Chapters Transcript Video The Effect of Intra- and Extra-Cardiac Shunts on Pulmonary Vascular Disease in sBPD Back to Symposium Learn how left-to-right cardiac shunts affect the pulmonary status of patients with BPD. OK, great. Thanks for the invitation to speak. I'm one of the cardiologists. I know a lot of people in here. I'm certainly not a BPD expert, um, but I am, uh, an international cardiologist and have an interest in Helping out on the pulmonary hypertension team and, and with some like EKD patients. And, and so I took the liberty of altering the title of this talk just a little bit. I know the title said intracardiac and Excardiac shunts, but I think from a physiologic standpoint, I group these together and it's a little bit easier to think about what we consider left to right shunts. And I'll go through those and describe a little bit more about what I mean by, by left to right shunts, um, as we go through the physiology. So again, I'm not an expert in BPD and you guys all know this, but I put this slide in here just to make the point that uh of course, BPD is uh results in um Immature lung prancuma and alveolar certification, and this is just basically to prove the point or make the point that when you have abnormal development of the lung, um, ranoma and of the alveoli, the vasculature develops along with those, and it, uh, oftentimes results in abnormal vasculature as well. And that's what's important when we talk about left to right shunts and how left to right shunts can affect the pulmonary status. Um, so fragile lung beds, uh, in BPD, uh, have an abnormal alveolar vascular surface area, and this results in increased susceptibility to left or right shunts. Patients at BPD we know are also at risk of some diastolic dysfunction, which results in left atrial hypertension and potentially some impact on the pulmonary gascature from the venous side. So, uh, these patients are more prone to pulmonary edema, um, from defects that result in increased pulmonary flow. And, and, and that's what left to right shunts really means. So we in cardiology think of shunts as, um, you can have physical shunts like a hole in the heart, but physiologic shunts are grouped as either left to right shunts. You can have right to left shunts, you can have to by direction shunts. But the left to right shunts are the ones that are a little bit simpler and, um, And physiologically, well, a left to right shunt is blood that comes from the left side of the heart, so it's oxygenated blood and it makes its way over to the right side of the heart back out to the lungs. So, so that's the left to right. It doesn't matter whether it's an atrial level, ventricular level, or a PDA. I don't go through all these, but a left to right shunt results in increased flow going to the lungs. And if you have abnormal pulmonary vasculature or abnormal, um, Uh, uh, pulmonary rama, that increased flow can have deleterious effects, and I'll, I'll show you some, some data, uh, on, on, uh, on the effects of these. So the most simple left direction to think of, or, and maybe the least noxious is, um, is an atrial septal defect. So that is a hole between the top chambers of the heart. And blood flows through the path of least resistance. So usually the compliance and the resistance on the right side is lower than the left. And so you get blood that goes from the left atrium over to the right atrium through the right side of the heart back to the lungs. And that's exactly why this picture here is shown the blue blood comes to the right atrium. There's some red blood that spills over and the right ventricle and pulmonary artery in this case are shown as purple because there's red blood and blue blood that's going to the lungs and it's increased. Uh, a ventricular septal defect, and this is what the title I think meant, intracardiac. So an ASD is obviously within the heart. A VSD is also within the heart, and this results in left to right flow at the ventricular level. Again, path blood goes to the path of least resistance, and the resistance through the right heart out to the lungs is lower than the left heart, so you get increased pulmonary flow at the expense of, of increased pressure as well when you have the VST, um. And then a PDA we'll talk a little bit more about PDA and this may be the most pertinent one that we all worry about is, is a connection, we all know, is a connection between the aorta and the pulmonary artery. And if you think physiologically, this is the worst of the three because you have continuous flow from the aorta that's constantly spilling into the pulmonary artery. So it's a pressure load and a volume load throughout the cardiac cycle. So, uh, just again to summarize, ASD is, is a low pressure. Left to right shunt, it occurs above the ventricles, but it still results in increased flow to the lungs. A VSD is a high pressure left to right shunt. That shunt is at the ventricular level and so the lungs are exposed to not only high flow but high pressure in systole, and then a PDA is a high pressure continuous shunt. So throughout the whole cardiac cycle in cystole and diastole. And so if you're worried about pulmonary vascular disease, uh, and the effect of each of these on the, on the lung bed. The by far, the one that we worry about the most is a PDA. Uh, patients that have large non-restrictive PDAs go into heart failure very, very soon, and they can develop covascular change very, very early. And, and those can be, um, actually quite a problem if they're not repaired early. Um, just below that would be a VSD still a big problem if it's not fixed early in life because of the risk of, um, of that high pressure and high flow and the effect that has on the pulmonary vasculature. And ASDs of the three are actually the one that we were about the least. And in fact, when it, and, um, patients without lung disease, when we see patients in clinic with ASDs, sometimes we pick it up because they have a murmur. Um, sometimes patients aren't diagnosed until they're in their 20s and 30s. They begin to have some issues related to either pulmonary status or, or arrhythmias or, or things of that sort. But many patients at ASDs don't have any symptoms. And in fact, if we have patients that we know have large ASDs, we usually follow them in the clinic and we tell them that it's a good idea to fix that at some point, but we usually wait until they're 56 years old, sometimes, actually tomorrow, we're doing a, uh, a 19 year old girl who just was diagnosed with a murmur. Um, so the point being is that most of the time, ASDs don't cause a problem early in life, um, even though there's increased flow, it's low pressure flow. Um, that usually doesn't cause a problem if your lungs are normal. So it's reasonable that then ask, well, we know if you have abnormal lung frama and your pulmonary vasculature is at risk and increased flow to your lungs, it probably doesn't help your pulmonary status. Does eliminating these left or right shunts improve pulmonary status in patients with BPD? And so if we start with the most simple or the least noxious of the defects I mentioned, ASDs, we generally think ASDs don't cause a problem, but in fact, there are reasons to think that, you know, that increased flow, even low pressure increased flow to the lungs is probably not good for a baby with BPD or, or underlying lung pathology. Um, and this was a cool little study just recently, um, and I should say the data are a little bit limited with regard to looking at the effect of closure in patients with BPD in part because up until uh really in the last decade, um, Uh, the, the, the way to close mostly defects with surgery. Um, really in the last 1520 years, um, catheterization has been more common to close ASDs, but I think people started to look at this population a little bit more closely, uh, recognizing that we can close defects without the need for surgery, even in, in young kids. So this was the group in, uh, Baylor, and Pam is probably friends with a lot of these people. Um, but they asked this exact question is, does closing ASDs in patients with BPD improve their clinical status? And so this was a retro retrospective study over about a 3-year period. Um, they took patients that were less than 37 weeks. They had to be, uh, less than 10 kg. They had moderate to severe BPD. And um, and again, they just retrospectively looked at who had closure of their ASDs. And there were only 10 patients in this group, um, but I, I still think there's a lot to glean from this study. You can see these are the kind of the baseline characteristics of the babies at birth. The median gestational age was about 25 weeks. Med birth weight is about 700 g. You can see it was a long time before they, uh, did any intervention. So the, these were not interventions that were done, um, within the first couple of weeks or even months of life. Um, but 10 patients you can see here that had, um, BPD. And if you look at the characteristics at the time they had the procedure done, um, obviously they were much older and much bigger, around 6 kg. Um, so these were babies that were in the hospital for many months. 9 of the 10 had device closure, and I'm actually gonna show you a little bit about device closure. One had surgical closure. But if you looked at um what they created, which is a scoring, severity score, basically, or a respiratory score. They called it a BPD ASD score. Um, and they took basically 7 characteristics. Um, I won't go through all these scoring details, but you can see that, uh, patients had moderate to severe BPD. Um, they tried to classify their respiratory symptoms, how much, uh, diuretics they were on, whether they had growth failure, what their degree of respiratory support was, whether they needed supplemental oxygen, and they got an estimate of what their RV pressure was whether they had pulmonary hypertension. So if you look at patients, time 0 is the time at intervention, so that's the time they had closure of their ASD. If you look backwards 8 weeks. And you look forward to 8 weeks, you could see that patients in general, as they got bigger and older, there was a general downward trend in the BPD ASD score, which you'd expect. But at the time of closure, or I should say after closure, the slope of this line was significantly steeper, meaning that their pulmonary status improved quicker after closure of the ASD. And if you broke it down even further and basically looked week to week, um, you can see that post closure here, this is broken down into week intervals. The largest improvement really was the first week of life, uh, uh, the first week after closure, and, um, and, uh, after about 4 weeks, there wasn't much change, but most of the improvement you could see was very, very early on in the first couple of weeks after, after closure. Uh, they looked a little bit more closely at some of the other characteristics as part of that BPD score. So, diuretic use, you can see in general, there was an upward trend towards using, as you'd expect, as their pulmonary vascular resistance fell. Uh, they probably get wetter lungs, so patients need more and more diuretics. And after closure, there was a, a reduction. Um, uh, there was a, a gauge of respiratory score which improved afterwards. Interestingly, growth didn't really change all that much afterwards, and growth velocity didn't change. Um, And uh their RV pressure tend to improve actually quite a bit. So, they concluded that ASD closure in patients with BPD, even small kids, can be associated with improved respiratory scores, decreased tic needs, and improvement in uh RV pressure. And, and therefore, I, I think, and I agree with this, that it's reasonable to consider whether we should close ASDs in, uh, patients with BPD in early in infancy, especially those with significant um respiratory pathology. I say that as an interventionist and uh, it's probably just, um, worth a couple of minutes to describe how we actually close ASDs, um, because we, we would almost never in patients that have reasonable size defects, almost never now close them surgically, and many of these can be done percutaneously. And I just thought I'd show you maybe a couple slides of how we do this. Um, this is an ASD device, um. This is the device that's been approved by the FDA for about 2 decades now. It's called the Ampplatzer device. People have probably heard of it. It's a double disc device. Um, these are the two discs. There's a disk that sits on the left atrium. There's a disk that sits in the right atrium. You guys see my pointer there you go. Yeah, I can see it. So, and this, um, waste in the middle is what sits right through the hole. Um, we can pull this device into a catheter, this blue thing here, and, uh, and we deliver the device and I have a little video I'll show you, but one disc opens in the left atrium, the other disc opens in the right atrium, and if we like how it looks, we basically unscrew it from the catheter. So, um, this is a 6 French catheter and um, We can, we can do this, uh, you know, without the need for surgery and in older patients, we do it with a TED, but we have done it in younger patients with transthoracic echo if we get enough pictures. There's another device, and I just showed this for completeness. There's a device which you prefer to use this device a little bit better. Um, this is called the Gore, uh, cardioform device. The, the last device I showed you, this is all metal. Um, it's a soft metal, but, um, but it's still metal, and if you put your hand on it, it's almost like a little brillo pad. And there have been cases, it's very rare, but this is the one thing we're worried about with big devices and small patients is that there Having cases of the device eroding through the wall of the atrium, and that can obviously be a big, big problem. Um, so we try to avoid using this device when possible. Um, this device is really made of almost entirely of a vortex, so it's very soft, um, and it conforms actually to the septum a lot nicer, you can see here. Um, this device, oh, I'll just show this is, so this is a little video, basically, I show this to families in. Clinic too, um, you know, we put a catheter in the thermal vein. We go across the ASD, um, and it's a relatively simple. We push one disk the device out, we pull it to the atrial septum, and we push the other disc out. Um, we do this with echo to confirm that we can see both discs on both sides of the septum. If it looks nice, then we can disconnect it from the catheter and we just take the catheter out. A little video tries to show here that parents always ask, you know, what happens? Does this need to be replaced, you know, does it come out? Um, what they're trying to show in this video is it just gets endothelialized with, uh, patient's own tissue. And so it stays there forever. Um, but really, um, long term, there have not been there, I won't say never, but the incidence of long-term problems is extremely low, um, and, um. The device stays in there forever and you tell patients that, you know, essentially their, their uh ASD is closed forever and they don't need additional intervention. So, um, so the aplater device I showed you, it comes in all sorts of sizes, from as small as 4 up to 40 millimeters. Um, obviously, most of the babies that we would do this and have defects that are probably in the order of 4 to 8 millimeters. We have done a couple of babies up there. Um, the last was maybe a year ago or so, and I think he got about a 6 or 8 millimeter device. It just depends on the size of the hole. Um, the nice part though with this device is, like I said, it'll go through a six-re sheath through the femoral vein. And in a 6 kg or even 5 kg, um, baby, that, that's actually not a big deal. Um, they tolerate that just fine. We do it with just, just through the venous axis. We don't usually need an arterial line. Um, and it's only good for sumome atrial self-defects that have good atrial septal rims. So occasionally you see some other weird defects like Um, they're more relevant to us like sinus spinosis defects or, or primal defects, and we can't clo those. Those are less, less, um, common though. Um, very small risk of advice erosion like I mentioned. Um, the problem with the Gore device, although we like to use this, is much softer and there's almost no risk of erosion. It goes to a much larger sheet. So we'd have to put a 10 French sheet. So for young babies and most of the patients that, you know, we'd be considering in, in the NICU, this would not be applicable. Um, there is, I just saw this out there because for many, many years, these are the only two devices that were approved in the United States. Um, now, just at the end of 2023, there's another device, uh, which was developed in China. It's called the Aquatech device. It looks a lot like this. Um, a Platzer device. It's much softer, um, and we don't have any experience with it here. The thought is that the erosion risk might be better, but that may be an option, um, for some patients in the future. So that's a few closures, um, and that is the least. Physiologically noxious defect, as I mentioned. VSDs, we worry about much more because not only do you have increased pulmonary flow, but you have increased flow at high pressure. So the pulmonary artery here is hooked, of course, to the right ventricle. And if you have a big hole between the ventricles, then the RV pressure is, is gonna have to be elevated and therefore, the pulmonary artery pressure is gonna have to be elevated. So, so this exposes the lungs to high pressure, high flow, which Which, which we worry about much more um with regard to their pulmonary vasculature. So it's reasonable to conclude that if ASDs we know, uh, cause an issue and, and that clinical status can improved after closure of ASDs, it, it's reasonable to conclude that the The same would be true with BSDs as well. One of the challenges though is that most BSDs are not amenable to device closure, so almost all BSDs, if they're hemodynamically significant, need to be closed surgically, um, and most of the surgeons don't love taking on higher BPD neonates. So, uh, so it's not something we have a ton of data for. Um, there is an intermediate step, which was the old palliation, which we still do sometimes, which is to put what's called a pulmonary artery band, so the surgeons can physically put a restrictor around the pulmonary artery to limit flow that way. Um, and now, really in the past couple of years, we've been able to mimic that. Physiology in the cath lab by putting what are called, um, flow restrictors. And, and this is really kind of new and I don't have a ton of data. Other than that, we have some experience with this and it's worked well. But, um, this is a device that is intended to be basically a vascular plug. So we can push this device through a very small catheter, a four-inch catheter, and it's intended, you can see there's a sheet of Gore-Tex here. It's intended to basically plug a vessels. So if there was a Um, or venous malformation or some collateral vessel that you want included, um, this, this will do that very nicely through, through a small catheter. Um, we have started to, um, lay around these devices and this is not our picture here, but we've been doing these as well where you can actually take, uh, uh, either a dial. or in this case, a little bobby and poke a little hole on the device, and, uh, essentially, uh, create a tiny little 2 millimeter hole. So it acts like a pulmonary artery band from the inside. So it sits within the vessel and that plug has now a 2 millimeter hole in it, and it restricts flow that way. Um, this is a baby that we did actually last week. Um, this is a small baby who's, um, with a, is a punus arteriosis, so physiology. Little bit different, but has pulmonary arteries directly off the aorta, so they get a ton of pulmonary flow, and this is a small baby. So you can see the heart is long, uh, the heart is big, the lungs are wet, and, uh, these are two flow restrictors that we put in each of the pulmonary arteries. And this is actually the following day. You can see the, the lung already looks a little bit better and it's been a way that we've been able to palliate some babies with increased flow. Um, who are too high risks of children, basically. So more to come. I don't have a lot of good data just yet, um, either from our institution or as a field, but this is kind of becoming a, um, a hot new thing, uh, in our field to try to, um, the surgeons like this because they don't have to try to operate on some of these really small high-risk, uh, babies and And the patients we've done, we've done about 12 patients so far and we've been able to at least improve the balance of their pulmonary flow to get them a little bit bigger, uh, before doing surgery to close the hole at which what the surgeons take these out, so. Um, and then last and maybe most important, um, or pertinent to this group is, um, our PDAs. So a PDA, again, we all know the anatomy, the PDA is a vessel that is there at birth, should close at a couple of days of age, but it is a vessel that connects the aorta to the pulmonary artery. It's an important structure in fetal circulation, but it's not important after you're born, unless you have a major Heart defect like hypoplasar heart syndrome, something that, but for babies with normal intracariac anatomy, persistence of this defect can be a problem because, as I said earlier, this results in continuous left to right flow throughout the cardiac cycle. So both in systole and diastole, the aortic pressure is higher than the pulmonary artery pressure. So for a given size defect, you're gonna get the most flow to the lungs at the most pressure with, with a, uh, a PDA. And obviously it's been long recognized in the BPD world that, you know, PDA is not um uh can have deleterious effects on the, on the lungs and the typical treatment is, um, has been for a long time cervical ligation, um. You guys know the morbidity of the patients, uh, you know, PDAs that don't close have significant morbidity and premature babies. Uh, there's an increased risk of that, uh, due to the dysto flow from the aorta, uh, chronic respiratory disease, uh, pulmonary hemorrhage, intricular hemorrhage, and even, and even death, increased risk of death and PDAs so close, um, again, you know better than medical therapy than me. I know there's a lot of, um, when I was innocent, now I know there's a bunch of different cyclooxidase inhibitors that have limited efficacy in babies that are very low weight, and, um, and they do have some side effects. So, um, this is a device that I think people are familiar with and as I mentioned previous to this device, um, the only real way if medical therapy failed was to do uh PA ligation, what the surgeons would do, um, even in the bedside at the NICU. Um, we, I can't remember the last PA ligation we've done surgically here anymore. And this, this device has kind of replaced surgery, um, because, and this was kind of a landmark study and not that long ago, 2020, um, this was a group from about 12 different centers, um, that evaluated this device called the Piccolo device. So it, the concept is very similar to the ASD device I showed you. There's a couple of discs. You can push it through a catheter and again, I have a little video I'll show you. Um, but this was a trial looking at percutaneous closure in babies above 700 g. And this is the trial that actually got this device approved by the FDA and so it's now approved for use in babies above 700 g, although I will tell you, I don't think we've done any babies above 700, but people now are doing 5 and 6 5 600 g, um, babies in clinical practice. Um, we do this through the femoral vein, and this goes through an even much smaller catheter, 4th French catheters, so you do not get anything in the artery, um, and, uh, we can assess the placement of the device on the aortic side with echo. Um, I'll just show you some data from this study. So this was, uh, you can see 100 patients, in 200 patients total, 100 were less than 2 kg, 100 were greater than 2 kg. I mean technical success was really excellent in all these patients. Interestingly, it, and this is our experience too. The smaller babies, believe it or not, it's actually a little bit easier to close the. Uh, they tend to have PDAs that are a little bit longer and tubular and create a little bit better landing spot for the device. The babies that, one of my colleagues, Doctor Almasari, he jokes that the 4 kg babies are the ones that are a pain because their darkness tends to be a little bit more tortuous and, um, a little bit less predictable, and it, it gets a little bit harder to put a device in those safely sometimes, but. So you can see the technical, um, uh, success was really excellent in both, uh, less than and greater than 2 kg babies. Uh, there are some complications, obviously, um, not trivial complications of about 4.2%, um, but overall, um, it's actually a, you know, really very safe, effective way to close the PDA. This is, again, I'll just show you a little video, compliments of the aplats or I don't have anything that's closed. I should have said that earlier. No, uh, commercial disclosure, but here is a catheter that we, um, again, just through the femoral vein. Obviously this is an animation, but, um, and, and interestingly, the anatomy in a, in a neonate is usually, it's almost a straight shot. Get a catheter up into the RV and it almost always goes straight down the ductus arteriosis. It's a nice smooth bend that actually makes it really pretty easy for us to um advance a catheter. And then this is a four-re catheter. And as we, um, Look by floor, we can advance this device out. And this is an ideal, and they, they're not this easy. I will tell you. This is a nice long tubular PDA and, um, they don't always look like this, but when they're nice and long like this, um, that device sits right in the middle, and then again, we can unscrew it. We look by echo on the aortic side here. You can't see what's going on in this aortic side if we don't have a catheter in there. So it's important that we're sure that this device doesn't obstruct the aorta. Um, and then we can unscrew it and, and, uh, and take it out. This is actually uh baby Doer Sawe did, um, I think it was last week. So this is a baby that came over from Saint Joe's. This was the X-ray. Um, the heart, you could see is almost hard to see. The lungs are really, really congested. The heart is big, and this is literally the X-ray the next, um, the next day. So significant improvement in the vasculature. The lungs are obviously not normal, but, um, this can have a really, uh, profound immediate impact on the, uh, pulmonary status sometimes, so. So it's a, it's been a great um device and development for us. So, in summary, left to right, again, physiology, left to right shunts are shunts that result in increased pulmonary flow, which leads to increased morbidity in patients with underlying pulmonary pathology like BPD. Of all the defects, PDAs probably pose the greatest physiologic burden because of the continuous flow that is a pressure and volume load. VSDs also result in a pressure and volume load, uh, with similar effects, um, but are a little bit more difficult to close, and ASDs are the least noxious of the three levels of shunting, but closure can still result in significant improvement in morbidity early on. Um, and so closure of ASDs and PDAs now we can do with catheters for PDAs, uh, you know, 700 g is probably the lower limit. ASD patients, uh, probably about 5 kg, um. And, uh, limited data suggest improvement in pulmonary status almost immediately. Uh, and I just write, you know, VSDs again are still a little bit of a problem. I think the concept of pulmonary flow restrictors is, is really cool and we've been a little bit more, um, innovative and aggressive about using those, um, although we don't have any data to support their use, but there may be a, a role going forward for that in some, uh, some patients with VSDs as well. So, um, with that, I'm happy to answer any questions and I hope I didn't know we have to do that. There was a question in the chat. Yes, so the question was After hearing about, um, you know, closure of sun's. To, um, what is your recommendation on PDA surgical closure or device closure on extremities that are chronically ventilated, and is there? Closure PDAs. I think surgical ligation has really, um, I, I would say almost everybody deserves a trial at having it closed in the cath lab. There are occasionally cases where the anatomy is too complex and, or maybe the patient's unstable, but, um, I think our outcomes would be good with device closure. Um, I should say we've had occasionally patients who are on an oscillator or really difficult to ventilate without conventional ventilation and, and from a practical standpoint, we just, um, Those are ones we can't really do because we just can't get the patients there, um, but, uh, otherwise I would say, you know, an attempt at device closure, um. Should be done as soon as. You know, you think the child has significant low quality. I have a question that is for the small PDAs like we sometimes get this on the floor and the NICU or it's like a small PDA, uh, hardly flow and then so my personal experience and I ask you that is that how significant that is in patients with um severe BPD um and Do you, do you recommend that they should be closed? Yeah, it's a good question. We get this all the time patients come to the clinic or someone does an echo and they see a little PDA and the The left to right shunt results in increased flow that returns to the left atrium. So one of the things we look for and one of the criteria when we're determining whether we should close one in, in the, um, DVD patients is whether there's any left atrial left ventricular enlargement. If there is left heart enlargement, it would imply that there's a significant amount of flow through there that it should be closed. Um, we, we sometimes have patients that have, incidentally have a PDA that's found and the left heart's normal and there are any symptoms, and we actually don't usually recommend, they don't even necessarily require closure, but if the left heart is dilated or if the patient has significant lung pathology, it sometimes it's cleaner and easier to just get it out of the picture, especially in older patients. Once you get to be above 3 kg, um. It actually is a very easy, safe procedure. You know, we do worry in the small bas at any point out here, and we had one baby where this happened to where, um, the tricuspid valve tissue and leaflets are really, very, very friable. And, and one of the biggest risks when we do this in the kids that are less than 1 kg is injury to the tricuspid valve. But once you get to be about 3 or 4 kg, that becomes really negligible and it's a very, very safe procedure. Go ahead. I have a question regarding the study that result regarding ASD closure in DVD patients. And do you have data of what is the traditional management, meaning you don't put device closure. And you see how the respirator starts improve. The reason I'm asking is because to do the device closer, I assume all these babies got incubated. If they were incubated then you support their cardiovascular status in a better standpoint of view. So the improvement, some may say that it was based on the incubation itself and not necessarily the device closer. The question I have a little trouble hearing. The question is, do we have data regarding COP? I'm sorry. We do have patients with PPD that have ASD. Do, do we have a comparison between these patients with the paper that you saw with the device closures? And the reason I'm asking because of all the babies that under one device closure not to undergo they had. Incubate they were invasively mechanically ventilated. So you have a relative undersupported baby previously you incubate them, you take out the That under support. So theoretically the cardiovascular system might have been improved as a consequence of the intubation. I suppose that's possible. I mean, typically when we do older patients with ASDs, they're immediately extubated like in the cath lab. Uh, they don't usually require a long term, and we, I, I don't, um. I'd have to look back at that study to see how many, you know, remained intubated for a long period of time, but it's typically not a procedure that required. They're just intubated for a brief period of time during the procedure. They always get extubated, even the smaller kids. I'm saying because I saw high flow and that's a significant support. And then their babies ended up with the cake. And that's a common drug that we would end up anyway, yeah. Yeah, I, I mean, this was a retrospective study and just a really small group of patients and it's really the only data we have looking at what happens to their pulmonary status before and after. But, but typically, most patients for um ASD coders don't require intubation for a long time. Thank you. Um, there are some genetic conditions on which lung is actually, um, not formed correctly and there is a left to right on the smosis like hey we and ACD patients, for example. Those patients also come with some heart abnormalities as well. I know they are not stable and very rare, but would you consider the close? A heart defect on these babies if they are more stable because some of them have like due we presentation of the disease. I'm just curious. Yeah, I think anybody with an ASD that is significant, meaning there's a decent left to right shunt through there where you see enlargement of the heart, there's almost no, um, we would close those on almost everybody. There's really no good reason leaving a long standing left to right shunt would be beneficial. The only exception would be patients that have severe pulmonary vascular disease where they're systemic, you know, the pulmonary resistance is higher than the systemic resistance will pop off. But, uh, almost everybody else, uh, with a defect and by significant an ASD bigger than about 5 or 6 millimeters is hemodynamically significant. So, um, that's almost, uh, almost everybody with a defect bigger than that will have enough flow that it produces some, uh, volume volume load on the right side, um. So, so the answer is yes, I would say if they have uh uh a significant defect it probably should be closed. In babies with established BPD, how often do you get human dynamics prior to closing or even evolving, almost BBD given the prevalence of of BPD associated pulmonary hypertension that something need to be is like when you get the cat, um. Yeah, that's a good question. So I think the concern is if it looks like the pulmonary pressure, the pulmonary resistance is higher than the systemic resistance, and that's the one instance where you know closing a PDA might be. Dangerous. We can get some sense of that from the echo. So Panos, you know, we look all the time at the direction flow to the to the PDA. Almost everybody has some component of left to right flow. If it's very briefly right to left in early Sicily, but the rest is left to right, which is usually the case, then, then almost always it's better to get rid of that PDA. But we have had some instances where it's purely right to left. And, uh, and we'll do, sometimes we do a cath to determine that, whether it's right or left. And the other thing we can do at the time of the cath is test their pulmonary reactivity. So put them on oxygen, put them on, on X-ray. So we had a baby actually not that long ago, they had a PDA. It was all right to left. And, um, when we put them on oxygen, it went left, right. We left them on oxygen for a couple of months and came back. Um, and after, after a few months, he was all right we will close it, but that'd be the one instance where you, you have to be a little bit um careful about closing, uh, a defect if, if there's just pulmonary is a supers systems. So just a quick related question would be as a pulmonologist for the oxygen stats, what are those stats, and that probably depends on what is how much is the intrinsic or hypertension versus left because of the overflow. So how do you tackle that in the cath lab and what? Yeah, that's a good question. We can so we can get some sense of that from the echo. So occasionally there'll be a baby who's desaturated, but we'll see the ASD or PA is all left to right, and then in that circumstance. It has to be the lung. It has to be the pulmonary vein is desaturated if there's any left, right flow. We, uh, but it is an important point, and even in our heart patients too, if they're desaturated, we sometimes want to resist their lung or resist their heart. And when we do, uh, and that's when a catheter, a diagnostic cathe would be helpful because then we actually, it's important for us to get in the pulmonary veins. So, especially if they have an ASD or many times they'll have a little PFO we can get a catheter from the venous side across and get into pulmonary veins draining from each, each of the lungs. And, and that's your answer, you know, if you have blood coming out of the lung that's desaturated, it's a lung problem. If you have blood coming out of the lung that's normally saturated, but the patient is desaturated, then there has to be a light to left shot somewhere, um, so that's a good question. Any other questions? OK, that was great talk. Thank you. Thank you. Published April 10, 2025 Created by Featured Providers Joseph N. Graziano, MD Cardiology View full profile
