Chapters Transcript Video TAVR Basics: Fire Drill Overview #1: Pericardial Tamponade/Effusion Dr Summers discusses the recognition and treatment of pericardial tamponade during a TAVR procedure. So this is, I believe our force in a series, uh we're calling our Structural Hard Education series. And so again, this was uh prompted a couple of months ago when we had a, a more complex case, a lot of people in the room and, and a lot of new team members and a lot of uh faces that looked confused about what each independent person's roles were. And so that was part of it. But getting everyone on the same page and getting a fundamental understanding of, of what we're doing with trans cather aortic valve replacement and what each person's roles are and how we can affect outcomes by working together more efficiently and effectively as a team. Um Some of this uh was born out of what they do in military training when there's multiple uh different uh types of people coming in and out of the team. And you have to deal with emergently in the field, uh very complex scenarios that tend to be rare as well and have that team work efficiently in a time effective manner to, to save people's lives and that's effectively what we're doing in, in tver. We have complication rates that are on the order of one in hundreds. And, but during those one in a hundreds where there's a flip of a coin mortality rate, the, the effectiveness of our team and how, how facile we are with these complications will dictate our outcomes in those scenarios. And we invest a lot in TVER to have those redundant mechanisms in place. I tell people. And I know I said this last week that we have 16 people in, in the room for a TVER. And we can functionally do that procedure just like a bav with four people in the room. Uh But we have that redundant mechanisms and that, that uh reserve in place so that we can save people's lives in the rare circumstances that some of these complications occur, but we have to be prepared for them and that's what this is all about. So we went through uh our program, the standing of the program, our history, we went through how we approach aortic stenosis, how patients get to the operating room where you all meet them. And then it's often the, the time where you all uh stop seeing them as well. And so we wanted to uh provide a basis for, for how we manage uh patients and, and get them to the operating room, what the decisions are. Um And the complexities are in the, in the work up and evaluation, but also in the uh post operative management and then also some of the things that come in through the operating room that uh arm taverns, which we went through last week. Now today was supposed to be annular rupture, uh which is a surgical, pretty, pretty much a surgical emergency, which is very rare. It happens between 0.4 and 0.6% of the time. Doctor Kemp, I think was up with a transplant and other cases all night. And so he's not able to do that. We're going to switch that to next week. And instead we're going to go through pericardial Tampa predominantly a percutaneous bailout scenario. And then so the sequence again, we're gonna go through these five major complications of tabor that should take 15 to 20 minutes every Tuesday morning. These would be didactic to start once we go through the, the different complications and then we'll start running these intermittently on TVER days. It's not gonna be a big deal. It's gonna be during time out. We'll get a random flag that says, OK, this is a drill on a Pericardial Fusion and we'll put up a patient's case like I'm about to do today and we'll go through the case very, very quickly and we'll call out, you know, like Maria, if, if we saw hypertension, what would you be concerned about? And we would all speak up, we'd all have the opportunity to, to talk. But after after going through these, we really want to promote everyone in the room as a set of eyes, pointing out things that they see that are unusual. It doesn't matter what your position is in the room, you're an extra set of eyes. All right. So even if you don't understand why it's happening or how to fix it, that's fine. There's people in the room that understand why it's happening and, and know how to fix it. But recognition is a sensitivity issue. When we're focused on other things, it doesn't matter how we, we approach it, how we fix it, how good we are at fixing it. Recognition is is the first step in all of this. So let's get into the pericardial tamponade and effusion uh complications. So this is relatively rare. But if you look at some of the reports up to 4% of patients undergoing tab or have effusions, so how you define those and whether it's a baseline effusion, whether it's changed, whether it's new, whether it's sub acute, those things uh vary quite a bit. We see about 1% of our tatters and that's about the rate of what a pacemaker perforation would be in the right ventricle. So just keep that in mind, it's about one in 100 patients, we have to deal with this. It can ebb and flow obviously, and we'll go through some of the reasons why patients may be at more risk for it. Um But by and large, think about it as 1% of our patients suffer this complication. And so again, we have to be prepared because minutes matter and the seconds matter sometimes. And recognition as a result is key because early recognition can shave minutes, uh sometimes, you know, 1015 minutes off of your ultimate treatment of a life threatening problem. The etiology is almost always right. Ventricular perforation from a non balloon tipped p fixation wire, paradoxically, the active fixation leads have a lower uh perforation risk. So, when we do the screw ins, they actually have a lower risk of, of perforation, you see that uh for cied implants, the the rates vary at least in modern literature, up to uh less than half of a percent. Um So why do they go up during TVER? And there's a variety of reasons for that anticoagulation, the patient population that we're, we're uh treating, we're doing um you know, in a lot of situations, uh we're treating patients with smaller hearts and more frail individuals. There's, there's a variety of reasons, but we'll go through all of those normally. Uh the pericardium can tolerate about 50 CCS of fluid. And if you've seen these effusions, which most, most of you have more commonly, even in the acute ones that we, we get controlled very quickly, we're pulling off hundreds of CCS of fluid sometimes more than a liter of fluid. Now, in the acute setting, the pericardium just cannot tolerate that much fluid. And so the large large, large effusions you generally see in more chronic processes um because people start, as you see on this pressure volume loop, people start having issues immediately if their, their pericardium is not preconditioned to that fluid. So again, just like everything in in cardiology, acute is uh a manifestation of not being preconditioned to the overall problem. And so these patients come in with a dry pericardium, they get a little bit of blood in it and they can decompensate very quickly. And that's the key takes as little as 100 CCS to get a circumferential effusion and you can get tamponade with as little as a quarter of a liter of fluid. This is what we currently use. So there's two types of pacemakers. We went through this last week, passive and active fixation. All that means is a screw or not. And then there's balloon tipped and non balloon tipped, non balloon tip. This is a pay cell this we use in 95% of cases. Uh when we're not at risk for conduction abnormality. At baseline, we talked about the proximity of the bundles and the conduction system to the aortic valve and where they live in the MEMS septum, how we plan for those and, and risk stratify for those uh before the procedure and the decisions that we make about active fixation versus passive fixation before the case. So we should have a good understanding of why basically baseline conduction disease. We're using active fixation wires. This one isn't used very much anymore. Um It's uh it's a combination of passive and active fixations. It's uh called a tempo wire. There's some merits to it but uh isn't really being produced. Uh Currently, there's, there's a few places that still use it, but it's, it's not as common and a balloon tipped is a little bit safer as far as working in the right ventricular apex. That's why there is a push to use those a few months ago when we had a few effusions related to the pay cells. So these are fairly straightforward uh clinical features here, I don't know why that's not playing. But the the short of it is is you see a large effusion. So it's very easy to recognize often, at least in the scenarios in which we're going to be encountering. Um But hypotension tachycardia, which may be blunted because a lot of these patients aren't beta blockers or getting anesthetics that, that can blunt that effect. Uh But Respi oas meaning the pressures change with breathing. This is what pulses. Paradoxic uh paradoxes is this is what you see as a result of loss of ventricular dependence. It's basically the ventricular beco uh the ventricles become uncoupled as a result of these, this fluid around the heart. And you're getting a relative inefficiency as a consequence of that. This is back his triad with soft intracardiac sounds with uh uh goose malls and um and pulses and So there's there, this has been recognized for a long time. But in practice nowadays, it's really as quick as we can get att te that we can recognize it. And so really, it's looking for some of these subtle features, oftentimes subtle features during the procedure that prompt an echo to recognize it and then get a drain in very quickly. You can see the relative sensitivity and specificity of each of these echocardiographic features. In general. We're looking for a large effusion with some sort of chamber inversion or compromise collapse, you can get down into the weeds about which phase that occurs in and and which uh chamber it occurs in. But but generally a large effusion with some sort of chamber compromise usually of the right side and then Respi ofa inflow variation is is fairly common thing that we look at. This is where we're looking at how the blood flows through the mi and tricuspid valves at different points in the breathing cycle. OK. As you change and change uh intrathoracic pressure. If you have an effusion, that effect between the ventricles is amplified, the recognition is key. We have echo in here. I don't see any when the echo text. This is why we have echo text in every tavern. It's for an effusion, it's for complications. So one of the key parts of this in early recognition is understanding the baseline by the time patients get to the or sometimes they are a month, maybe more from their index echo that prompted them to come to see us. And so some people have heart failure and interval heart failure progression and can get effusions uh between their index echo and when they come into the or. And so, one of the, the key things here is while we're prepping the patient, we want the echo tech to just put the probe on the chest, make sure there's no change in LV or RV function and that there's no change in that can happen in a matter of seconds at the beginning of the case, while the patients getting transferred over and we and is getting clean and prepared. But we need to start doing that in every case for this reason because what happens is if they have an interval effusion and then we check first after the valve deployment gets very, very difficult to understand what's changed, what's new, what's not what we need to put a drain in for and a drain is not a benign thing every single, every single time we place them. And so that first echo when a patient comes into the room, an updated echo for ef and baseline effusion is very important for that reason. We should be getting standard TT es after every single deployment and after any valve intervention including predilation and post dilation. If there's a hemodynamic change, Katie, you do a really good job of this, you point out blood pressure, even when you're on pacemaker, when you're prepping the valve. Our Cath lab techs do a phenomenal job. JD. Uh Mia, they do a phenomenal job at pointing out abnormalities. And I'd like to encourage everyone on the team to do that. And so if you see an unexpected drop in blood pressure, the heart rate go up a little bit, you know, don't just assume that the anesthesiologist and me or Doctor Kemp are having those discussions or thinking about these things. Uh At the same time, we, we generally are, but it's a sensitivity thing. If we've got other things going on, our sensitivity changes from 99.9% maybe down to 95%. So when we're dealing with these issues, that can result in 5% of our patients having an issue that it is not recognized as early as could be. So I want to encourage everyone to speak up during these procedures. Any hemodynamic change leads to an echo. You all have seen that where we keep asking for echoes over and over and over again when we're concerned, that's why as we're looking for an effusion and we're worried about one. So if you see us repeatedly asking for echoes check and see if we have a Peric cardio synthesis kit in the, in the room, I mean that happened the other day, we didn't have it upstairs because it had been used by P or something. But that's, that's an extra step that someone can be doing while you see us calling for echoes uh repeatedly. You know, we're worried about an effusion if we don't verbalize that, that's what we're worried about deploying the valve. Obviously, there's, there's big things like annular rupture which are a more dramatic presentation. We're going to go through those with Doctor Kemp, I believe next week and what some of the surgical repair options are and sort of what the outcomes are. The short is is that they're not very good when you have an annular rupture. The way we treat that is by preventing one in the first place these patients, it's very, very difficult even in the hands of some of our excellent surgeons to salvage a scenario where there's an annular rupture, but they do it and they do it very, very well. And your, you know, their teams, you all do a phenomenal job of this, but the mortality rate is still very, very high. And so again, early recognition is key. Um the key parts of the procedure is placing the pacemaker. You see us having difficulty uh putting in that pay cell and the blood pressure drops. You know that that's, that's key. Those are the kind of things that we're thinking about if it's after crossing the valve and the valve is difficult to cross. Worry about an LV perforation that straight wire as you all see, when you feel the, the tip of it every time you hand it to us, even, even the correct end of it isn't totally benign. And a, and a little old lady with a small ventricle that's on chronic steroids that's got a thin, uh LV. I mean, all of these things add up to where the risk is, is not zero. The rapid treatment is important. There's two different approaches. Almost all these you'll see is subxiphoid. That's because if I hit the, the right ventricle or an artery, uh on top of the right ventricle with a needle, I'm I'm very unlikely to cause a permanent problem that requires a sternotomy. You can pull that back if you hit the RV and you've already got access into the, the pericardium. You have a drain in general venous bleed, stop of protamine in general. And so, Subxiphoid is safer in that, in that uh setting because you're right next to the right ventricle. Now, all of the um perforations and all of the effusions don't happen in that fashion. So some of them are apical. That's why in apical the equipment that I like is this micropuncture kit. So if you do hit the left ventricle, the consequence is less. It's just like we do with the femoral arteries. You know, we don't use a cook needle on the large board side because the consequences of hitting it and then having to wait and having a bleed are different than on the small side. So for the same reason if you, if we call for a pericardial uh synthesis kit, also pull an extra mini stick max. The stiffens also pull a wooly wire. It's good to I put this here. Not because uh I don't want you to see the, the length. It's a long wooly. Ok. So the long wooly allows us to get a ton of purchase in the pericardium with the wire and not lose pericardial access as opposed to walking back a short wire, putting in a dilator so long wooly pericardiocentesis kit, mini stick max or you guys call them stiffens. And then it's uh reversing the anticoagulation when that's safe. Protamine is very important that almost always solves RV, perforations from pacemakers which are the most common. If it's an arterial perforation, it gets a lot more complex. And we'll go through a case of that, determining the ideology is fairly easy. It's uh you can, you can tell kind of clinically what's going on. The, the speed of the accumulation, the speed of the drainage, not being able to keep up with uh the drainage with auto transfusions. All of those are uh manifestations of an arterial or LV injury versus a right ventricular injury. But you can get sats and you can check if the sat's 65 70% you know, it's Venus, if it's 100% you know, it's arterial. So you can analyze the pericardial fluid. So that's why we do that. And then an aortogram. If you don't have an ideology, very clear in general. If you have an annular rupture, you know about it right away. We're talking about ECMO, we're talking about opening uh trays to, to open the chest. It's not a subtle thing when it happens. Neither is left ventricular injury as far as the effusions. You all have seen one at least in this last year from uh that savvy wire where we had issues with it and we could not keep up. We had to open up. We were auto transfusing as fast as we could and the, the fluid was accumulating faster than we could pull it out. That's an arterial injury. I'll show you a more subtle one, but it's still very, very apparent and you, you kind of know that it's gonna happen before it actually happens. The more subtle ones that require really early recognition are these venous perforations that happened from the pacemakers. This is the first case. So the idea with these is we're gonna go through a couple of examples and then again, starting once we're done with this didactic session, we're gonna pull up randomly. These are real cases, real cases at the beginning of our, uh tver day, it's gonna be unannounced. Um I try to figure out how we're gonna do this. I think Danny is, is going to have random days almost like a true fire drill and we're just gonna show a case and we're gonna talk about it, like we're talking about it right now, we'll talk about what the, the ideology might have been. We'll talk about what the equipment we need is. We kind of wanna have you put yourself in that position as a member of the team thinking about what you individually would do in those scenarios. Does that make sense? And so if you don't know what you're doing in those scenarios, maybe you, you don't have a role in those scenarios. That's fine. But instead of spectating, um sometimes the, the answer is to get out of the way and let the people that do have roles take over and that's what we have to define. And so we may not need all 16 people for every one of the complications. But you have a very important role in every single procedure. And even if it's not dealing with that specific type of, of complication, the goal of each member of this team is when we have these drills to think about what you would do in a real situation, what your individual role would be and what you can do to help recognize the the issues sooner along with the rest of the team. So this was uh an 8081 year old lady. Uh she had class two heart failure symptoms in the setting of pretty severe aortic stenosis. See her gradients are what we would call critical or, or very, very high uh gradients it's got a little bit of aortic insufficiency. She's got some mild coronary disease. We're talking about doing a cath. This is a key here. Rheumatoid arthritis. She's on chronic steroids. A F creatinine is normal blood counts. Ok. Sinus and narrow. So we're not going to use an active fixation wire, right. She's not at risk for a pacemaker necessarily because she's narrow and sinus, she's got good iliofemoral access is about as clean as it gets from her annular anatomy. It's fairly benign. It's a tricuspid valve. We have good coronary heights. There are over 10, so are not at risk for coronary occlusion. We don't have a horizontal aorta. So we shouldn't get caught down here in the gutter. It shouldn't be hard to cross the valve. Um The only difficulty with crossing the valve should be from the high gradients and we should probably pre dilate or bab as a result of that. It's intermediate risk. Salvage is very high. Doctor Unger said extreme surgical risk and we are under limited surgical conversion options here. So that means that we went into this case with a plan to not do a full sternotomy. All right. This is baseline tt but it didn't put here. Is it two months before the case? All right. So that's, that's why we need those updated ones. There was a very small effusion in the interval. Uh but it wasn't subtle once we got to the, the meat of the case So this baseline looks like normal left and tr of the function, a little bit smaller LV cavity, the right ventricle is small. You know, these, these patients come in dehydrated because they're NPO, they're dependent on a higher preload because they've got uh LVH and an, you know, an aortic valve that's not opening. And so they're already sort of set up for badness before they even get to us. They're already volume down, They're already a little bit behind the eight ball and then we compromise their, their ventricular filling further with any effusion. And we're off to the races towards badness. We had standard access. The patient was stable throughout all the access and placement of a passive fixation, non balloon tipped pacemaker wire. So remember the context is key. I had a really difficult time putting this pacemaker in. She was dry. The, the uh pacer kept sticking on every little branch vessel all the way up. She had a, a vertical heart, not a horizontal heart. And so getting in making an angle into the right ventricular apex was very, very difficult. But ultimately, like all these cases, we did this without too much of an issue, but it was a little bit more difficult than usual. So that, that should be a flag if you see us struggling a little bit with the pacemaker because patient's anatomy in our mind, what Doctor Kemp and I are, are thinking about as we're doing that, we're we're thinking about, did we, are we potentially at risk for a pacemaker perforation by doing this? Should we switch to a balloon tip? Should we just put in an active from the, the right IJ, that actually has a lower perforation risk. So we're thinking of all these things and we're also flagging in our mind that if there's any blood pressure issues, we just had a difficult time with the pacemaker. Standard Heparin was given the first AC T was very high. That's another trigger we really need over 250 for these. When we're in the lab, our anticoagulation is a lot less robust. It's because when you come to the or we're used to putting people on pump and doing high doses of Heparin, you'll commonly see that first AC T I know you all see it, it, it, it tends to be very high. But if it's, if it's above 350 or so, and we're having trouble with the pacemaker. That's sort of the recipe for this. We performed uh bav first because of those high gradients. And then we deployed this self expanding valve without issue and then she started getting a little bit hypotensive. Initially, it was after the BAV, we didn't do a repeat echo. Um We, we instead moved quickly with the valve. We were concerned that there was a little bit of aortic insufficiency after the BAV. So again, it's not necessarily enough to sit through there and think about the differential diagnosis. During these cases. I had an attending, uh, Jonathan White, tell me he used to be a referee in, in, uh Australian Rules football and, uh, in the professional leagues and he would say it's, it's not enough just to know the different types of penalties when you see one and say, OK, this could be, you know, X penalty and this is the, you know what you get as far as yardage reduced. And all these things, you recognize it in real time as a penalty and you're already making the call. And so the way that translates over to us is it's not enough for us to say, OK, there's hypotension. What are the five causes of hypotension after a ta or this could be this, this, this and this, you have to be moving for the initial treatments of the presumed primary cause before you break down the differential. In other words, hypotension after valve deployment, we should be reaching for pericardiocentesis kits even before we do the echocardiogram. So it's recognition. Yes, but it's also two steps ahead in getting the stuff necessary for any of the complications that that recognition could prompt. And so we weren't improving with anesthesia interventions. We were initially a little bit worried about A I but we were, we had the valve ready. We're gonna put the valve in and get it in very quickly and take care of that. OK? But things kept getting worse. I know we had this very easy to see. Right. Subcostal approach drained roly wire sequential dilators. 65% sat, she had no significant hemodynamic consequence. With all this, it's just some subtle, low level blood pressures and we were flagged to it early. We were worried about the pacemaker from the get go. We reversed protamine, put a drain in. She went home two days later just because we watched her for an extra day. There's no ill effects from this at all. She had one extra day in the hospital. That's still a complication. It's still something we should try to prevent. But if we get out of these life threatening problems with an extra day in the hospital with a little discomfort from percutaneous drain, that is a massive win. Ok. Uh in the setting of a sometimes lethal complication. So this is what we should strive for and this is what we can accomplish in the vast majority of cases with early recognition. Um But again, Katie had the pericardiocentesis kit already out. Um I mean, I, I couldn't get a needle in uh faster than I was being handed equipment for this case. And that shouldn't be the expectation that we're, you know, you're thinking, you're trying to think of what we're thinking every single time, but it should be a process where if you see something and we're worried about something, you see us getting repeat echoes. You're starting to think about these things to help us take care of the problem by grabbing a pericardiocentesis kit, grabbing a wally wire, grabbing a mini stick max, the echo tech making sure you're scrubbed should be scrubbed already. But getting prepared to help me with the pericardiocentesis, we have to get into the pericardium very, very quickly. So we're putting a big needle in underneath the, the xy trying not to hit the liver, trying not to hit the heart and we're doing it in the middle of hemodynamic instability. So it's our focus is very technical and so focusing on what equipment we need should really be a secondary thing and that's what you all can help us with. This is the second case and this will be the last thing here before we get going. Um But this is an 85 year old female, had a different outcome. And so she has a severe aortic, she had a balloon uh for syncope uh with her A S and and more rapid prog uh progression, but she also had vocal cord dysfunction and some pretty severe uh depression. And catatonia was on an MA O I inhibitor, had some cerebral vascular uh history um and had a concern for mac and, and the lungs. It's different kind of mac than, than we usually deal with, but she wasn't healthy at a baseline. She was on also on some chronic steroids, had a small LV, what we call the little old ladies, right? 85 year old lady that's uh, got a BM I of 20 has a small ventricle, small heart. These are kind of the things that when Doctor Kemp and I, and, and doctor Taraia go into a case, we're already sort of thinking about this. This is what we're talking about outside the room when you guys are getting ready. As we're saying, this little old lady, what kind of wire are we gonna use? What's her risk of vascular injury? She's got tortuous iliofemoral, but they're clean. Um We're worried about the annuls but not about annular rupture. It's pretty benign looking annul. It's not horizontal necessarily. At least it doesn't look like it in this but intermediate risk for sure, high rate of uh bad outcomes if we have to convert. We used a navato in this setting. So standard access patient stable throughout access fixation on balloon tipped pacemaker wires because there's no baseline conduction abnormalities. It was a self expanding valve. You all learned last week that that's got a higher pacemaker rate. And so we're already thinking about if there's any conduction problems, we would switch to a right IJ and an active wire. We had no difficulty with that Pacific wire. The first ac T again was 450. Not terribly unusual. We had difficult, a lot of difficulty crossing the valve. And so sometimes after bavs the anatomy changes enough to where it can be more difficult to cross. It's usually easier but sometimes it can be more difficult. We had to use the glide wire, multiple wire position changes was the key. So with these self expanding valves, we do something called cusp overlap deployment. You've probably heard us use that term. But what we're talking about is using a technique that allows us to deploy the valve very, very high away from the conduction system. That's all that is. And we do that in a view that allows us to see the heart and its long axis. So it's generally generally safe, but sometimes the wire position can look uh atypical from our typical views. What we we did with this in this, this cusp overlap is best done with stiffer wires. So in the evolut trial, that showed its benefit lowering pacemaker rates, single digits Lunder was used. That's why we use double curved Lunder with all of our evolut. And that's why we had been using Navato we've been using since self expanding valve. We've been using uh L Lunder. In this situation with a small LV, you'll see we had uh a significant difficulty releasing the avatar. And as a result, we had to be very aggressive with their wire manipulations. And because it was a Lundquist, we ended up having an issue, we also ran into a horizontal aorta, we had to re bav and so a lot of these things were struggling to get wire position, the wire position in the ventricle, the whole time Sarah and I were uh concerned about it. We, we, we kept saying we, we hate the wire position. Let's get another pig tail. We're trying to uh adjust the wire position. Um This is why we call for pig tails and why we, we try to rewire this often. Why we switch to a safari or conta or circular, the pre shaped ones. Um But bottom line, it was very difficult and we kept calling for TT E SI at almost every step. I think I had called for att E about 10 times before there's actually an infusion. And that's because we're worried about these things because of certain aspects of the case as we're doing them. But ultimately, the, the failure here and I want you to look, this is a soft part of the wire, this black part, this is a coat hanger, it is as stiff as a coat hanger. The techs know that we are fighting relentlessly to try to keep this black part in the apex so that it doesn't cause you see how this is starting to fold that can get very, very, very sharp in the apex. And some of these little old ladies with BM I of 20 have trans loosen apexes. They're so small, they're on chronic steroids, it can be prone to injury just with putting a wire in there. So when we're having difficulty, that's why we're, we keep looking at echocardiograms and then this has been a problem with some of the novatos when there's tortuosity and when we're using stiff wires is they fail to release. So the, the failure in this case wasn't that we picked the wrong valve that we did anything technically abnormal. We did all the best practices when we, when we could, we, we use a stiff wire to help with a higher valve deployment to reduce pacemaker risk. That's in spite of her having a small LV and being a little old lady, this is how we typically do every one of our evals. Um We were concerned about some things at the, the front end, but ultimately, we, we ended up doing everything we would typically do, but we found that her aorta was very horizontal, it was hard to get across. We had multiple wire manipulations had to adjust the stiff wire several times. And then when we had all that tortuosity in the ileo femorals and then the descending aorta and when we had the stiff wire in none of that torque is getting transmitted including in the release. So if you guys remember this case, we spent probably 10 minutes trying to get the valve to release. This is a non sternotomy patient. This someone you said had limited limited surgical conversion. So we can't leave the valve in place. Two of the three tabs ended up being released, not all three, we can't leave the valve in place uh because we can't get it to, to uh remove itself from the delivery system. So we can't take this out of her with unless it's surgically. And so we either have to be more aggressive with the wire to, to get this out or we have to open our chest when that was not part of the plans initially. So we chose the lesser of two evils, so to speak. And we were more aggressive with the wires. This is why we kept calling for echoes. She ended up having a big effusion. You can see this is the next image. This is a wooly wire. This is why I like this. It's wrapped around in the pericardium. It's in no chamber. I can see that I have tons of wire purchase when I'm putting dilators and I don't have to worry about losing uh wire purchase or wire access. So this is why we use a wooly and this is why we take these pictures to confirm that we're in the pericardial space. So ultimately, we ended up getting very good valve deployment, but we had a huge arterial perforation. Um And this was the one that we had difficulty keeping up with. I did Subxiphoid. We had 750 out almost immediately that we ought to transfused SATS were 99%. So we know what's going on. This was not a failure in us getting to the patient quick enough, we were already ready for it. We already had a pericardiocentesis kit on the table before we even had a Pericardial Fusion. And that's how we, that's how we win these. Right. But even then they're not all winnable, we reversed anticoagulation. I was able to get the valve released. But, but with a lot of positive pressure on the Lundquist Wire, um Sarah said she felt like she was getting nauseous during the case and she, she had sort of the same guttural response just looking at that wire the entire case, but really didn't have any other options other than opening her chest to remove the valve system. And so, um, we ended up watching this and this is the nature of the arterial perforations. The Venus one should stop or they don't if it's a big big hole, but they stop 99% of the time the arterial ones linger. We're staring at a fusion. We're draining the drain can stop working because it clots. It's sort of a more dynamic process. And this was case in point of that. Once we got to 715 reversed anticoagulation. We had no fusion. It's trivial. We watched that for 30 minutes. We were going to leave the room. I know you all remember this from last month. And then as I'm talking with the family saying, look, this is a big complication, but we got through it. The team did a great job. We, I think, I think we got her out of the woods. I get called back to the or that it's starting to get larger again. So we actually electively doctor bro. And I said, look, let's just take care of this. Now, let's just do a window. Now, get it taken care of so that it doesn't come back at seven o'clock at night in the middle of chaos. And the whole team is here all night dealing with a more serious problem. So Doctor Barrero actually did a, a window and found a small little area of bleeding that he repaired. The patient went back to the IC U completely stable. She was a window, not a full Stronomy candidate. And then about four or five hours later, she just opened up that injury continued to progress. She had quite an extensive tear in the inferior lateral wall of her left ventricle that wasn't apparent necessarily when you're doing the window and was able to be controlled through conservative measures. But then opened up later that night, Doctor Cortina did an incredible repair and I know a lot of you were were in that case late into the night. Um She quite literally has zero chance, zero chance in the hands of other teams. Um Most teams don't even try with an extensive injury that much, especially in an 85 year old and got her fixed. She died a week later, not because of her heart. It's a downstream consequence of her vocal cord dysfunction or catatonia. We couldn't get her to wake up and her family didn't want a tr but we, we, we didn't win that one. Right. Because a patient didn't survive. She's very high risk and these complications will happen. But it wasn't because the team didn't work incredibly effectively. We gave her every single chance in spite of a scenario that that often is, is one we can't overcome. And so I think that's, that's the, the big picture here in my mind is there's complications that are mild, that shouldn't be a big issue that can end up being a big issue if the team doesn't work effectively. And that's what we don't want, but we also want to win, so to speak, a lot of these rare things because we have the talent in the team, uh and the, the support we have cardiac anesthesiologist. In every case, we have a team of 16. In every single case, we have all of this machinery put in place and this team put in place to where we can get people out of these life threatening, usually devastating, almost universally fatal complications. A lot of people in a lot of centers don't classify people as conversions and bailouts and these kind of things like we do because they know that when one of those one in 501 in 100 risks happen, there's not much they can do anyway. And so it's not even attempted here, we do everything we possibly can for an 85 year old who was mowing the lawn six weeks before and was doing pretty well besides her aortic stenosis. It's important to understand that she wouldn't be around in six months if we didn't do this. And in our hands, she got the best possible treatment and in spite of a complication that will happen if you do enough of these, we got her through that complication and gave her a chance. What happens after they leave? The ors is often out of our control. It's really out of y'all's control because it's usually when you stop taking care of the patient unless they have to come back. Um But we did everything in our power and the team worked incredibly efficiently with early recognition. We identified the problem right away and we set her up for success even though ultimately, she didn't uh have the outcome that we wanted. And that's I think what we should strive for in every case, we shouldn't, we should be trying to prevent these things first and foremost, but we should be rapid in the recognition of them and the treatment of them so that we win these very, very rare complications that have such a bad outcome universally. And that's basically it, they can occur up to 4% where at 1% we do a variety of things intermittently like switching to balloon tip pacers. If we see an uptick in these, uh since that case, we aren't using Lundquist with uh Navato anymore. We're using their circular wire. There's some thought that the uh the spline on, on it to make it more agile on the flex nav uh make it transmit torque, torque less, especially if you use a stiffer wire, maybe that's uh uh stalled a little bit. And that's why we're having issues with valve release. It's not the first time we had an issue with valve release using a Lundquist so that there's things that we, we continually do for uh quality improvement. This is part of it, having these conferences. Um but early recognition, getting the equipment, we need everyone being engaged, everyone looking out for these things. Every single member of the team is important. Every single member of the team can recognize these things. There's only a few things that happen, hypotension, tachycardia, we can all, we all have those monitors in front of us, what I want to encourage and which is often not encouraged in operating rooms or in cath labs is that every single member is an active participant in the procedure, you all key members of the procedure. And as a result of that, one of your key roles is to speak up when you see something. That's what makes these teams uh working in these kind of scenarios, life, life or death scenarios uh at the cutting edge of medicine where we're using brand new device, therapies to take care of problems that we didn't have answers for, at 10 years ago, 10 years ago, remember I said I sent half these patients to hospice because they didn't have any options. And now we're getting these 85 year olds into their nineties. We see them in clinic every single day doing incredibly well. And that's what we're trying to accomplish for people. But to do that, we have to be prepared for these rare complications. And I just want to encourage everyone again. You see something speak up. It doesn't matter who's in the room if that's not encouraged by anyone, surgeons, interventional cardiologists, we need to point it out and call it out. So it should be the culture of the operating room of the hybrid or to where every single member of that team is actively engaged and it should never be something where you feel like you can't speak up. Makes sense. Published December 17, 2024 Created by Related Presenters Matthew Summers, M.D. Sentara Cardiology Specialists View full profile
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