Chapters Transcript Video Right Heart Failure Dr. Sudhan Nagarajan reviews RV pathophysiology and discusses management from a surgeon's perspective. We would go straight up, straight to the uh presentation today. So I wanted to talk about right heart failure, uh, from a uh surgical uh perspective. It's a very wide topic and um we would like to uh share with you like what we experienced, um, in our practice, uh, is with regards to the right heart. So some wise person said this, the poor right ventricle is far too often the forgotten ventricle. It is sneaky, however, and it can catch you off guard if you're not actively paying attention to it. So I just wanted to lay out the presentation as what, what should I talk, you know, the objectives would be uh to talk about the anatomy and the physiology of the right heart, especially the right ventricle, uh, understand the pathophysiology of um uh right heart failure. Um, go into the etiology and how it manifests in both acute and chronic, uh, conditions, and also, um, how we manage, um, specifically from a surgical perspective. The right ventricle is different from the left ventricle. It's a thin-walled, um, it's got a similarly inlet um uh and uh body and an outlet. Um, it's a crescent shaped compared to the left ventricle, which is more spherical on cross section, and it is very designed for low-pressure pulmonary circulation compared to the left ventricle. It's highly preload dependent, and it very poorly tolerates afterload. When you compare the two, as I was saying on the cross section, this is the normal configuration of the RV and the LV and any overload or dilatation can push the left ventricle, push the septum, and narrow the left ventricle, the phenomenon which is called ventricular interdependence. The intervention the function of one ventricle directly affects the other, what this phenomenon is about. And it's dependent on both the intraventricular septum and the pericardial space, which is more or less fixed. They also share common myocardial fibers, so that also plays into this phenomenon. Because the heart sits inside a relatively non-compliant pericardium, when one ventricle fills or enlarges, it limits filling of the other. And You can see that in physiological states where you have, um, during inspiration, there's increased uh preload into the RV which limits the um uh sys, I mean, decreases the systolic blood pressure, which is very mild, and it's a physiological variation. However, in, in tamponard, this is exaggerated and causes a low output state, and that explains why you would have a low systemic perfusion directly, indirectly resulting from RV failure. There are 3 components, just like the left ventricle. Preload, after load, and contract loading. If you have any, um, you can have overlap of these and pathological conditions, or you can have, uh, singular pathologies, as they are outlined here. Most often what we see is right ventricular infarct as an acute MI. And uh chronic states like tricuspid regurgitation can cause volume overload. Acute situations like acute left heart failure, ARDS, or pulmonary embolism can cause increased afterload, causing the right ventricle to fail. Now, looking at the uh pathophysiology. The pressure volume lobes compared to the left ventricle are not very, uh, you know, it's it's not a very rectangular shaped uh pressure volume loop compared to the left ventricle. It's more triangular, small volume, small pressure. However, the characteristics are pretty much the same. When you have volume overload, your end-diastolic pressure volume relationship gets pushed further towards the right, um, whereas in systolic overload, I mean, ah, pressure overload, um, it, the volume loop itself becomes very narrow, um. And if it's a hypochondracile RV, it becomes smaller and flatter. And this gives an algorithm, like, you know, it was published in CHS, and it gives an overview of how both volume overload states and ventricular afterload states can cause heart failure eventually, by causing increased wall stress, hypertrophy, and because of the ventricular interdependence, you can have decreased cardiac output and left heart failure as well. Just to go into some of the important ideologies, what we see in our practice. In acute situations, like I said, in a myocardial infarction, or secondary to acute liver, I mean, uh left ventricular failure, or in pulmonary embolism are the most common things that we see. Obviously, if you have myocarditis or uh sepsis, you can have increased preload um in sepsis, uh, or in severe stress in uh Takatsuba syndromes, can cause RV failure as well. LVAD is a whole different entity, which we will see in the later part of the TA, um, which also causes acute RV failure. Chronic states like pulmonary hypertension, lung disease, and, uh, left ventricular failure can also lead to right ventricular failure. The clinical manifestations. The symptoms are broad, like fatigue, dyspnea, and exertion, back pressure leading to abdominal distention, mesenteric congestion, and loss of appetite. They also can have exercise intolerance. And the classic textbook signs are um jugular venous distension, epitomegaly and um ascites, and peripheral edema. EKG for the completion's sake, um, we do not diagnose it entirely by EKG, but there are signs like right axis deviation or right ventricular hypertrophy, the classic S1Q3T3 in pulmonary embolism, and um the MI changes inferior wall MI. Echocardiogram is a very key test. It describes the interventricular dependence. Uh, it shows the interventricular dependence very clearly on this. If you would see. Um, This is a normal, you can see the. septum, the LV is bigger, the RV is crescent shaped. This is mildly enlarged RV. You can see the septum right in the middle. And this is severe RV dysfunction. The RV is very enlarged, almost looking like an LV where the LV is very small and the septum is all pushed all the way to the left side. What else do we see on the echocardiogram? Fractional area change based on comparison between the difference between systolic and diastolic area as a function of diastolic area. It is less than 35% uh signifies significant RV dysfunction. We can also use RV size more as a relation to the LV size as a parameter to um. Denote RV dysfunction. In acute situations, new regional wall motion abnormalities in MI. Uh, can, um, uh, predict RV dysfunction, and also intraventricular septal flattening like we saw, uh, especially in pulmonary hypertension, can, um, uh, denote RV dysfunction. Tapsy is a quick bedside echo measure of RV's systolic function. Tricuspid annular plane systolic exertion. It assesses the longitudinal systolic motion in the four chamber view and takes an MOID measurement in the lateral tricuspid lys. A threshold of 17 millimeters a cutoff, less than that would indicate RV systolic dysfunction, and it's prognostic and pulmonary hypertension, RV infarction, and post-surgery. However, it doesn't reflect global RV function because it's a measurement taken more at the septal plane. Um, I, I mean at the Anglola. And it's also operator dependent. However, you can, uh, people have started using TPSi pulmonary artery systolic pressure ratio, which is a potential marker of RV coupling, RVPA coupling. What do we mean by that is RVPA coupling, it measures the balance between the heart's pumping strength and the resistance it faces, which is the afterload. And in right heart catheterization can be measured by taking the ratio of um Elastins of the um Elastins by um. Uh, and the ratio about 1.5 to 2, and less than 1 is uncoupling between the RV and the PA. A Swangans catheter, which we normally use in the operating room for most of our cases, um, also known as a pulmonary artery catheter, gives you all these parameters, um, central venous pressure or the right atrial pressure, pulmonary artery pressure and pulmonary capillary wedge pressure. The right atrial pressure and pulmonary capillary wedge pressure ratio can also be used as a parameter to study the RV. Uh, PAPI, which is pulmonary artery pulsivity index, we'll talk about in the next slide, um, is also, um, used as a measure of RV function. The, the wave forms, as we know, in our um right atrial pressure, the A wave, which is the atrial systole, and the X descent is when the atrium is relaxing. Uh, the V wave is when the atrium is getting filled up in its stents, and the Y descent is when the atrium is emptying, when the valve opens. RV dysfunction causes a, you know, elevated RA pressure, um, very prominent A and sometimes giant V waves in certain conditions, and uh blunted and variable Y descents. These are the parameters that can be used from the hemodynamics. So this was a very good article in um um by by uh in in Hart. And right aid to pressure more than 15 millimeter, especially after LVAD, which is what we worry about all the time after LVAD implantations. And um The ratio of the radiatoral pressure and pulmonary capillary wedge pressure, if it's more than 0.6 after LVAD or more than 0.86 after acute MI. Pulmonary artery papillary, uh, pulmonary artery pulsivity index, which is the ratio of, uh, the pulmonary artery pulse pressure to the, uh, right atrial mean pressure, less than 1.85 after LVAD and less than 1 after acute MI, uh, we get concerned about. Right ventricular stroke work index, pulmonary vascular resistance, and PA compliance are also the other indices. None of these are absolute indices for RV function. It's a combination of these parameters and based on the clinical evaluation as well, and the situation. Pulmonary artery postility index predicts RV failure post LVAD and also is useful in acute MI with RV involvement. It guides therapy and mechanical support decisions, but it also is an invasive measurement, and it can be influenced by preload and after load conditions. How do we manage right heart failure? This is a, you know, basic overview of how to manage it in, uh, based on each of its components. You optimize the preload. If they're in right heart failure and they are hypovolemic intravascularly, you can cautiously give them volume for, for the most part, we have to remove volume with diuretics because they're most often congested. Uh, otropes, the most common used, which we use in our practice pretty much every day, is dobutamine, which is a selective beta one, agonist, and, um, um, milrione, which is a phosphodiesterase inhibitor. Vasopressors are very, are used in low doses, because we don't want to vasoconstrict and cause any afterload um increase. We want to reduce the afterload by use of either inhaled nitric oxide or uh prostacyclins or sildophil. Also important is to manage ventilation by reversing hypoxia or hypercarbia, which can be triggers for pulmonary vasoconstriction. Most importantly, we should treat the underlying cause, which involves a multidisciplinary team approach. Heart failure cardiology, CT surgery, interventional, and uh the PERT, which is a pulmonary embolism response team, includes vascular surgery, and I'll go over that in the subsequent slides. And this gives a rough overview of each component, which we can address. To treat, uh, right heart failure. This is a more comprehensive uh uh algorithm published in circulation which addresses everything, starting from pericardial disease to acute conditions like MI, pulmonary embolism, sepsis, and also, uh, control of arrhythmias, which is very important, and preload optimization. And also maintenance of perfusion by uh vasodilators and ionotropes. And if all of these are if it's re reflected to all of this, then we progress to uh mechanical circulatory support, which we see in a lot of our patients being at a tertiary care center. So, over to mechanical circulatory support for right heart failure. And briefly, if you were to have isolated right heart failure versus biventricular failure, we see biventricular failure more often, but there are certain situations where we see isolated right ventricular failure. If it is associated with respiratory failure, then you need some kind of oxygenation, uh, support also, where we do VA ECMO and RAD with oxygenator. Um, Protec Duo we'll talk about. No, if no need for respiratory failure, there is a role for Impela RP or FLEX, which we'll talk about, but we use it very uncommonly these days, and I'll, I'll share with you later. Bventricular failure, most often we use VAECMO. So, just to categorize them as to um how we can do the right ventricular support is indirect RV bypass, where we cannulate the um you know, major vein and a major artery, typically the femoral vein and the femoral artery and um through a pump and an oxygenator, and that indirectly bypasses the artery, relieving its relieving it of its preload, um, and oxygenating the blood as well. Direct RV bypass is essentially you're taking the blood from the right atrium, uh, or from the venous side of the circulation, and, uh, Delivering it into the pulmonary artery side, taking away the right ventricle out of the equation of the circuit. The Impella RP is, is uh the older device which goes through the groin, and um there's an Impella RP flex that you can access through the right internal jugular vein. The tandem right ventricular device is you essentially have two cannulas, one in the right atrium, one in the pulmonary artery. It can be either done through an open chest, or it can be done through femoral vein access. One femoral vein using a cannula to position in the RV. Another femoral vein can be accessed to position the cannula through that into the PA, and they get connected to a centrifugal pump, and that becomes a right ventricular assist device. The Protec Duo is is is similar, but I'll show you the differences, but essentially, only the impella is the axial flow, everything else is extracorporeal centrifugal flow. The Impela RP or the Flex, it was the first percutaneous RVAD approved by the FDA. It is catheter-based, it's transfemoral in the older device, the RP. The RPFlex is smaller and used via the right internal jugular vein. The advantage is it can, it can make the patient walk. Uh, while you have the RPFlex, they both are approved for 14 days, and they have microaxial flow pump up to 4 L per minute. They can be used in acute right heart failure and malignant ventricular arrhythmias and also after PE interventions. Bleeding and hemolysis are known risk factors. Uh, we don't favor it very much because of the risk of thrombosis and, um, uh, the need to, uh, do repeat interventions. So we, in our practice, we favor the Protec Duo more. It's a dual lumen coaxial cannula. As you can see, the, the inflow is from the uh venous site of the circulation in the right atrium, um, and he uses an extracorporeal centrifugal pump. And the return cannula is inbuilt in the same catheter, and it's in the pulmonary artery. So we position this in the operating room using um echocardiographic and fluoroscopic guidance. The advantage again with this is the patient can ambulate once they are off the ventilator. An oxygenator can be spliced into it, and the device can be removed at the bedside, although we place it in the operating room. Val arterial emo. Um, is a viable alternative to acute MCS. The big advantage, it can be placed, uh, very quickly, percutaneously at the bedside for initiation of emergent support, and it also supports both ventricles. It comes with an oxygenator, so it takes the lungs also out of the equation. The usual configuration is femoral, although you could use a right internal jugular vein for inflow and the axillary artery uh for the outflow for the VAECM. It can be used as an adjunct to interventions in massive PE when the patient is really unstable and needs oxygenation. So these would be the common clinical scenarios for percutaneous AED use. Initial RV failure, there's no increased oxygenation needs. We use a Protec Duo or or or an impeller, less often used, but essentially you're just bypassing the blood from the right atrium to the pulmonary artery. If it is initial LV failure that progresses to RV failure, you need a support device for the LV, which is an Impela 55, uh, commonly in an acute situation. And in addition to that, you need a right ventricular assist device. If it also has, you know, ventilation failure, you may want to add an oxygenator to that. I if it is an initial biventricular failure situation, then we most often use VA ECMO in an acute situation, or um we can use um both the Impela 55 and the Protec Duo. The human dynamic effects of percutaneous RAS. So in an isolated RV failure, um, an RV unloading device works really well, and it addresses all of the hemodynamic uh abnormalities, whereas in a biventricular failure, it's, it's better to use a VA ECMO rather than an RV unloading device for obvious reasons. And also it can cause pulmonary edema due to RVLV uncoupling. How do we wean these devices once we have placed them? So, this is a rough algorithm. It was, um, you know, it mirrors most of our practice. You know, we want end organ perfusion to be good and end organ function to have normalized or improved. Um, we want the lactate to normalize. We want the co-ops to get better. Um, we use bedside, uh, echocardiography monitoring both transthoracic and transesophageal, make sure that the RV is not dilated, that the septum is in optimal position. Um, we don't go by tapsy very often, but that's an index that you can measure as well. And the patient should be off of, uh, uh, reasonably off of isotropes and vasopressors. And hemodynamically, the central venous pressure should be more optimal. And once you have achieved all of that, um, once we target all of these, we also go down stepwise on the flows in the RVAD, uh, gradually over a period of days, and we carefully watch all of these parameters. And if they continue to successfully wean, then we wean and remove the RVAD. If not, we increase the flow back and we proceed again with weaning. And in case of consecutive failures, we always have to think about next step. Sometimes they're suitable as transplant candidates and um sometimes they're not, and they go the palliative route. Up upscaling to a durable device on the right side is very tricky, and we'll get to that a little later. So to summarize the tips and tricks for acute right heart failure with percutaneous or vans. You have to recognize them very, very early, um, because they can go in a very downward spiral very quickly. Um, you have to make sure that the RVAT is positioned well, uh, by doing serial imagery every day, um, and regularly monitoring the hemodynamics with a PA catheter, uh, or a swangan's catheter, which we mostly have for all of, all of our patients in the ICU. And regular echocardiographic assessments, um, you look at RV size, function, all of those parameters you may not be able to look at, they, they can be unreliable, like tap, uh, tapsy and fractional area change, but you can get a fair idea with the RV size function, interdependent septal position. And you optimize the RV pulse pressure better with inotropes, uh, improving the contractility and dilators, reducing the afterload. And you have to wean them gradually and not rush into rush into it, because uh gradual weaning always is more successful. We have to anticoagulate these patients, understanding the risks and benefits of anticoagulation in each particular situation. And I cannot emphasize this more, this is a multidisciplinary approach, uh, between the surgeon, cardiologist, and the intensivists, um, every day. So, in a, in a, from a surgeon's perspective, when do we see this during surgery, the most common risk factors, like if the patient risk factors preoperatively, if they have pre-existing pulmonary disease, if they have COPD, or if they have prior RV dysfunction from multivalvular disease, all those patients, we are worried about RV dysfunction. Surgical factors in coronary artery bypass grafting, if we are unable to revascularize the right side or if they have early graft failure in the immediate post-operative period. Inadequate myocardial protection from long class climb times or long surgeries, um, tamponard from bleeding after surgery. And uh special situations of when you can get RV dysfunction once you have supported the left ventricle after an LVAD. So I'm going to show you a few cases. So the first case is a 76-year-old gentleman. Um, not, not much, uh, comorbidities. Press with shortness of breath and leg swelling two weeks after a bout of fever. He has pronounced Juglavina's distention and muffled heart sounds. CTHS shows a large pericardial effusion and You would see that Um, this, this, uh, representative image showing how this was acute compared to a CT six months ago, which was taken for a lung cancer screening. And you can see the uh. He's pretty much floating in a in a sea of pericardial effusion, and with the right ventricular diastolic collapse, and the IVC also was dilated uh with no respiratory collapse. And this is where the patient was urgently taken for a pericardial window, which was done through the sub-xiphoid route. And once the window was done, you can do a pericardiocentesis too, if available. And once um That was done. You can see there's no pericardial effusion, and RV function gets gets better. I'm sorry, that's a very short loop. Um, another, another patient, 70-year-old male, road trip 5 days ago, presents with shortness of breath, chest discomfort, fatigue, and dizziness for a day. He's hypotensive in the emergency room, and CT angiogram of the chest shows a big saddle embolus and also intransit right atrial thrombus. And you can see. In the transthoracic echocardiogram, you can see a floating thrombus across the tricuspid valve. And Arby's playing. And The patient was emergently taken to the operating room and You can see the intransit big clot from the right atrium being taken out, and pulmonary embolectomy was done under cardiopulmonary bypass as well. After which the right heart improved. So this can also be done. We do this more often with our vascular surgery colleagues' help, uh, endovascularly. Sometimes you may have to do them open. Uh, the key is to treat the primary cause of acute, uh, right heart failure, uh, in this case, uh, pulmonary embolism. This is a different situation. This is a 62 year old gentleman, multivalvular disease with aortic stenosis and regurgitation, mitral stenosis and mitral regurgitation with severe mitral annular calcification of a small aortic root. Uh, class 3 NYHA symptoms. Pre-operative left heart cath was normal, no CAD, but with a left dominant circulation, with the LPDA supplying most of the RV in the inferior wall. He underwent elective root replacement, mitral valve replacement, was technically challenging, long cross clamp times, had severe RV dysfunction coming off cardiopulmonary bypass. The RCA, which still was functional, uh, I mean, patent and a decent size, was preemptively bypassed. We were reluctant to bypass the left PDA, um, preemptively because of the risk of AV dissociation from a severely calcified mitral valve analyst. The RV instantaneously got better. So, However, on post-op day two, there was recurrent RV dysfunction. We got the help of our cardiology colleagues and you can see The. The ostium of the LED and also the circumflex right here is severely stenotic. The button, the coronary button is fine, but there probably is a slight twist, which is very hard to see in the operating room and very hard to predict. But that completely takes away the, you know, the LPDA circulation to the inferior wall of the RV. So the only option at this time was to stent both the LED and the um uh circumflex, following which you can see, um, The LPDA filling very nicely and the RV function, um, uh. Expected to improve. However, we had to place an additional device. You can see that faintly right here, that's the Protec device to help with the RV recover from the myocardial stunning. So, like I said, it's a multidisciplinary team approach. You have to have your colleagues in every aspect of care, uh, of these patients. This is another patient, 43 year old gentleman, transferred with cardiogenic shock, classic heart failure symptoms. And had normal coronaries and left heart catheterization. His classic picture of non-ischemic cardiomyopathy, and you can see that he has biventricular failure. So this patient, uh, definitely needs uh biventricular support, and as you can see here, that's the Impela Phi-5 placed in the operating room, and also the Protec Duo placed. You can see that's a TEE probe. So, some patients definitely need biventricular support. Now to right heart failure after LVAD. I wanted to make this a good part of my talk in the second half of my talk, because these are patients that we see very often. And um you can see, for example, in this patient, 60-year-old gentleman with chronic ischemic and non-ischemic cardiomyopathy on Milvinone and uh was being evaluated for LVAD. He was a suitable candidate for a left ventriculosis device, which was a HeartM 3 we use nowadays. And, however, postoperatively, he had severe RV dysfunction and reduced endogen perfusion. The RV was borderline in the operating room. There was moderate RV dysfunction. Uh, however, we, it, it looked better after we, um, uh, placed the LVAD, so a decision was taken not to support the RV at that time. However, his systemic profusion, decreased on post-op day two, and he needed um. RAD placement on post-op day 2, which was a Protec Duo, and supported for 9 days and weaned off gradually and recovered completely and discharged home with the HeartM 3. Another patient, 67-year-old gentleman, referred for um stage D uh cardiogenic shock, acute and chronic uh congestive heart failure. Um, he had an Impela 5 initially and transitioned to a durable LVAD after he was a suitable candidate. He had severe RV dysfunction while weaning from the cardiopulmonary bypass during the procedure and needed a concomitant RVAD on the table and required 17 days of, uh, support, um, for the right ventricle. Again, gradual vein and, uh, full recovery are very important to be patient with these, uh, uh, people. This is on a follow-up after RV Arvad was weaned off and removed before he was discharged home. And you can see the RV much better. The Intramax uh definition of RV dysfunction is persistent signs and symptoms of RV dysfunction and, um, CVP greater than 18, index less than 2, and worsening hepatic or renal dysfunction with all the peripheral signs that we talked about, in the absence of left heart failure, tamponard, or any other mechanical effects like pneumothorax or arrhythmias. Um, requiring RAD implantation in severe, uh, conditions, severe right heart failure, or requiring, uh, vasodilators and inotropes for more than 14 days in moderate right heart failure. What happens to the RV once we place a left ventriculosis device? There is decreased afterload from decompression of the LV. But there is an increase in the preload to the right side of the heart, because you're flowing more on the left ventricle. However, the right atrial pressure is still unchanged. Initially, it does not improve or worsen. And, uh, this paper in 2016 from the Journal of Heart and Lung Transplant followed 60 patients who had LVAD for over 3 years post LVAD. And the RV load was measured by effective arterial elastins, uh, pulmonary vascular compliance, and, uh, PVR. And. If you can see, the right atrial pressure actually increases a little bit from the increased load and then slowly starts to uh decrease down and then plateaus. Every other uh parameter actually improves with the LAAD. So, It's a very mixed picture for the right ventricle after the LAD. And This study was done retrospectively analyzing more than 5000 patients of continuous flow LADs um between 2014 and 2016 from the InterMax registry, and they showed that the prognostic significance depends on the number of signs and also the type of right heart failure. The persistent right heart failure is some amount of right heart failure at the time of LVAD, and then it goes on to continue. Uh, after 3 to 6 months, whereas resolved is once they have completely resolved, even if they were present initially to a mild extent at the time of LVADT. De novo is completely new right heart failure that arises after LVAD placement. And this is a very interesting uh slide which shows once you have uh uh de novo um right heart failure at one month, The persistence is actually lower compared to if it is late onset uh de novoid heart failure, where the persistence is much more. Um, And if you look at the survival of these people, um, the manifestations of right heart failure, if they have more manifestations, the 3-year survival is much lower. Which RVs need support is a very important question. Like, how do you assess these patients, uh, to know when, when to, which patients will need RV support? Anywhere from 10 to 40%, based on the existing literature, patients who have LAAD need right heart support. It's because of heterogeneous definitions. Every group that studies it defines it differently, so the incidence is very variable, and there have been multiple risk scores that have been, um, uh, calculated to predict right heart failure or the need for RAD following LVAD. A lot of these have been done during the pulsatile LVAD era. Um, the group from Penn published this paper in 2013, came up with a good prediction score called the CRIT score, which analyzes a CVP RV dysfunction. Um, intubation, pre-op, and then, um, tricuspid negotiation and tachycardia. And, uh, from what they found, the more number of risk factors you have from the score, your need for RAD becomes more and more absolute. How to support the RV? Again, we go back to our previous um uh picture. How do we support the RV? We commonly use the Protec Duo for temporary support uh for all our uh patients who need RVAD after LVADT. Uh, any of the other modalities can be used, but their, uh, feasibility and, um, uh, complications are more. Especially when you compare VAECMO versus RVAD, all of these complications, especially GI complications and limb ischemia, mortality, everything is higher, um, with VAECMO when you compare it to RVAD. Not, not to mention, you can make them more mobile with uh placing them on percutaneous hour beds. Um, important thing about how, when to time this RV support after LVAD, whether you do it immediately or whether you wait and see how the patient does, um, how do you plan that? Um, this, this group in 2009 published, uh, analyzed 266 patients, um, out of which, uh, a third of them required RVAD and LAAD, um, and. They found that a planned BAAD, actually, the survival was much better than a delayed BAT. Um, now, these are all temporary, uh, RVADs, and the trend towards bridging to transplant was better with planned BWAD versus delayed BVAT as well. And they found that the risk factors that would suggest is very similar to the risk score that I spoke about. If you have pre-op RV dysfunction, low RV function pre-op, elevated creatinine, all of that are red flags. What is the price of delay? What if we delay, uh, placing the RVAN, and you can see the survival definitely drops, the one year survival if you, uh, wait to, uh, do them sequentially rather than doing them concurrently. Um, this study also, this, this registry also uh analyzes temporary versus durable RADs. And as you can see, the durable RVADs don't have much higher survival compared to the temporary RVADs. Um, Also, you could use a durable RVADT for long term, but it's not well favored because of the risks of using durable RVAT. It's not like the left-sided circulation. There's increased incidence of thrombosis. There is a space issue keeping two durable devices inside the pericardial and inside the thoracic cavity. So, um, durable RVADs are not very widely used. There's always total artificial heart, uh, which can be used as a bridge for transplantation. Um, and the most common one is a synchardia, uh, two-chambered with two outflow tracts, uh, preserving the atrium on both sides, uh, but they are used as a bridge for transplantation. And if nothing works, then, um, do orthodopic heart transplantation, um, I think that's for another day. To summarize, RV function predicts outcomes. Um, poor RV function translates to higher mortality directly. RV physiology is very unique. It's very preload sensitive and uh highly intolerant to afterload. Um, the key is to recognize it early and address all the components of RV function afterload, preload, and uh contract. Mechanical circulatory support, it needs to be initiated sooner than you think, um, and definitely a multidisciplinary team approach is mandatory for these complex patients. And. These are the references questions. Published February 2, 2026 Created by Related Presenters Sudhan Nagarajan, M.D. General Surgery, Surgery - Cardiothoracic, Vascular Surgery View full profile
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