you can bring down the venous pressure and the surgeon operates in a field and with the venous pressure is reduced, but acceptable for adequate cardiac output, then we think that could improve our outcome. We need to demonstrate this in randomized trials. But that's been our experience that could help. The only problem with this is that there's some areas which you cannot control. And as William Boblin and Sunini showed you, we're doing also a transcranial locker in our patient. And you can see in some patients, you have thousands of emboli, lots of emboli. And we recently documented that the number of emboli is directly proportional to your complication, post-op complication. Because you know if you have lots of emboli, you're going to have RV dysfunction. And if you have RV dysfunction, then things will go badly. So it's not by giving in a vasodilators that you're going to prevent air emboli. So that's why there's also a confounder which could explain why the randomized trials that we've done just with merino didn't work before because we're not aware at that time of the importance of this confounder and the outcome of our patient. Because the number of emboli clearly is associated with a typical suppression from bypass as we suspect. But definitively, the lower the venous pressure, the better the surgeon will be in operating because the bleeding will be much less. That's our experience. Jocelyn, any comment? Oh, I think it's very complicated. In a critical care, we'll use also the portal of inflow to say maybe it's enough of volume or maybe need diresis and inotropes. And as we said before, and we'll try to have a baseline and to see after intervention, is it getting better or worse and what we can do. So it will be integrated with all the other emotandes. I made data and so I think that's the use of that. Based on what you said and become routine in your practice to look at pulsatility, if patient is not responding to therapy, not responding to diuretics, did you notice that you are introducing greener replacement therapy earlier or it's difficult to say at this point? Yeah, I would say in the ICU, if it's not responding, we would start to the age very rapidly in those patients because and you'll see as you're gonna reduce the venous pressure, your vasoactive support will come down. And we've seen this and the renal function will improve. So we'll be much more aggressive, but that would be based on individual patient. And it's not the strategy that I would use. There's just been recently in the Canadian Journal of Cardiology a study on emofiltration and cardiac surgery. And I don't do it on every patient, I just do it in those in which I know there's excessive fluid. So again, I would be careful not to try to treat everyone the same way. Like I always tell that there's no universal dentures that does not exist and it doesn't work. Everyone is different. And our role with ultrasound is to get as much information on this particular patient to say, well, if we do an intervention, we think we hope we hope because it's not always possible that we're not trying to make it worse. And that's really one of the things I've learned over the years is that if you don't want to make your patient worse, you want it to try and maybe to try to avoid complications. So I think that's why it's so important to know what's exactly the venous condition of your patient. Regarding the reversibility and the response, Jasmin, what are your strategies in cardiology or in the ICU in those patients? But if the patient didn't have any venous congestion with no pulse activity, and he develops RV filler with and you see the diuretics goes down and even with maximum dose of diuretics, that would be the kind of patient that will be aggressive on their renal replacement therapy. But as you said, it's not a universal strategy. I think we have to integrate those data with all the rest and I think in cardiology, like patient, like external patient, if there's venous-consistent venous pulse activity with pure RV function, that's the one that will be faster on referral for evaluation to advanced therapy. So that's might be the patient who will not have a good evolution of their disease. So that's maybe how we use that. Perfect. I have one question regarding renal resistive index. I know that William is not with us, but perhaps you can try to answer the question. You presented very interesting data showing importance of early post-op increase in resistive index. What about looking at this information before surgery? We know that every second patient coming to big cardiac centers as impaired kidney function has reduced GFR, any data on that? Yeah, well, there's been some studies showing the renal resistance index as some prognostic value, especially in cardiac surgical patient. The only problem, and we mentioned this, is that most of the study where they look at renal resistance index, you just look at the renal resistance index. They didn't look at the splenic resistance index, the hepatic resistance index, or the cerebral resistance index. And that's a problem because if you just have a normal renal resistance, and the rest is normal, you have a kidney problem. But if the resistance index is reduced everywhere, that's not necessarily a renal problem. It's a systemic problem. So that's why I said one of the rule, never analyze a Doppler signal alone in isolation. You need to find another, you need to find a friend that tells you, oh, okay, that's a problem with the kidney? No, no, no, that's a systemic problem. Okay, so it's very important. And most of the studies, unfortunately, on renal resistance index, often I've just looked at the kidney. They haven't looked at the other organs. So if the renal resistance index is high because you have the arctic insufficiency, it doesn't know, I don't know. There's so many factors affecting the signal that in isolation, I don't think there's as promising as we might think about. Perfect. And there was a question from panelists. You already answered it, but I believe it's very important to all participants. You basically mentioned that in your study when you did passive left lecarizing and increasing cardiac output, in those patients who are responders, renal restrictive resistive index went down, which was a good trajectory. So that's very important information. I believe we have three more minutes. There is one more question from one of participants. And it's Dr. Kwank Shim. A renal outer medulla is the most vulnerable portion of two hypoxic injury. And accordingly, it's the proximal tubules that are caused of AKI. What do you think about grading the renal blood flow according to the region of interest? Yeah, that's interesting. The problem is that we don't always get good renal Doppler signal in all our patients that was mentioned by Dr. Swinney. But what's becoming interesting in that some work of Dr. Silverton is that people now are looking at the urinary P2. What's the kidneys pulling out in terms of the analysis of the urine and we've been correlating this with the renal outcome? So we're, I think the kidney needs attention and there's some elements that we need to see, but sometimes we don't have all the information with the Doppler signal. And I think there's other methods for evaluating renal function that are promising, looking at biomarkers, urinary urine content. And some people often even look at the oximetry, but keep in mind if you use a non-invasive oximetry, you have to know what's the distance between the skin and the kidney because if it's too much, you might not really grab this information. But if you have great renal Doppler signals, like we showed you in one of the secretaries, then you could probably explore this avenue. Unfortunately, it's not always the case for all your patients. So that's, I would say, a mutation for all this kind of application. Perfect. I think our time is up. Thank you again for putting together for excellent, excellent session. I think it stimulates lots of questions. It stimulates all of us to expand beyond cardiac echo. I'm sure you'll get more questions to your emails. Any housekeeping information from Annette or from Azat before we go for lunch or dinner for people who are in Europe? If not- No, we're all good. We're all good. Okay, we have 45 minutes break before we come back. Once again, thank you very much, Andrei. Thank you very much, Zansimo. And pass our thanks to William. Good.