Thank you very much, Dr. Cajigas, and thank you for the opportunity. So we're going to talk about three or four tips in terms of aortic valve ultrasound in the ICU, and this is looking into the perspective of the intensivist or the person at the bedside. So I'm going to talk a little bit about regurgitation and stenosis. So in terms of regurgitation, there's mainly three things that we need to look for when we're talking about the aortic valve in terms of regurgitation in the ICU. One, we need to describe the anatomy or notice the anatomy, and we need to know that the aortic valve unit is an apparatus. It's a complex, both between the aortic annulus, the cusps, and the aortic root. So the aortic root is crucial. Any of those elements can fail, producing regurgitation. The other thing that we need to know is that the dimensions of the cavities, particularly the LV cavity, will tell us a lot about chronicity. So aortic regurgitation in a normal-sized ventricle is usually a very, very extreme clinical emergency, because usually we're dealing with acute AR in a patient with a ventricle that is not adapted for it. There's also a functional classification. We'll talk about this in the mitral valve disease. This is called the L-Co-Uri classification. But in general, it tells us that the aortic valve can be regurgitant because of the root being dilated or the valve being perforated, restricted, or flailed. And sometimes it's very evident. This is a case from our ICU at Mayo, a patient referred for pulmonary edema and shock, and we can see very clearly a flayed valve with a giant vegetation. In terms of the functional part of things, so aortic regurgitation is a volume and pressure loading disease. So it generates severe increases in the LVEDP and also the LVEDV, so produces pressure and volume overload of the left ventricle. There's this concept of the regurgitant volume, which is going to be very important both in aortic and mitral regurgitation. So our therapeutic target in aortic regurgitation is that regurgitant volume. The decreases in the antegrade stroke volume, which is not so prominent in aortic regurgitation, produces shock, hypoperfusion, and end organ damage. But the increases in that retrograde stroke volume or regurgitant volume is what's going to give us pulmonary edema and respiratory failure. There's a couple of measurements that tells us how quickly those pressures equalize between the aortic root and the LV, and those are dynamic. Probably the most notable in all of our point-of-care machines, including the SonoSite devices, they all include this feature. You can measure that slope of how quickly the continuous wave Doppler decreases the velocity. That's called the pressure half-time. Classically, less than 200 milliseconds is severe. That means that the pressure equalization is very quick, so the pressure gradient is very large. So this is, for example, our patient with a very short pressure half-time. Although this has not been evaluated as a therapeutic target, when we use vasodilator therapies, these numbers should change to some degree. So there could be a value in following this in the ICU when we're treating patients with acute aortic regurgitation. So how to define aortic regurgitation? We define it in several ways, but here I highlight the ones that are accessible to us in the ICU and that we can do in the ICU. So first of all, if we have a largely abnormal valve, so if we can see flail leaflets, such as in that picture, that is going to be severe regardless. Noticing this and evaluating aortic regurgitation is very important, particularly because these patients would have an important consideration, can be considered having a contraindication for balloon pumps, and they will have troubles with peripheral cannulation for VA ECMO, or with paracorporeal VADs. So severe AR in the ICU, when can I suspect severe AR? If you have a flail leaflet, if you have a vena contracta of more than six millimeters, and I'll show you that in a second, if the jet occupies more than two-thirds of the LVOT diameter, if I have reversal of the flow in the aorta at the end of diastole, and if you have a short pressure half-time. This is a classic jet. You can see there how the vena contracta is the narrowest point in space. And then the jet height, you can measure that and compare it to the diameter of the LVOT. A very severe jet will occupy the entirety of the LVOT. And you can measure that in M mode, or you can go to the descending aorta, and you will have a complete reversal until the end of diastole of the flow. Then these are the parameters that the echoes, the formal echoes, are going to give us. The regurgitant volume, which is how many milliliters are coming back into the left ventricle during diastole. The regurgitant fraction, what proportion of the antegrade shock volume is coming back, and the orifice area. That's what I had in terms of aortic regurgitation. One thing about aortic stenosis, so aortic stenosis, although it's much more significant because probably it's more common, it's more straightforward in terms of the ICU ultrasound. One thing that is important, if you see on 2D imaging that the aortic valve opens completely, it's very unlikely for that patient to have severe aortic stenosis. You need to make sure that you put the color Doppler both in the LVOT and the aortic valve, and the acceleration needs to happen at the level of the valve, just to make sure that we're not dealing with a valvular stenosis. And then the difficulty is that we really need to align the Doppler to obtain the highest velocity. So always take your highest continuous wave Doppler velocity, and ensure that you're aligned. So usually you have to tilt your view a little bit to be aligned with the LVOT and not with the ventricle. If you have a good short axis, you can trace the area, and in general, what's severe aortic stenosis, if you have a maximal velocity more than four, or a mean gradient more than 40. That's our quick in the ICU to know that we have aortic stenosis. And finally, the other important point is the presence of dynamic obstructions. So always when you have a very hyperdynamic ventricle, particularly in a septic shock patient, 22% of those patients have dynamic gradients, and they die more frequently, and they have striking volume responsiveness. So you have to screen the left ventricular outflow tract, both in 2D and with color Doppler, and you have to screen the mid-ventricle as we're doing right there. Here we have a patient with full-blown systolic anterior motion of the mitral valve. If you place the color Doppler, you have that very bright red-blue, red-blue, red-blue interface there. That's aliasing. That's very high velocities. And then you can measure the gradient with your continuous wave Doppler, and the key to that is that you have to have that deflection, that convexity to distinguish it from true valvular stenosis. That's what I had. Thank you. Thank you all for staying. I'm going a little bit early. I have to get back to Atlanta. So I have nothing to say. That was great, and you know all about the aortic valve, but I will try to tell you something. I'm going to try to get this done in 10 minutes. So the objectives are to understand differences in pathophysiology and presentation between acute and chronic aortic regurgitation. You heard a little bit about this. And then we're going to talk about aortic stenosis, and we're going to talk about high gradient, low gradient, low EF, and if we have time, maybe a little bit about low gradient preserved EF. I have no disclosures with the relationship to this talk. That's slightly different from saying I have no relationships whatsoever. And I'm going to try to get you to think. So here's aortic regurgitation. Here are the main causes, particularly in the ICU. You've got endocarditis. You've got aortic dissection. You've got trauma, and occasionally, iatrogenic when my cardiology breathmen start messing around and get themselves in trouble. So the pathophysiology, as you heard about, is acute aortic regurgitation is different from chronic aortic regurgitation. You have sudden valve incompetence. You have low forward stroke volume, and you don't have a high pulse pressure. High pulse pressure is chronic. So acutely, you have a low pulse pressure. Don't get fooled. And you wind up with cardiogenic shock. So one of the reasons, the reasons why do you have low pulse pressure, well, the left ventricle doesn't have time to dilate. The stroke volume, and thus the pulse pressure, is not increased. The effective forward stroke volume, right, some of it's going forward, but all of that's coming back, is decreased. And the LVEDP is very high. So in addition to that steep slope that you just saw, you can actually have the pressure goes up in the ventricle. You can actually have diastolic mitral regurgitation. If you see that, you know you have severe aortic, acute aortic regurgitation. Here's the treatment. Relatively straightforward. Keep calm and call the surgeon. Until you do that, afterload reduction with parental vasodilators, assuming you have enough pressure to do that. Hemodynamic monitoring is very useful. But you want to minimize the time to definitive therapy. Mechanical support devices you can think of, but they aren't really much help. The intra-aortic balloon pump is contraindicated. It inflates the diastole, makes the regurgitation worse. An axial flow pump, otherwise known as an impella, is limited because it pumps it out, but the blood just keeps coming back. ECMO increases left ventricular afterload by taking blood from the right side of the heart to the left side of the heart. That's not so great, but it may be all you have for circulatory support. All right. Let's move on to aortic stenosis. We'll talk about valve disease stages. We'll talk a little bit about imaging and quantification. Then we'll talk about timing of intervention, earlier intervention, a little bit about valve disease centers, and then integrated approach. Much of this comes from the, if you really want a comprehensive look, much of this comes from the ACTHA guideline in 2020. Rick Nishimura is a guy from Mochester, Minnesota, you may know. So we'll talk about disease severity, and it depends on which perspective you're looking at. You've got the patient, symptoms due to valve dysfunction. You have the valve, leaflet anatomy and pathophysiology, which you may have heard of. You have the valve hemodynamics. We'll talk a little bit about the flow. And then you have, importantly, the ventricular response. What's it doing? Hypertrophy, dilation, dysfunction. So here are the stages of aortic stenosis. Cardiologists like to go from A to D. And so A is at risk, risk factors for development. That just means everybody has them, right? You go there to B is progressive, the valvular heart disease is getting worse. And then you have stage C and D. So D is relatively easy. It's severe and it's symptomatic. You have severe symptomatic aortic stenosis, not such a big dilemma in terms of treatment. The asymptomatic severe is where the challenging comes, and they come in two flavors. C1, asymptomatic in whom the left ventricle is still compensated, and C2, they're asymptomatic, but their left ventricle is decompensated. And you can imagine that the urgency is higher in that group than in C1. Here's just a little thing about aortic stenosis severity. You heard a little bit about this in terms of measuring the gradient, the jet velocity, the pressure gradient by the modified Bernoulli principle, four times the velocity squared. And the continuity equation basically says that the flow in the outflow tract has to equal the flow across the valve. So if you look at the terms, the area of the aortic valve you can solve for by the outflow tract area times the ratio of the velocity across the outflow tract divided by the larger velocity across the aortic valve. So we talked about the two stages of C, right? You have the asymptomatic severe with a normal ventricle and without a normal ventricle. But symptomatic aortic stenosis also has three flavors, D1, D2, and D3. D1 is the classic high gradient severe aortic stenosis. D2 is low gradient severe aortic stenosis with a low ejection fraction. So in D1, the velocity is high. In D2, the velocity may be somewhat lower because, remember, the velocity is dependent on the flow and the ventricle is not so good and the flow is not so great. So then the question in D2 becomes, is the valve not opening because there's no flow to open it or is it not opening because it's tight? And then you have low flow, low gradient severe aortic stenosis, which is slightly different. So low gradient, low EF aortic stenosis is a bad ventricle. And it looks like this. And the way to distinguish this is to try to increase the stroke volume. So you have low flow and your valve doesn't open. If you increase the flow and your gradient goes up, then the valve is really stiff. But on the right, you have low flow and the valve doesn't open. If you increase the flow and the valve opens up, then you have what we're going to call pseudo severe aortic stenosis because, remember, the gradient is dependent on the flow and the aortic valve area. This is what it looks like. I won't really go into this. But you do this with dobutamine echo. You attempt to raise the stroke volume and look at the resulting gradient. If it goes up a lot, if it goes up as expected, it's a valve problem. If it doesn't go up quite so much because dobutamine is opening the valve, then that's pseudo aortic stenosis. So just very briefly. Then there is this. So you can understand how a ventricle with a low ejection fraction might not be opening the valve. But then there's this paradox of a low flow, low gradient severe aortic stenosis despite preserved ejection fraction. So that's an afterload phenomenon. And it's associated with reduced survival. It used to be. So people didn't really know what to do with this, but I'm going to show you a graph in just a second to show why we think this happens. Here is, on the left, you have normal flow aortic stenosis. And on the right, you have paradoxical low flow aortic stenosis. The idea is that the ventricle is so hypertrophy that the stroke volume is low because there's no room in this ventricle to fill. So the stroke volume is low. Even if the ejection fraction is preserved, it can't pump enough stroke volume to produce a gradient. And that turns out to be somewhat intermediate. It's still aortic stenosis. It gets somewhat better when you fix it, but not as good as when you have normal flow aortic stenosis. Now you have to be a little careful about this. You heard a little about this before. Some cases of low aortic valve area may be due. If your valve area is low because you measure the aortic flow outflow tract low, that's not aortic stenosis. And even if the outflow tract is tiny, you're going to put a tiny valve into a tiny aortic outflow tract. Not going to help very much. And remember, the outflow tract diameter is squared. Increased afterload may be limiting aortic valve openings. So the classic view is that you don't have to worry about the afterload in the aorta because it's the valve where the obstruction is. But actually, in moderate AFs, actually, the afterload may actually matter. And also, left ventricular, even though the ejection fraction is okay, left ventricular performance may not be entirely normal. People say it's 30% of cases. Probably not nearly that common. But it does happen. So here's just a little bit, a quick diagram from the guidelines talking about what to do with low gradient aortic stenosis. If the LDEF is less than 50% over on the left, this is classic low flow aortic stenosis. You do a W to mean stress echo and you're done. If it's this EF greater than 50% and the stroke volume is low, then you have paradoxical low flow. And if the stroke volume is high, you have normal flow. And probably the best way to deal with this is to do a CT scan. If you have a ton of calcium on this valve, it's stenotic. And there's a Housfield units 1,200 in men and 2,000 in women. So CT can help in these patients to try. You're looking for calcium. You really can't see the valve open, but you're looking for calcium. So in the last couple of minutes, let's just talk a little bit about intervention. You have the timing of intervention, the choice of intervention, the valve type, and the surgical versus transcatheter. So here's a little bit of a choice of intervention for aortic stenosis. If you're at low surgical risk, you ought to have a surgical valve. If you're at prohibitive surgical risk, you either have a TAVR or you have nothing to do. And if you're at an intermediate surgical risk, you kind of, at least in the current guidelines, you get a choice of TAVR, of transcatheter aortic valve or surgical valve. We're going to talk a little bit about this because the conceptual frame has to do with the amount of benefit and the amount of risk. And as technical evolution happens, the amount of benefit goes up. Risk becomes easier, and the risk goes down. These valves are getting better and better over time. There are complications with TAVR, peripheral vascular complications. These people have atherosclerosis, stroke, heart block, and paravalvular leak. This just basically shows the progression from 2002, the first TAVR, down to 2021. Valves get smaller. They're tested in lower and lower risk patients, and the results get better and better. So we've kind of evolved to this. So if we go back 25 years, the only thing you had to do for aortic stenosis was surgery. And then we said, well, surgery is the gold standard treatment, but we have this other technique we haven't really evaluated. Then we said, well, surgery is the preferred treatment for low and intermediate risk patients, but the high risk patients probably do better with TAVR. Then we get transcatheter interventions are performed in intermediate risk patients. That's sort of where we are now. Some people are doing surgery there, but many people, you give the patient a choice, you get a lot of people who want a TAVR. Where are we going? We're going to surgeries performed in patients with contraindications to a transcatheter approach. And the surgeons, this is why heart teams exist. The surgeons are helping to put these things in because they want a part of this thing. So key points. The presentation of acute aortic regurgitation can be quite different from that of chronic aortic regurgitation. Interventions for aortic stenosis are based on disease severity and also on staging. Some cases of aortic stenosis do not present with a high gradient, and evaluating the severity of aortic stenosis in these cases can be challenging. And therapeutic options are evolving as technology advances. Thank you very much. We're going to go ahead with the focused evaluation of the tricuspid valve. Since this was the original, the first talk, I wanted to talk about the general framework of valvular disease in the ICU. So the main things that the ICU team really cares about the valvular abnormalities in the patient is whether they are severe versus non-severe in terms of being a potential contributor to the hemodynamic status of the patient. So really, we look for two things. One, are we dealing with a life-threatening or treatment-requiring etiology, such as endocarditis, perforations, or things that require immediate treatment? Or number two, are we dealing with circulatory repercussions of the valvular disease, either low systemic flow or congestive repercussions? Those are the main things that we look for. An important etiology, low flow, and congestion. Those are the three things that are important in the ICU. Going into the tricuspid valve, it's very important to note that we're going to talk mainly about tricuspid regurgitation, since tricuspid stenosis is so rare, particularly in the first world countries. The main etiology for tricuspid regurgitation is annular dilation. And the annular dilation occurs not in the same plane. It occurs in this abnormal heterogeneous plane. And then the lesson behind this is that that annular dilation is dynamic. And tricuspid regurgitation begets tricuspid regurgitation. The more you dilate, the more you dilate. So this is a vicious circle. And we have evidence that volume removal techniques preventing further annular dilation is possible with medical therapies. And this is done in outpatient settings. But if you have a patient with severe tricuspid regurgitation, preventing further right ventricular dilation is going to try to break this cycle. So having an abnormal annulus, it's going to be a vicious circle. So what are the definitions of severe tricuspid regurgitation? And we have, fortunately, an expedited definition. As in all valves, if we have a major 2D abnormality, for example, if we have a valve that in systole doesn't close visually, right, here we have a visual gap in systole. Or if we have a flayed leaflet, this is TEE, so this is your right atrium and your right ventricle. If you have flayed leaflet, by definition, that's going to be severe tricuspid regurgitation. And then, fortunately, we have this expedited definition based on the previous guidelines. But this is something that we can look for. So if you have a dilated IVC and dilated right ventricle, in the absence of other etiologies for dilation, if you have a jet area that is more than 10 centimeters squared or a vena contracta more than 7. And I think in the ICU, vena contracta is probably our friend because it's probably the easiest measurement to make. If you have systolic flow reversal in the hepatic veins, or if you have this dense triangular continuous wave Doppler that is as dense as the normal flow, those are signs any of those would be severe tricuspid regurgitation with more than 90% agreement. These are the measurements that your formal echo are going to give you. But in general, if you have an abnormal valve, a large jet in the right atrium with a vena contracta more than 7, a systolic reversal in the hepatic vein, or dense triangular continuous wave Doppler, you are talking about severe TR and you need to look for organ injury from venous congestion and signs of RV volume overload of RV dysfunction. Now what happens if I have a severe tricuspid regurgitation jet? The tricuspid regurgitation jet should represent the gradient between the right atrium and the right ventricular pressure, right? That's how we calculate our RVSP in the majority of our cases. Now it's classically taught that when you have severe tricuspid regurgitation, you really lose that ability and in severe tricuspid regurgitation, you cannot estimate RVSP. That is probably not true altogether. The tricuspid regurgitation, when it's severe, you lose that gradient because there's practically no gradient between the RV and the RA, and the jet becomes smaller and triangular as we can see here. But that's still representative of the gradient between the RV and the RA. The problem is that you have very high RA pressures that your IVC is not going to be able to estimate, right? You won't be able to estimate them. But we have evidence, this is out of Mayo, showing that that tricuspid regurgitation jet is still representative of that gradient. The problem is that your RA pressure is too high. But in the ICU, we have that solution. We have central lines on everyone. So we can measure an invasive CVP and still monitor the RVSP of our patients, even with severe tricuspid regurgitation. If not, we can use the pulmonary acceleration time of the pulmonic valve. And if we have a known RAP, we can really estimate all three pressures. We can estimate the pulmonary diastolic pressure if the patient has pulmonic insufficiency, and we can know the mean pulmonary pressure. The last tip that I had about the tricuspid valve is, patients with tricuspid valve disease and tricuspid regurgitation, they really suffer from congestive organ failure. So how to measure with ultrasound the congestion in the ICU? So you know that in the hepatic veins, we usually should have almost always flow into the IVC, so the flow is gonna be negative, only these minor deflections. When tricuspid regurgitation is severe, we have red flow, particularly in systole. And in systole, here after the QRS, we have the reversal of flow, and that hurts the liver, and that hurts the kidneys. So you probably have heard here about the VEXA score, and that's a score of congestion. I'm not gonna go in detail about the VEXA score, but it's really measuring that congestion, making it into the hepatic veins, the portal veins, and the kidneys. And we know that patients with tricuspid regurgitation and pulmonary hypertension, if they have high pulsatilities in the portal veins, in this study out of Mexico, they have higher mortality. So measuring the VEXA score and congestion with ultrasound can be helpful for titrating your diuretic therapy. And the last extra tip, if you have a patient with low RVSPs and a bad ventricle, and it's really hard to know whether this is from elevated RVSP, there's a potential non-invasive way of measuring pulmonary vascular resistance in the ICU by dividing the peak velocity of your tricuspid regurgitation by your RVOT VTI, which is similar to measuring your delta pressure divided by your flow. If that index is more than 0.12, you probably have elevated pulmonary vascular resistance. That's been validated in patients with PVRs less than eight. And that was my last tip, thank you. Okay, we're gonna talk about the tricuspid valve now. The tricuspid valve is interesting because no money has been invested in the tricuspid valve until now. So there is something now that could be inciting to have a little bit more of help that we didn't have before. So I think that that's important that we have to understand that this is more fashionable. Now it wasn't. So we're gonna try to learn, we'll understand some of the realities of tricuspid valve in that particular tricuspid regurgitation. We're gonna learn a little bit of epidemiology of this classification and some encounters in TR situations in the ICU and what can we do about. So what are the realities of the forgotten valve? This valve wasn't liked by anyone because there was really nothing to do about it. So it was an innocent bystander. So usually you said, it's because of the MR, or it's because of the mitral disease. It's not a tricuspid regurgitation problem. But survival has been noted to be progressively shorter with increasing severity of TR even after adjusting on comorbidities. So it is a real disease. Diagnostic challenges and problems with timing on intervention contribute to the increased mortality. And the prevalence of clinical significant TR is four times more common in women. So we have to really understand these epidemiological facts so we can understand when to do something about it. What are the clinical key points in severe TR? Chronic right heart failure, that's what we all think about. And everybody thinks about pulmonary hypertension, right heart failure. But yes, in truth, that's usually what happens and what's the most common cause. It creates congestion, decreased absorption, decreased cardiac output, exercise intolerance, dyspnea. And they could be in the ICU already thinking, having all this. And then they go into cardiopathic, cardio-renal syndrome. There are strong predictors of that, of hospitalization for heart failure. Important fact, atrial arrhythmias. In patients who have a normal LV function, AFib results in more tricuspid anal dilation than mitral annular dilation in the same patient. So rhythm control is associated and it's proven to a reduction in the tricuspid regurgitation. Again, these are facts not necessarily in the ICU, but in general. But what type of patient do you expect to have in the ICU with TR? You're gonna find an elderly female with atrial fibrillation, elevated pulmonary artristolic pressure, an increased left atrial size, and rapid progression, particularly in those with the presence of a new pacemaker or defibrillator lead, tricuspid anal dilation that wasn't present before, it's getting worse, and or any valvular heart surgery without concomitant tricuspid surgery. So who gets these patients? We all get these patients all the time. The question is, when do we have to really make any attempts to do something about it? How do these patients do it? They don't do well. One year mortality rate of 36% with medical management alone. So it's pretty high. They do die a lot. This illustration is from actually a retrospective study on comparing those patients who had tricuspid interventions to the ones who didn't. And we're talking about interventional treatments, not surgery. So those patients actually who did have intervention and follow-up months, they had freedom of heart failure and they had improvement in survival. So they did do better in this retrospective analysis, which led to a prospective analysis that we're gonna talk about. So all-cause mortality was higher for tricuspid regurgitation than for aortic and mitral valve in the UK Biobank. Again, retrospective data, but very important. So tricuspid valve needs to be looked at. So now we have to understand what cardiologists talk about. If you are cardiologists in the audience, you know this. But if we are pulmonologists, we need to learn about TR. So atrial versus ventricular. This is the new terminology or the terminology that is used more commonly. What is atrial-related or ventricular-related tricuspid regurgitation? Atrial secondary tricuspid regurgitation is less common. This is the one that usually starts with atrial fibrillation. Anular dilation is not that bad. You have a normal or relatively normal RV. This is what all cardiologists want because this is easy. These patients do better. But what happens? We end up finding this more in 80% of the cases that ventricular tricuspid regurgitation, that these are the ones actually that are most often male. They have significant remodeling of the RV. They have actually the valves, because of the dilation, the papillary muscles get displaced. And then you have a significant degree of anular dilation. These patients do have increased pulmonary artery pressures, most commonly as the etiology. So primary tricuspid regurgitation is when you hit the valve. When the valve is a problem and the problem started there. Infection, endocarditis, trauma, etc. We'll talk briefly about it. But secondary tricuspid regurgitation is what we get the most, is what we need to understand more. Secondary tricuspid regurgitation, approximately 80% of the cases, mostly ventricular, and that's usually from post-capillary PAH, usually heart failure of left valvular disease, due to PAH, again, common as well, but not as common as this one, or primary RV dysfunction, those patients who have had RV infarction and so on. Atrial, secondary tracheospital irritation, those patients who have had, like I said, dilation of the right atrium, because they did end up with a lot of atrial fibrillation and they had anatomical changes, and they end up having significant degree of anodylation from that perspective. And then when we have catheter-related tracheospital irritation, which is in a minority of the cases, but it can definitely be, it should be in our minds, because we can see these patients in the ICU. What about infective endocarditis? This is a primary disease of the tracheospital valve. We see that. We see significantly. How much of the, how many of these patients go in shock because of this? Not commonly. We don't see. Shock is not the reason for this. We get very concerned about how much bacteria we have there. Do we have abscess? Do we have a surgical indication? So there is no significant difference in short-term outcomes with surgery in this valve. But there was a meta-analysis of 44 studies of angiovac-assisted vegetation debulking, and they found that the vegetation size was reduced by more than 50% in almost 90% of the cases. So there is a potential option of angiovac of those vegetations as well. I don't know if Dr. Guerrero will speak a little bit of mitral, but in some other valves on the left side, they have done this type of procedures as well, which sounds crazy, but it can be definitely an option to think about in the ICU. Traumatic rupture of the tracheospital valve, usually due to blunt chest trauma, and they usually appear late. So if somebody works in the surgical ICU and somebody had a car accident with blunt trauma to the chest, you have to suspect this is a potential complication. But again, it's more seen as a chronic TR. And after heart transplantation, if you are exposed to these patients, 20% of the cases actually can come from this, and it's usually in the first month. And they think it's related to cardiac allograft vasculopathy, but it's not really known. So some people say that too many biopsies is doing this as well, and we are injuring the tracheospital valve significantly. Devices. When do we have to call EP and say that lead is bothering me, is bothering the patient? We don't know. That's a problem. But approximately 25 to 29%, they do have TR. So the presence of TR. But is the cause of the bad TR in 7 to half of the patients? What is the big number here? I don't know. When can we say that's the cause? Usually when there is consequence or we have the situation kind of defined from that moment. But removal of the lead can cause worsening in 10% of the patients. So it may not be just that simple to remove that lead. Want to make the proper diagnosis, Dr. Ortiz mentioned to you about ECHO, but color doper is very potential to underestimate. It has to be multi-parametric, and cardiac MR is considered to be the standard for RV size and volumes. And a regurgitant volume of at least 45 mLs or a regurgitant fraction of at least 50% identifies patients at the highest risk for death. This is what we, the kind of the numbers that we end up need to remember, because those are the highest risks. And what are the therapies? Again, not fulfilling, not happy about it, diuretics. So we are really in the ICU not using oral diuretics because number one, they probably are congested and they are not going to have significant good volume of distribution. Diuretic resistance is associated with worse prognosis. Rhythm control, is this an indication to do cardioversion in the ICU? Obviously not. We really need to weight all the risks and benefits, but we know that atrial fibrillation makes more annular dilation in these patients that already have TR. And guideline-directed therapy for left heart failure definitely needs to be still applied. Surgery in this valve is high, the mortality is high, 10 to 12%. This is way higher than other valves, and it is considered to be a class one level of recommendation if you have to do left heart surgery. So it's going to be very hard to make a surgeon convinced to fix your tricuspid valve alone. So it's not really a surgery even less in the ICU. But then we move into transcatheter therapy. So what are the current devices? We can do annuloplasty, leaflet coaptation devices, heterotopic valve implantations, or orthotopic valve implantations. This is a very nice review from Dr. Becky Hand in the New England Journal that is this year actually that explains the anatomy that you need to have because sending a patient for tricuspid valve repair needs to have certain parameters. It's not everyone. One of the things is that usually patients with pulmonary hypertension don't qualify for these trials or for these potential treatment options. I'm not going to go through the ideal anatomy, it's just for you to know and to see the reference. But again, you can have coaptation devices, you can have valve implantation that could be actually in the inferior vena cava and the superior vena cava to try to reduce the degree of congestion. They could be a suture annuloplasty system, ring annuloplasty, or transcatheter replacement. Those are the options that exist. So we are not out of options for this. It's just that we need to be careful about who has to have that. In the trivalve registry, which is a registry, again, they did find improvement in survival in these patients. Again, these are outpatients. This is not ICU cases. They never included anybody in shock. Met analysis of 21 studies, mortality 5% at 30 days and 25 at one year. But then there was a triluminate study, this is the one that was prospective, and that actually showed and was published this year that after a year, death, surgery, and rate hospitalization did not differ between device and medical treatments, so bummer. So it didn't really work in prospective trials, but there was a very significant improvement in quality of life. So is that a good reason? Could be. So when they actually graphed the quality of life difference, it's very significant. When we measure by the QCCQ scores, at one year, they did notice that it was independent of the severity, there was a significant change in how these patients fell. And this is what they do. They basically put the device of the mitral clip that was used before, just trying to approximate those leaflets, so you reduce the tricuspid jet. There has been one case reported, I could find, of somebody who had RV dysfunction after doing this, if you didn't calculate this patient do okay, you imagine you all of a sudden reduce your tricuspid jet and you have an RV that actually doesn't know what to do with that increase in preload, so that could be a risk. But again, we have to remember, these patients did not have pulmonary hypertension, none of these ones. I think the limit was 70 millimeters of mercury and systolic pressure for these cases. The ICU patients with cardiogenic shock were excluded from the transcalator trials. The focus is on the management of RV failure, so all what you already know, optimization of preload, afterload, rate and rhythm, prevention of acidemia, hypoxemia, hyperthermia. I tell my fellows, this is probably the first thing I tell everyone, acidemia, this increases your pulmonary vascular resistance like four times more than hypoxemia. We get very focused on hypoxemia, but acidemia is way worse in PVR. And the treatment of pulmonary vascular disease, if we have the opportunity. So in conclusion, tricuspid hypertension portends poor prognosis in any clinical scenario. There are no studies done during shock state, so I wish I would be able to tell you more. But it's important, and we as pulmonologists and intensivists, we understand what is primary, secondary, atrial, ventricular. So when we talk to cardiologists, we know what we're talking about. And we know that ICU states may worsen this, so we have to start investigating options. Maybe we need to study in these cases if they can do better and the transcatheter therapies are evolving. Thank you very much. Again, happy to get any questions if you have it right now, otherwise we will move on to the next session. All right, we're going to talk about the ultrasound tips of mitral regurgitation again. We're going to focus on regurgitation in the ICU. I think the first thing we need to know when we deal with a patient with mitral regurgitation, particularly in the ICU, is what is the mechanism. And that's where this kind of classic classification can be helpful for us, even in the ICU. Because if we know the mechanism, we can look for the etiology. This classification, or the Carpentier classification, was designed to determine whether a patient had a repairable valve or not. However, it's helpful for etiology in terms of investigation. So Carpentier 1 is a valve with normal cost mobility, right? It can be regurgitated because of two situations. One, the annulus is dilated, so that's secondary because the valve is okay. Or two, you have a perforated valve or a cleft. So that is usually accompanied by a central jet. There's exceptions, but that's the general rule. Carpentier 2, it's where the valves have excess mobility. And the classic example is a prolapsed valve or mitral valve prolapse. The key is that the jet is gonna be directed in the opposite direction of the pathology. So it's gonna be aimed away from the lesion in Carpentier 2. Carpentier 3 is a valve that has decreased mobility. 3A is when the valve is limited both in systole and diastole, and that's classically patients with rheumatic heart disease or in our context, mitral annular calcification. If the pathology is symmetric, the jet can be central. But the most common one is gonna be this one, Carpentier 3B or restricted. That's when one of the valves is tethered, usually from ventricular pathology, most commonly dilated cardiomyopathy or ischemic cardiomyopathy. And then the key is that the jet is directed towards the pathology. So the direction of the jet, and whether it's aimed away or towards the pathology, that's where this classification is helpful. Why? Because if we have a flail leaflet here, for example, we're gonna look for mitral valve prolapse, the rupture of a papillary muscle. If we have these here, we're gonna look for endocarditis causing a perforation. So these are a couple of examples. This is a flail valve here of the anterior valve. And then you can see how the jet is directed away from the pathology. Here, this is a restricted dilated heart. The pathology is restriction most prominently of the posterior valve here. So this is 3B, the jet is directed or aimed at the pathology. How do we define severe mitral regurgitation? The same. If we have an evident 2D abnormal image, so for example here a flail, that's severe, regardless of the other measurements. And here we have another flail leaflet. Here you can see how they don't co-opt and this valve is aimed above the annular plane. That is severe just with your 2D imaging that we can do in the ICU. Otherwise, how else do we define severe MR? So any 2D abnormality, flail, perforation, cleft, that's gonna be severe. Again, in the ICU, although it's probably too basic for our cardiology experts, vena contracta is our friend because it's easy to measure. If you have a jet that is large and occupies more than 50% of the left atrial area, we have systolic reversal in the pulmonary veins, the same as the hepatic veins with the tricuspid. And if we have a dilated LV with normal function, that means that this is acute. So this is a general demorphology of regurgitant jet. This is just to know that the vena contracta here is the narrowest point of the jet, and it's usually not the same as the anatomic hole. It's downstream from it, and that's what we're gonna measure. This is a mild MR and a severe MR, and we should not be fooled by the fact that the jet occupies the entire left atrium. Really what makes it severe is how thick that vena contracta is. We see here the vena contracta, the narrowest point. And why I say that? Because if you have very high afterload, you can have more volume with a moderate MR, and this is how you measure the area. This is the normal flow in the pulmonary veins. We're looking from the LV, so everything should go into the LV. When we have severe MR, we have in systole reversal of that flow. These are the other parameters. Other indicators of severity, when you do your continuous wave Doppler, this is not severe, so it's rounded and incomplete. When you have very dense and triangular shape, that's also severe. This is a patient from many years ago back home. If you have this dome, this spontaneous dome here, right? You have what the cardiologists call PISA, without manipulating your color scale. If you see that dome, that hemi ellipse there, spontaneously, that is severe. If when you go to look for your diastolic function, your E wave, your diastolic E wave is more than 1.2, those are other clues of severity. And this is very important. Asymmetric jets can have this effect of hugging the wall, and that can make them look smaller. This is called the Coanda effect. These are severe jets by definition, because if you apply other measurements, they're gonna be underestimated. And this is probably the most important part in terms of management in the ICU. Mitral regurgitation is a volume loading condition. And the important target that we need to keep in mind is the regurgitant volume. When we have our end diastolic volume here, the ventricle starts ejecting and it has two pathways. The left atrial pressure is always lower than your diastolic pressure in the aorta. So it's gonna be easier for the left ventricle to eject into the left atrium. The decrease of this anti-grade flow gives you shock, again. And the increase of this retrograde flow gives you pulmonary edema. That ratio, what our cardiology experts will give us as regurgitant fraction or regurgitant volume, that is our therapeutic target. We wanna increase this by and decrease this. And it's hard to measure this bit to bit. But if we follow the anti-grade stroke volume here, as we do when we're measuring cardiac output, if we measure that, we can certainly see indirectly that we're reducing the regurgitant volume. For example, this patient, 180 over 90 blood pressure. A lot of regurgitation, high velocity, stick jet. And this is backwards, I apologize. So this patient probably had this low VTI, low stroke volume. By decreasing the afterload with vasoilators, probably we can see that the stroke volume, the anti-grade volume is increasing. And that's a representation of lowering our regurgitant volume. And my last tip, so that's our therapeutic target. Our therapeutic target in the ICU is the regurgitant volume. And then the last tip is that when you have wide open MR, particularly if it's centrally located and you can align it well. So you can think that the MR is gonna be the representation of the gradient between your LA and your right ventricular systolic pressure. So you have the gradient in between those two, and then you know your LVSP, which is your same arterial systolic pressure. So if you have severe MR, if you subtract the peak gradient of your MR from the systolic blood pressure, you can have a continuous measurement of your left ventricle pressure non-invasively in the ICU, and that can help you manage your pulmonary edema. And that's what I have. Very good. Any questions? Okay. Thank you very much for the invitation. It's really an honor for me to be here. I appreciate the opportunity of sharing with you the perspective from the interventional cardiologist in regards to mitral valve in the ICU, when and how to act. And let me just figure out how this works. So these are my disclosures. Our learning objectives today will be to identify causes of severe mitral stenosis and regurgitation leading to cardiogenic shock, to describe treatment options of mitral stenosis and regurgitations complicated with cardiogenic shock, and to evaluate outcomes of transcatheter mitral valve repair and acute severe mitral regurgitation complicated with cardiogenic shock. I would like to start with a real case question first. This is a 76-year-old female with history of hypertension, atrial fibrillation, on warfarin, chronic kidney disease, and severe mixed mitral regurgitation, which she has had for years. And it's mixed etiology due to thick leaflets as well as tethering and annulus dilatation, which is second, I mean, functional MR and primary MR. She presents to another institution with GI bleed, in shock, and acute dyspnea. Her blood pressure was 40 over 30, heart rate was in the 50. No regurgitation or stenosis murmur was noted in the examination in the ER, at this low blood pressure. The troponin was more than 5,000, lactate 3.7, hemoglobin of 8, Y count 12, and INR of 2.8. And the EKG showed inferior posterior stemming. Dopamine, atropine, IV fluid resuscitation, and she's transferred to your institutions. Urgent coronary angiogram shows 80% middle AD, 80% proximal, and 90% distal left circumflex stenosis, as well as 100% distal RCA stenosis with collaterals, which is thought to be the culprit, but because of active GI bleed, no PCI is done, it's treated medically. So she remains in cardiogenic shock requiring IVP, balloon pump, and mechanical ventilation, and this is what the TTE shows. LVEF now is 37% previously normal. There's inferolateral hypokinesis due to the inferior posterior stemming and severe functional mitral regurgitation due to feathering of the posterior leaflet. So ischemic MR along the entire line of coaptation. So this is bad MR. So which following strategies would you recommend? And let's just do a show of hands if you want. So PCI of the LAD and left circumflex. Surgical mitral valve repair and bypass. Transcatheter mitral valve repair or palliative care. So anyone who wants to do PCI? Anyone who wants to do surgery, repair, and bypass? Yeah, that would be great if a patient can tolerate surgery. Anyone who wants to do transcatheter repair? Good, a couple people. And palliative care, good. Yeah, we don't go palliative care until we're run out of options. So perfect. So the next of the slides, I divided them into chapters. So stenosis and regurgitation. And these are the conditions that you're going to see in the ICU with severe mitral stenosis. So you have rheumatic mitral stenosis. This is rare to be seen in the US to give you a cardiogenic shock. You have degenerative MR or MS, I'm sorry, due to mitral annulus calcification. This is what we call also calcific MS or MAC. This is the most common pathology that you probably are going to see. It's associated with poor outcomes. These are usually all people with multiple comorbidities. And sometimes you also have stenosis and mechanical prosthesis due to thrombus, which is the more common. Sometimes you have panos formation in the prosthetic valve. And the treatment for this, well, you have two options. Medical stabilization, you know, where you can do heart rate control or AFib, if you have AFib, then restore the sinus rhythm. I'm sorry, I've been using the mouse here as a pointer and I just realized it's not working. So you can do rhythm control if you have atrial fibrillation. But if you need pressures, avoid chronotropic agents and then diuresis. But the key is mitral intervention. And you have vaguloplasty or you have surgery, replacement of the valve, either transcatheter or with surgery. So basically, this is a mechanical problem. There's very little that we can do with medications. The key is early referral to the heart team. And by that, I mean both interventional cardiology and not just the surgeon. It has to be the heart team. And if we don't have a heart team, then transfer to a facility that can offer the patient a multidisciplinary structural heart disease, heart team approach for, so we evaluate it for all the options that we have, which now, thank God, are many, not just surgery. So you can do valvuloplasty. The top images are the single balloon with the inovaloon mitral valvuloplasty. This is a double balloon technique. And those are the results that you can see in hemodynamics. In black, you have the severe gradient that is reduced after valvuloplasty. This may not be known to you. This has been going on since 1984. But this is more new, and maybe you have not seen this. This is actually what you're going to see in the ICU. This is what we call MAC, mitral annulus calcification. And this patient has severe calcific stenosis in the setting of MAC. You can't fix this with medications. You can't fix this with valvuloplasty. You need replacement. And these patients have high risk for surgery. So the surgeons are usually going to say, no, thank you. You're on your own. But this is what we can do. We're seeing this more often now that patients survive TAVR. This patient has already had a TAVR. So all people, they come for TAVR, and they survive. And then years later, now come back to us with stenosis of the mitral valve. This is the calcium of the mitral valve. These are the ribs. You see this mitral valve is darker than the ribs. They're really like a bone. So what we can do is we can do transcatheter mitral valve replacement through a transeptal access, all transvenous, all we need a vein is in the femoral vein. And this is a TAVR device being deployed in the mitral valve. This is not approved by the US, I mean, at the US by the FDA. It's being evaluated in clinical trials. And there are other devices also being evaluated in clinical trials. So it's off label. I need to let you know that. And this is what you see after. This is an LV gram. And there's no regurgitation. And this is what you can see now on TEE. So before and after, big difference. This is what patients need, a new valve. Now, changing to the second chapter, which is mitral regurgitation. I further divided this one into native mitral valve and prosthetic mitral valve. So here, you have ischemic MR, like the patient that I presented to you, due to dysfunction in the setting of mitral infarction or ischemia. You can also have papillary muscle rupture in the setting of MI. You can also have non-ischemic severe MR due to rupture of chordae or infective endocarditis, trauma, acute rheumatic fever, or iatrogenic, like sometimes that are ruptures of the survival apparatus during procedures like TAVR, LVAC, lampoon is the percutaneous laceration of the anterior leaflet that we need to do sometimes during T and VR. So bottom line is it can be also iatrogenic. And then, in prosthetic mitral valves, you can also have acute regurgitation due to rupture in the setting of endocarditis, or degeneration, calcification, or also thrombosis in the setting of a mechanical valve, or infection, or panus, or paravalvular leak. And again, two treatment options, you have medical stabilization, which include diuresis after low reduction, like NIPRA will decrease your vascular resistance, decrease MR, increase cardiac output, and decrease pulmonary congestion. You can also place a balloon pump. But bottom line is you need what was until now a standard of care, which is surgery, like repair or replacement. In the guidelines, I have two sets of guidance here, some old ones and the new ones for you to see. In 2008, surgery was indicated in patients with life-threatening congestive heart failure and cardiogenic shock. In the newer ones, they also tell you, prompt mitral valve surgery. The problem is these patients have high risk. This study is from the 70s and 80s, 55% in hospital mortality with surgery. So not everyone can have surgery. Yes, it's the ideal treatment, but they have high mortality, because it's very invasive. Obviously, it's better than with medical treatment, right? I mean, this is a mechanical problem. If you do nothing, mortality is almost like 100%. So 55%, a few decades ago, didn't sound too bad. But can we make it better? And the answer is yes. This is another study with surgery, more recent, but still from the 80s, a study in the 80s, still high mortality. So case reports of mitral clip in a cardiogenic shock. This is from 2016, this is 2017, 2019, and this is when it was approved in the United States in 2019 for secondary MR. This is then a series of cases, 12 patients with cardiogenic shock here that were treated. The STS predicted risk of mortality was 33%, and it was only 17. They observed mortality, so less than half of what was predicted, or about half, so much better than with surgery. Then you start to see single center reports, single sector experience, like 29 patients. This is the amount of MR before, in blue, is four plus. Most of them had four plus MR in post-procedure. Most of them had one or two plus MR, so significant reduction of mitral regurgitation. With that, there was increase in cardiac index, and the survival rates are now 82%. I told you, like half of them die with surgery. Now it's more than 80% survival with mitral clip in that particular study. And then you start to see now multi-center registries, 114 patients. This is, I think it's from Canada, and 87% of them had device success, meaning, or defined as decreasing MR by one grade, and absolute less than two plus. And patients who had, this is a significant reduction in mitral regurgitation, and the ones who had device success, compared with no device success, had even lower mortality than when you have failure or no device success. And this is the most important one. If you want to read just one paper, then read this one. This is from my colleague at Mayo. This is from the TBT registry, which is the entire US registry of mitral clip patients. 3,700, so the largest data so far. This is a reduction in mitral regurgitation. Patients in shock, treated with transcatheter edge-to-edge repair with clip. And significant, most of them, one or two plus MR after the clip. And this is a survival course. In patients who had success, less than two plus MR compared with no success. With a number needed of three to only five patients to save a life. And this is mortality and heart failure hospitalization. So there will never be a randomized trial, I don't think so. So this is the only one paper that you need to know, because subsequent to this will be just follow-ups of this study, I think. So just the last one to end. You can do transcatheter mitral valve replacement in shock in patients with bioprosthetic valves. This one was an 84, I'm sorry, 80-year-old female with a prior bioprosthesis who had sudden ulcer of dyspnea, comes to the ER in cardiogenic shock, EF 78%, hyperdynamic in the setting of severe MR due to a rupture of one of the leaflets. In shock, intubated, SDS-CoR predict the risk of mortality of 42%. So the surgeon called me and said, can you fix it? And this is how we fix it. Transceptal, you can see a balloon pump here. This is just going through the vein, femoral axis, which is very, I'm just gonna show you a real life case. And this is how long it takes, less than one minute probably to place it there, in most cases with good planning. And then this is a deployment. Here is a bioprosthetic valve, it's very difficult to see. This is a biocord, it's hard to see. But this is how long it takes, less than one minute. I'm just gonna let it play a few more seconds. To inflate that under rapid pacing. All transeptal, transvenous, and now we can do this patient under conscious sedation. This patient did well, in the interest of time, I'm just gonna tell you that she survived to celebrate one more anniversary, 57 anniversaries. Her heart was very happy. Few case reports, no large studies yet, so this is relatively a new option. So going back to our case, I won't repeat what this case was about, but basically it's a patient who had a lot of MR, ischemic MR. And this is a baseline TEE, I just want to show you, interestingly, this is on balloon pump, and this is on standby. If you stop the balloon pump, this is what happens, very severe MR. So we placed one clip, and after one clip, there was still some significant mitral regurgitation. We placed a second clip, and this is how it looked after two clips, now mild mitral regurgitation. The patient was still sick at the end, ended up having two stents to LAD, just to complete revascularization, just like surgeons do. Did well, was discharged two weeks to a nursing facility. So did not go home yet, but at least she survived, and surgeons were not offering her anything. So in summary, these are your options in addition to medical treatment. You have repair, you have ovuloplasty or transcatheter edge-to-edge repair with clip, or you have replacement. You can do transcatheter mitral valve replacement, like valve-in-mag or other devices, or valve-in-valve. So a lot of transeptal options for these patients who may not be a good candidate for surgery. So in conclusions, severe mitral regurgitation and or mitral stenosis can lead to cardiogenic shock. Common causes of acute MR include ischemic, just like papillary muscle rupture or dysfunction, or non-ischemic in the setting of ruptured corte or iatrogenic. Mitral valve surgery is associated with high mortality in patients with cardiogenic shock, but outcomes are better than with medical treatment alone. And transcatheter mitral valve repair is emerging as an alternative to surgery or as a bridge to surgery in acute severe mitral regurgitation complicated with cardiogenic shock. Transceptal mitral valve-in-valve is an option in acute bioprosthetic mitral regurgitation complicated with cardiogenic shock. Thank you very much. Thank you.

severe mitral regurgitation

mitral stenosis

ICU setting

treatment options

mitral valve repair

mitral valve replacement surgery

transcatheter mitral valve repair

medical stabilization

mitral intervention

high-risk patients