All right, let's do it. I think we're past the point of needing introductions. We all know each other by now. I see we've got a mighty group of learners here and we're gonna switch over from lectures to more questions and case-based formats for the next two sessions. We'll try to get through things in good time. And I've been assigned to go first. I'm the warm-up act, so I'll give you some nice, easy bread and butter things, things that you're used to doing in everyday life in terms of visually estimating things. So it's just to get you kind of warmed up to things. I've got the audience response questions that we didn't quite get to in the first day because we had a very packed agenda that day, if you'll remember. And so we'll go through those quickly and then I'll get into some quick cases and then head off the batons. Okay, so I got the chat going here, but I'll leave it to you to moderate. So we have a bit of a slight technical issue with Zoom. So for these first response questions that we're getting caught up on, we're gonna just use the Zoom chat window. So I'm gonna ask you guys just to put your answers up in the Zoom chat. This will get your fingers warmed up and it'll be lots of fun, I promise. So we're gonna start with a basic session here or basic questions, which is eyeball assessment of left ventricular function. So the options here are normal function, moderate dysfunction, or severe dysfunction. So what do you guys think for box A? Let's see some life in the chat. I feel like I'm a YouTuber. There you go, okay. I'm gonna just wait for two or three answers and then we'll go. So I see votes for moderate. Yeah, that looks right to me. Let's go for, yeah, you can just put the first letter if you wanna be really efficient. What do you think about B? Yeah, yeah, we got some votes for normal here. Sometimes normal is a little bit underwhelming. We talked about that last time, but that looks pretty nice and normal. The walls are moving in on all sides. If you put your finger in there, it would pinch you on all sides. The walls are moving in about, say, 50% of the linear dimension, but that would convert easily to an injection fraction of 65, 70%. What about C here? C is broken. Okay, well, we can guess that C was probably severe given by how dilated that was. Technical difficulties abound. Okay, here's an April 4th Chamber view. What do you guys vote for one here? All right, we got some votes for normal. You know, what about, so let's look at all three of them and then we'll compare. What do you guys think for B here? So, we're looking at B here. Yeah, yeah, okay, we got some discordance. I think the majority has severe. You know, I think this really reminds us that we shouldn't make any determinations based on a single view, either on the exam or in real life. You know, the adage really is that one view is a hypothesis to be confirmed on a second view. Remember that you're only looking at two of the six walls in view B or any of these views, for example, and so you're missing a considerable amount of the information. So, what I recommend is that you make a hypothesis based on a view, and then you go and confirm that hypothesis with a second view. Oftentimes, you'll also find yourself debating between two, and that's pretty normal. So, it sounds like for B, we're debating between moderate dysfunction and severe. Personally, I would go with the majority here and lean towards severe. What do you guys think about C? Yeah, we got two votes for three votes for normal and a moderate. Yeah, I think it looks relatively normal. I've got a little sneaking suspicion that the apex might not be normal, and we'd have to go confirm that on another view, and that might kind of downgrade your function a bit. And then it brings us back to which one is A. I think it's okay to be in a debate between moderate and normal. You know, you might get a mild, whether you consider that a category or not, and what's really important clinically, of course, is discovering severe left ventricular dysfunction. So, sometimes you have a hard time pinning it down between some mild or moderate dysfunction or normal LD function, but if you can say this is a not severe left ventricular dysfunction, then that's certainly useful clinically. All right, here we've got some parasternal long axis views. So, what do we think about A? Yeah, I would tend to agree there. This looks pretty severe. Again, you don't see the apex well in an apical four chambers, so you're really only seeing the mid portion of the base of two of the six walls. So if you go back to your 17-segment model, we're only seeing four out of the 17 segments. So just, you know, tread very carefully in that situation, but certainly severe. And we get some accessory information here, you guys. The eMERGE docs are fond of doing this EPSS, or end-point septal separation. The anterior leaflet of the mitral valve here should open up widely and bang into the septum here. It's coming nowhere close. If the distance is greater than one centimeter, that's abnormal. So the options when you see that are twofold. Number one, there could be something wrong with the mitral valve. That's less likely here because the valve looks quite thin, which is usually a sign of health. The other option just is that there's not much blood leaving in the preceding beats, which means there's not much space in the LV cavity for new blood to enter in the following beat, and that's why the valve is not opening very much. So this poor opening of the mitral valve and a high end-point septal separation is certainly a good sign that there is significant left ventricular dysfunction. What about beat? Yeah, we got some good votes for moderate, I think. So you see you get this hinge point here, and then often that's a sign, you can almost imagine it here, to when we get a better look at the apex in another view, we're gonna probably discover that the apex is not great. And so we've got a typical situation here where the base is preserved, certainly the better vascularized territory, and then the apex is potentially toast. And so this would lead you to be moderate. This might actually even be worse than moderate once we discover the other segments, but certainly as a hypothesis, I think moderate is okay. And then what do you guys think about C? Yeah, I think we can all pretty much agree that looks normal, this is a good view. We see a lot of the heart, we don't see the apex, which you're not supposed to. We see the myocardium here moving, we see it thickening. This is really the image quality that we'd like. Notice the contrast here with the end-point septal separation where that anterior leaflet just jumps up and slaps that septum point aggressively. Okay, question here is I want to talk about the various segments of this left ventricle. So I want, now instead of assessing global function, we can assess the movement of each individual segment. Segments get rated in terms of there being hyperkinetic, normal kinetic, hypokinetic, akinetic, meaning not moving at all, or more properly, not thickening at all, or diskinetic, meaning dead meat and moving in the wrong direction. So let's start by looking at the base of the heart here. So look at the wall here and the wall here. Would you describe those segments as being hyperkinetic, normal kinetic, hypokinetic, akinetic, or diskinetic? It's quite a mouthful. Yeah, we got some votes for normal here. I think that's pretty reasonable, right? We want to see, do we have the image quality here to see the endocardium, to see the myocardium thickening? Yes, looks like it's thickening reasonably well. You got to ignore the papillary muscle that comes in here. Okay, let's move up a little bit and let's look at the mid portion here of this. It gets a little tricky here, but what do you guys think of that mid portion? Is it hyperkinetic, normal kinetic, hypokinetic, akinetic, or diskinetic? Yeah, I'm torn like you guys are. It depends really specifically where you look. If you look here, it looks pretty normal. If you look up here, it's starting to not thicken as well. So it's really a question sort of subjectively of where you draw the line. That's a tough one. What about the apex? What do you guys think about the apex? Yeah, yeah, I see hypo for sure. It's at least hypokinetic. You start to wonder when you get out to the very top here, is that it's moving a bit, but some of that movement is just the toing and froing of the beating heart. Is this segment of myocardium actually thickening? Doesn't really look like it. I'm worried that this apex might actually be akinetic. So you know, these are really free points on the exam. So hopefully you guys are doing very well. Hopefully you're in a good position to answer these. You'll get some of these questions, just eyeball LV function. What's this segment doing? And you guys can bang these out real quick, gain back some time and get some free points. Question here, which wall is moving abnormally? Look particularly at the base. So which wall? You gotta know your walls, guys. All right, I see basal inferior septum. So I guess the question is, what view is this? Let's start there. It's an apical tube chamber, correct. This is funny, I'm like speaking into the void. Good, so the wall on the right of the screen, what wall is that? Yeah, interior, and on the left? Correct, inferior. So good, know these walls, three points. So the basal section of the inferior wall is not moving normally here. It's hypokinetic, if not achinetic. Muhammad, I liked everything you said there, I just wasn't sure about the septal part. There's no septal viewed here, but everything else you said was perfect. Okay, so it's not inferior lateral, right? Inferior lateral is a different wall. That's what we used to call the posterior wall. We're gonna see that in a second. It's the anterior wall on the right and the inferior wall on the left, okay? So again, know these walls, get your three points. All right, question here. What two walls do we see in this view? So look at the left ventricle in the bottom right-hand corner of the screen. So what two walls are we assessing here? This is all in that American Society of Echocardiography document. There's some beautiful pictures. So just take a minute and commit this to memory. It's useful in real life, it's useful on the exam. So it's a two for one. So what two walls do we see? Let's start with the one at 12 o'clock up top. What LV wall is that? I've frozen the chat, I've stunned them. Yeah, great, inferior septum, that's correct, John, good. So the subcostal four chamber shows you the same walls as the apical four chamber, which is kind of the twist here, right? So just a thing you gotta commit to brute memory is that in those four chamber views, it's obviously part of the septum because we see the right ventricle on the other side, and you just gotta commit to brute force memory that in the four chamber view, it's the inferior portion of the septum that we see. Again, three points. What about the wall that we see at six o'clock there on the bottom of the screen? What wall is that? So if we're seeing the inferior septum, what's opposite the inferior septum? Antralateral, right. The word anterior always abuts or is opposite inferior and lateral is always opposite septal, that's the memory trick. Very good. Okay, what wall is moving abnormally here? Good. It's a trick question. They're all moving pretty normally. What I wanted to cue you on here is just to be able to do your different walls in a subcostal four-chamber view or a parasternal, oof, sorry, a parasternal short axis view or less commonly a subcostal short axis view. So this is obviously the septum because we see the RV here, anterior septum, anterior, anterolateral, infralateral, inferior, infraceptal, around and around the clock you go. Make sure you can do that in your sleep. Okay, I'm going to skip this one. I don't like this one. And then the last question is, please rate the right ventricular size. Is the right ventricle normal sized, moderately dilated, or severely dilated? Okay, wait for a couple more votes. Good. Yeah, severely dilated. So rough eyeball rule of thumb. Is the RV bigger than the LV? Yes, that's consistent with severe. Who owns the apex? RV appears to own more of the apex here, although it's close. We would call this tentatively severely dilated RV. Okay, so that's my ARS questions from the first talk. So let me just end, get out of presenter mode. There we go. We're going to close this one down. We're going to open up the second one and go to presenter mode. This one will be slightly more painful, but thrilling nonetheless. Let's do my diastology questions from my second lecture the other week. No doubt you guys are thrilled to see these waveforms. I would like you to take a best educated guess as to whether this pattern is consistent with normal diastolic function, grade 1 dysfunction, grade 2 dysfunction, aka pseudonormalization, or grade 3 slash 4, meaning significantly elevated filling pressures. So okay, we got a vote for 3-4. Grade 1. Excellent. I like the disagreements. We need a tiebreaker here, Chad. I don't think that actually there is a person named Chad participating yet. I'm cosplaying as a YouTuber. Dear students, do we have a tiebreaker? No one willing to venture a guess? I know it's intimidating. Well, let's just break it down here. I won't break it. That's okay. We got a tiebreaker. So I think, you know, in diastology, I'm not going to pretend that this is an exact science, right? Remember the tips that I gave you. One of them was to look at the E-A ratio. So an upside down E-A ratio, meaning with an A wave greater than an E wave, is consistent with what grade of diastolic function? Our friend the iPhone had it. It's mild diastolic dysfunction. Right. Grade 1. So if you just looked at this picture, you would call this probably grade 1. I would also say that it's very unlikely to be grade 3 or 4, meaning very high filling pressures. Because remember, the rule of thumb is that if your A wave is contributing meaningfully, it means that the left ventricle is still not that stiff for our wimpy little thin walled atrium to be able to contribute meaningfully to filling. And so when you see a big A wave like this, it's really inconsistent with severe diastolic dysfunction. So that's another eyeball trick. And then we can move to our E and our A wave. It gets a little trickier here because there's always technical errors here. This is a an annular. So it's the medial annulus of the mitral valve here, meaning that we don't expect as much out of the E prime wave. But we've still got a decent E prime considering it's medial. We're getting close to 9 or 10 there. So again, you'd expect that to be lower if it was severe diastolic dysfunction. So all in all, I think the votes are in for kind of grade one or mild diastolic dysfunction here. We'll look at the pulmonary vein flow. This is not useful in real life, certainly if you're dealing with inpatients, because you can never achieve this in at the point of care. This is for the echo lab. So we're not going to spend too much time on this. What about this one? Is this normal diastolic function? Is this mild or grade one, moderate or grade two? Or is it severe grade three, four diastolic dysfunction? Okay, we got one vote in. This is tricky stuff, you know? It's tricky stuff. It's not easy. So don't be too discouraged. Anybody else willing to go in on a limb here? The astrology is definitely my least favorite. I'll say it. And until you heard me. Until I heard you, yes, of course, yes, yes. Revitalized your perspective on it. Yes, yes. Abnormal, yeah, iPhone. I wish I knew your real name. The iPhone here. A teak, I can do it. You're not Apple AI. Yeah, so let's look at this, right? So let's look at the basics, the E to the A. So we've got a pretty decent size A wave. So right away, I'm leaning against there being severe diastolic dysfunction, okay? We've got a pretty normal E to A ratio, meaning that the E is like 1 1⁄2 times the A-ish, and that's pretty normal. So that means it's either normal or it's pseudonormal, right? So we're probably dealing with a normal or a grade two. And how can we break the tie? We can look at the E prime. This is a medial E prime. Again, it's subtle, right? It's not that different from the last one, but we're getting down towards like five, six here, and that's pretty low. So I'd probably lean, this is also an abnormal pulmonary vein inflow. I'll explain that very briefly in a second. So I think overall, you're probably gonna lean towards this probably being pseudonormal. So I agree with the teak, and you would do a Valsalva maneuver if the patient is able to do so to kind of unmask this. All right, how about this one? We'll go a little bit quicker. Normal, grade one, grade two, grade three. What do you think? Okay, I'm going to vote for normal. Anyone else? Yeah, I think so. I think you guys are getting it. Good job. So, you know, again, I like how they throw up some 2D imaging here, right? You know, don't forget to do this. How bad is your left ventricular hypertrophy? How big is your left atrium? These are important clues. So looking at the E to the A, we've got a pretty normal ratio, like one and a half, getting a little up there. We've got a decent size A wave. So is this normal? Is this pseudo-normal? Well, we've got a nice, big, deep E prime wave. We're getting out towards like 14, 15 there. Probably a pretty normal pattern. Okay, and then lastly, through process of elimination, we won't belabor the point. We've got a big left atrium. We've got a huge, thick left ventricle. Here, the A wave is a little bit of a trick. We've got a kind of a two-to-one E to A pattern, and we've got a really tiny E prime. All told, this is probably consistent with more severe diastolic dysfunction. Okay, we'll skip over these questions. I want to show you this. Let's actually do this. Which of these, A, B, C, or D, is consistent with normal diastolic function? Okay, anyone else? Yeah, D looks pretty normal, doesn't it? We've got a good E to A pattern, we've got a significant A wave, we've got a pretty good looking E prime here, getting up to about 10. And then if you're wondering the pattern of pulmonary venous inflow that you wanna see, it fills in all cycles, right? It fills in systole, it fills in diastole. We're talking about now the left atrium filling from the pulmonary veins. And it fills nice and equally through pretty much all phases of the cycle. So that's pretty normal. Which one is consistent with grade one diastolic dysfunction? Grade one is what we're all developing as we speak. As you get older, you get some stiff heart in grade one. Yeah, C pattern, right. We've got this big A wave. Remember your A is your buddy is trying to help you out as the heart gets stiffer. We've got an E prime that's okay, but getting a little smaller. And then you'll start to see that you get some loss of the diastolic component of filling early on, and you get more early filling in systole in terms of your atrial filling. Which one is moderate dysfunction? So grade two or pseudonormal? Yeah, A, very good. So you can see how A up here looks not unlike D in terms of your E to A. So one of these is normal, one of them is pseudonormal. The best way to break the tie if you can is an E prime. This one's pretty small compared to this one. And then as you get pathological, you get the flip here where you get more of your left atrial filling in diastole. And then you actually get some late diastolic inversion here, and then of course by elimination, B is your severe. You can see your E wave is two or three times as big as your A now. Your E prime is really bad, and then you get really the lion's share of your filling in early diastole in terms of your left atrial filling. So again, just look at these patterns and quick pattern recognition hopefully can get you some quick points. Okay, let's do a little bit of math here. Let's assume that we're gonna cut this off. Remember, shave the beard here, right? So let's call this, this is a tricuspid regurgitant velocity and it's three meters per second. I'm also gonna tell you that the central venous pressure of this patient is 15 millimeters of mercury. So tell me what is the systolic pulmonary artery pressure? Man, that's fast. You guys are so good at math. Right, 51 is the answer. So how did we derive that? Three squared is nine times four is 36 plus 15 is 51. So again, a nice free question. If you really wanna show off to your friends, if you've got a pulmonic regurgitant jet that you can capture usually in an apical, pardon me, in a parasternal short axis view, way up at the base of the heart, the end of this tracing is two meters per second, right? So remember this occurs in diastole. So your end diastolic velocity is two meters per second. Same patient, they've got a CVP of 15. What is the diastolic pulmonary artery pressure? Yeah, very good, 31. So same formula. We don't do this one as much, but it's just a fun party trick if you're so inclined. The end diastolic pressure, there's two. Two times two is four, four times four is 16. You add on your 15 for your right atrial pressure and you end up with 31. So some nice free math questions there. Okay, Joanna, I'm gonna switch over to my complex cases now. All right, go ahead and put that PowerPoint up and we'll get the polls going. Yeah, so these are a couple. I think at least one of these is stolen from Gisela. So Gisela, as always, thank you for this. You gave this to me years ago and I like the case, at least one of them, I think. So good job by you and full credit to you. Gisela's always got the best cases. So this one is one of my old ones. This is from my early days as an ultrasound nerd and we were teaching at a course, I won't say where, and we have a perfectly healthy 20-year-old, you know the models of the courses, right? So I'm gonna show you a couple pictures here. And there is an abnormality here. Subtle though. Is that all you get? Hold on, oh, I'm stumped. Is that enough? Yeah, you know what, that's enough. You can do it, guys. I can't see if anyone's voted yet or maybe because I can't see anything. No one's voted. We've got about four responses currently. Okay. I think we can chop it there. Let's see the results. Yeah. Very good, guys. The LV function looks good as best we can tell in a single view. RV size, there's this rule of thirds, one-third, one-third, one-third, left atrium, and hey, wait a second, it's not the RV that's violating that rule. It looks like it's the ascending aorta. We haven't talked about this much. There is a specific and dedicated PDF document from the American Society of Echocardiography talking about aortic imaging. It's worth a quick look. Only about an order of it is echo, but it's worth a quick perusal. I'm stuck here. I cannot advance my slides here. What have I done? What have I done? There's four locations where you can measure the aorta. Again, I don't think you need to spend a ton of time on this, but it's worth a passing knowledge. A is at the level of the aortic valve. B is the sinuses of valsalva, which is the largest diameter. C is wrong. C is the fourth one. C would be the proximal ascending aorta, usually a centimeter or two distal to the sino-tubular junction, which is right between B and C. It's where the sinuses taper off to the regular aorta. The cutoffs here are really kind of tricky. They vary by age quite a bit, and they vary by gender as well. So the widest part is always gonna be your sinuses of valsalva. I remember as a rough guide 3.5 centimeters for men and three centimeters for women. It's a very rough guide though because it's heavily dependent on your age. We all dilate our aortas as we get older. So this young man is 4.1 centimeters. So he was 20 years old. That's quite dilated and quite pathological. We put the probe on him to see. This is precisely the view you don't wanna use to look for aortic insufficiency because of course we're perpendicular to the angle of incination that we need, and so we will not see much. He did have a little bit of aortic insufficiency, and what's the end of the case? It was an incidental discovery at an echo course, and it's not the first time that we've found some pathology on one of our models, and this was a big, huge, tall guy with really flexible fingers, and turns out he had Marfan syndrome and an aortic aneurysm, and he came back the following year with a sternotomy scar and showed off his repaired aortic arch, which was kind of cool. So maybe being the model might have saved his life, which is kind of neat. Okay, here's a second one. I think this is Gisela's case. We see this all the time. This is a 75-year-old female who's found down in shock, kind of undetermined as of right now, history of recurrent urinary tract infections, and she gets a bit of fluid. She gets put on a bit of Levophed, and then people are unhappy, so they put her on some dibutamine, and she actually gets clinically worse on dibutamine. So that's a bit of a clue. I want you guys to look here, and I want you to tell me what is the abnormality here. Again, it's relatively subtle. How are we doing for votes? Five, oh, six so far. Amazing. Hit it. Let's see the damage. OK, OK, so the majority rules here. We've got an LVOT obstruction. Is there an abnormality of wall motion? It's a good question. I don't think that's overtly wrong. I would certainly question it. I think, generally speaking here, we only have the image quality necessary to make that judgment on this, remember, infraceptile wall. We can see pretty well here at the base. It's definitely moving. It looks like it's thickening. You want to go out on a limb and tell me that it's a bit hypokinetic. I'm not going to fight you on that. Looks like it's moving and thickening here. And then the rest is kind of fuzzy, so it's hard to say. But look at this anterior leaflet here. I'm really having trouble with the PowerPoint here. I'm sorry. Gisela has really slowed it down here for us. So pay attention to the mitral valve apparatus here. And there's two kinds of SAM that you can see. We'll go frame by frame here. This is great work by Gisela. So you can see here the coaptation. And we've got the anterior and the posterior leaflets here. And then there's a redundancy in the coaptation. And the high five that they're giving is redundant. And there's a lot of extra tissue there. And then that tissue gets drawn. Remember, now there's blood being forced down here through the LVOT. And it's going to entrain that and tip it over there, potentially obstructing the LVOT. That's one kind of SAM, or systolic anterior motion, that you see. This would be more properly called a LVOT obstruction, as we've called it. Sometimes what you see is that instead of redundant coaptation blocking the LVOT, more commonly what happens is just this anterior leaflet gets peeled off and bumped up into the septum. And that's even worse because that obstructs the LVOT and gives you pretty rip-roaring mitral insufficiency. That's the more common one. This one we're seeing here is the less common one. But you'll see this pattern a lot if you take care of patients with sepsis, hypovolemia, hyperdynamic patients, if they have pre-existing left ventricular hypertrophy, they will tend to manifest this physiology. And it's important to find it because it dramatically changes the way you care for these patients. And then Gisela's showing us that the right thing has been done. You get rid of the dibutamine. You even get rid of the levophed and put them on phenylephrine, something that doesn't have beta. And then you give them fluid. And then if you're really brave, you beta-block them. But that's pretty sketchy because they're usually, you know, shocky. And they get better. Yeah, this one was like strictly, like they did it strictly by the reverse protocol, like when the reverse protocol. And so there was like dibutamine, add dibutamine when you think you've adequately fluid resuscitated. So that's why they added the dibutamine. Well, in those days, you know, people would put dibutamine on blindly, right? And there wasn't widespread POCUS. Now, I think, you know, my view of this is that if you're going to dibutamine, you need to do it under image guidance, which means you got to be able to do a basic point-of-care echo, which, you know, all of us can do in this call. So great. All right, I think we'll maybe do one more case and then we'll hand it over to the team here. This is, again, another example of abnormal pathology. This is a 60-year-old gentleman who doesn't see the doctor very much. And he presents with severe dyspnea. And he is just in that worst kind of shock. And it's very, very unclear initially when he comes in and what kind of shock he is in. So I'll show you a couple pictures here before we start the quiz. I'll let you know, Joanna, when to start it. So there is, you know, obviously very difficult views here. The only thing we could get initially was a half-decent subcostal pore chamber, which you see here. This gentleman was so sick, he just got immediately whisked up to the ICU before any kind of diagnosis was kind of made. He was just in horrendous shock and multi-organ failure, although curiously still sort of awake. Here's a second view. So the pathology we want to talk about is starting to manifest itself here. And I'll show you one more picture, twin picture. And we can start the poll here, Joanna, please. All right, what is the abnormality seen here? You won't see too many of these, any more anyway. I would do it on both. We're all in. Fire it. Send it, as they say. Yeah, you guys are great. So this is a VSD. Again, I wouldn't, a casual perusal of the different types of holes in the heart is worthwhile to do. I don't think they perseverate too much on this exam. Certainly if any of you are gonna punish yourselves with the comprehensive exam, there is a fair bit of ink spilt over those kind of questions. But in the critical care exam, I don't think that would be as relevant. We see, close up the poll here. We can see here in 2D, it looks like an abnormal connection between the right ventricle and the left ventricle. And when we put some color on here, we see the connection highlighted with blood flow from left to right, as you would expect. And yeah, we got some further history from his wife. He was feeling unwell about 10 days ago with lots of chest pain. He refused to go to the hospital. He stayed home. He basically was a missed MI. And one of these complications of acute MI that you hardly ever see anymore because the care has improved so much. But post-infarction ventricular septal defect was diagnosed within a few minutes. So I think I'll end it there at 540 after 40 minutes of punishment. Any questions from our students here or our co-presenters? Great cases, thank you. Well, thank you very much. All right, guys. Well, I will be back on Thursday to help moderate. And I wish you guys the best of luck if I don't speak to you again. And it's been a real pleasure. I'm gonna share my screen unless there's any questions that anyone has before we move on. Okay, I'm gonna just start with showing you a couple of things. I wanna go over an exam prep guide real quick, and then I can go on to my cases after that. Just wanna go over this really quick. Suggestions for exam. Exam length overall, 200 questions. And I'm gonna go over a couple of things before we move on. So I'm gonna go over a couple of things. Exam length overall, 200 questions. There's five books. It's about four and a half hours in length. And you have about approximately 1.35 minutes per question. So remember that when you're doing your calculation questions, just to, it's not a super time crunch exam. You have enough time to finish it for sure. But remember that it is four and a half hours in length. And totally doable. You have enough time per question. I should ask if we need a break, Joanna, before we go further. Do we need a five minute break, bathroom? I put the chat on. Let me know. I'm totally okay with that if we need to. Okay. Oh, yes, no. Five minutes. Okay. We'll do five. Okay. We'll take five minutes, let you use the bathroom, and then we will come back. So 547, we'll start again. I'll just pause right here. Okay. So that's the exam length. The NBE website has the outline of the exact course content. This course was based upon that outline. But I would definitely get familiar with that outline, make sure you know all the different pieces of it, and that you are ready to go. So look at the NBE website for that exam outline. Basic echo text. If you haven't already started reading that, definitely is important. I like the auto test the best. Feigenbaum is extremely dense. It has everything, but really goes into too much detail on it, and you'll get lost in it. But the auto one is just the right amount and is easy to read and is a very good book. So that's the one I would recommend. But any of these three will have the information that you need on it. A critical care ultrasound book for the non-cardiac stuff, I think, is important. The one from Levitoff is great. Neelam Soni's one is a case-based one. And the other one is also a very good one. So one of these books to look at things that are not cardiac is a very helpful thing as well. And then there's a really good question book. So there's this question book that I'm showing you now, Kline. It's extremely hard. It's meant for the cardiology echo boards. It will frustrate you, but it'll really, really test you on your knowledge and really push you. There's another one called 1200 Questions for Critical Care Echo. That one's totally on the level of, that one's totally on the level of the exam that you're gonna take. It's a very good book. It has a lot of questions on it. And I would definitely suggest that you look at this book for question practice as well. So those are the two question books. The other book will frustrate you, but it will push you. So I like it for that reason. Basic physics. Dr. Edelman has this, there's a PDF floating around online. I'm not allowed to give it to you because it's copyrighted, but if you look online, you'll find it. It's, you just need the chapter that goes on over basic stuff from this. And that PDF is floating around. So look for it. Know the physics. Be able to answer those questions really quickly. They're giveaway questions and will help you get basic quick points on this very easily. Websites. Jonathan Greenstein, a former fellow of ours has this website, advancedcriticalcareecho.org. It's great. It goes over a lot of things that you need to know for this exam. And then there's another one, a Facebook group called Critical Care Echocardiography Group. Both are very good, both of which goes through a lot of things, but Yoni's is great. It also has a full ECHO exam on it, a sample of it. So when you start to work on your logbook, you'll be able to look at that for reference as well. So look at that website as well. As much as you can, hang out in the ECHOLab, watch cases, be able to do the calculations of cardiac output and valve area very quickly. Those are questions that will definitely come up and will definitely be tested. So be able to do that. And the give me's for you guys are lung, abdominal, and DVT. There's a lot of questions on that and it's very easy in comparison. So know all that stuff, cold, the anatomy of the DVT, basic abdominal stuff and lung, which you should definitely know as well. Once you've passed the exam, you're called a testamore. And in order to get certified, you have to do 150 full exams and there's different ways that you can do that. So if you need help with that, please reach out to me. I'll put my email again in the chat and I could definitely be your supervisor. I can help credential you on that. I can also send you to somebody else if you prefer, whatever you want, we can help you get through that training pathway as well. So remember that there's also a TE pathway now you have to do 25 TEs, which you can do as well. And you just need someone to look at those. So we could do it via Dropbox or other ways. If you need help or someone to supervise you, let me know. A full echo exam is defined in the certification handbook and it has to have some Doppler in it. You have to have a reason for doing the exam. And I have a sample log that I can send you if you want. Once you're through the exam, you can reach out to me if that would be helpful to you. Okay, this is what the full echo looks like that you need to do 150 of. This is a sample log, it's in here actually. Very simple, keep track of all the echoes that you do so that you can do this later. I have a study guide that I'm gonna show you now. I'll have it forwarded and put it in the chat for you so that you have that. It's just basic stuff that you can reference it real quickly and it will help you just do last minute studying for the exam, it's not enough to study on its own. Here's my email address, Scott's address, all of the faculty's addresses on here. So take a look and email any one of us. We're always open to discussing things if you have questions, concerns, wanna run something by us, wanna talk about an interesting case, email one of us. Okay, let me show you the study guide. So this is the aortic valve review going over mild, moderate, severe for aortic stenosis, for aortic regurgitation, dimensionless index, rheumatic heart disease, mitral valve, again, severe, very severe, mitral regurge as well, what that looks like, tricuspid valve, pressure halftime, vena contracta, regurgitant orifice, pulmonic valve, same thing. And then going over just systolic function, what wall motion, what thickening looks like, what the walls are, what you see in the two chamber, the four chamber, the long axis, the short axis, the apex, which vessels distribute to which wall, so you have that as well, you need to know that for sure. The diastology for normal EF and the diastology for not normal EF as well, PW for hepatic vein, so you recognize constriction versus restriction. That's a very nice testable question, how you distinguish between the two and how inspiration, expiration helps you, right ventricular and left ventricular inflow with tamponade physiology, MI complications, congenital heart disease, which is definitely something that is tested on, so no basic stuff on that as well. I know you have that lecture, which septal defects are which, VSDs, where they're located, and then PDAs, Epstein's, and then prosthetic valves a little bit, just what you need to know, not too much. And then some M mode, really basics, mitral valve, SAM, what it looks like, mitral valve prolapse, mitral stenosis, aortic regurgitation, Holcomb, early systolic closures, and then diastology, really basic ones, what some abnormalities look like, Lambel's expressions, lipomatous hypertrophy, and what a crista terminalis and eustachian valve, where they're located. I'll share this with you guys as well, so you have it, just a basic overview, and then we can go through some of my complex cases. Any questions before I go on? Okay. Just come off mute, please, and just ask your questions if there are any. Nothing in the chat. Okay. Okay. This is what a normal M mode of the mitral valve looks like, just so that you can see it, what it looks like. You should know about the E wave, the A wave, what that looks like, what the closure of the mitral valve is, what early opening looks like, where it's located, and just decreased EF, what the EF looks like when it's decreased and how it changes the slope. And then at the end of systole, when there's scalloping and depression of the leaflet tip, that's what you see in prolapse. So the normal M mode of the mitral valve is definitely something that you should know. So looking at this mitral valve, I just can't even see. What does this M mode show? Take a minute to look at that. Is it mitral regurg, mitral stenosis, septal thickening, or a septal B bump? I can't see the chat. So Joanne, I'll just depend on you to tell me what's happening. Nothing in the chat. Okay, thank you. Okay. So this is mitral stenosis. There's thickening of the mitral valve leaflets. I'm sorry, let me move this out of my way. And there's a flattening of the E to F slope. You can see how different it looks than the last one. It's very flat here and the posterior leaflet moves a little bit anteriorly and diastole. You can see it, there's a slide up. So this is mitral stenosis, it's classic. Definitely know what that looks like. What does this M mode show? Is it mitral valve endocarditis, mitral valve prolapse, mitral annular calcification, or a flail leaflet? Go on, this is prolapse, there's some systolic bowing of the mitral valve. You can see there's a little bit of slurred bowing right here. And that's mitral valve prolapse with systolic bowing of the anterior leaflet. It's very well seen in M-mode and it's a very good question to ask in M-mode. What does this M-mode show? Mitral stenosis, aortic stenosis, LA mass, or MAC. I'm going to keep moving because I know that we still have another one to go after this. This is an LA mass, there's a hyper-dense area just under here, this thickened area, this is that mass that you're starting to see right here in the LA that you're catching here in this area here. So it's a bright hyper-density and it's seen throughout the cardiac cycle and you have functional mitral stenosis, the mitral valve is sort of pushed and it's very narrow. This is a normal aortic valve M-mode. You can see very thin leaflets, barely visible, a nice box right here that's nice and open. This is the aortic valve, nice and open, thin leaflets, not calcified. This is an aortic, normal aortic valve. So you're looking to see in systole, do the leaflets oppose the aorta? Are the leaflets thick or calcified? And are they open throughout systole, which would be consistent with the hookum or a low output state? That's what you're looking for. What does this M-mode show? This is also through the aortic valve. Is it an aortic vegetation, a unicuspid valve, aortic stenosis, or an artifact? This is aortic stenosis, thickened, calcified, very bright walls. And dense echoes that you can see are persistent. And thickened LV, which also goes along with it as well, the walls of the LV itself. It's a pattern recognition thing. This is through the LV, this is the third place that you would put the M-mode. So the first one was through the mitral valve, then through the aortic valve, and now through the walls of the LV. Here you're looking for wall thickness of the LV. You're looking for chamber size change in systole and diastole. And you're looking for any intraventricular masses as well. What does this M-mode show? Does it show severely reduced LV function, mitral valve prolapse, RV collapse, or LV hypertrophy? So it shows LV hypertrophy, you can see the thick walls of it, and most of you got that. And you can see thick walls, and you can see sometimes, you can see SAM in this patient population, where that anterior leaflet pulls up and systole, and it hits that wall. And this is just an example of that anterior motion of the leaflet with septal hypertrophy. What does this M-mode show? We've switched from heart to lung. Does it show stratosphere sign, seashore sign, lung point, or plankton sign? This shows lung point here. Basically, you're looking at lung sliding that ends right there, and then there's no lung sliding over there. How do I know that? You can see this barcode straight line sign past there. And you can see that this is normal lung sliding here. So the interface between the two is a lung point, not normally used in M mode, but just to show you what this looks like, is lung point in M mode. Any questions? This is what stratosphere sign looks like when there's a complete pneumothorax. I'm just gonna skip the poll cuz I already told you about this. Straight lines all the way across like a barcode, and that's called stratosphere sign. That means there's no lung sliding, and it's a sign of pneumothorax. This is what it looks like when there is lung sliding. This is called seashore sign. Again, not something that I really use. I just look at the lung sliding, but these are very testable concepts, so I just want you to have seen them. So no lung sliding to the left and lung sliding to the right. And you can see this is called seashore sign because it's like waves crashing on the seashore here. And that's just lung movement with respiration that you're seeing here, and no lung movement with respiration on the left. All right, we're gonna do another case. This is TE, which is completely fair game for this exam. So I'm gonna go through the different views that I have and then ask a question at the end. So aortic valve, short axis view, color. Long axis view. Color. So four chamber view, mid esophageal four chamber view. Remember, it's TE. All right, what is the abnormality seen in this TE? Is it the tetralogy of Fallot? Is it unmoved coronary sinus? Is it an osteosagundum? Or is it a super crystal VSD? If you need me to go back to any images, let me know. I would say replay all of them again, please. Really? That's what I would have probably like just coming into this now. Put the question first, then put the images and then put the question again, which is what I'm doing in some of mine. Okay. It makes it easier, I feel. So the answer is in this image, it's the bicavel view. Here's my SVC to the right. Here's my RA. And here's my IVC to the left. This is the intraatrial septum that you're looking at here. And you can see in the next image that there was good flow across that intraatrial septum, telling you that there's a hole between the right and left atria with flow going from right to left here. And that was a, I'm sorry, let me go back and just go over the answers. It was an ostium segundum. Good. 100% of people got it. Very good. So basically for TE, know what views are which, what the angles are showing you. It's the short axis of the aortic valve. It's the long axis of the aortic valve, the four-chamber view, the bicavel view, and then the short axis view of the LV and the aorta and the pulmonary artery. Those are the views that you need to know and what the big abnormalities are in each of those views. Very good. Okay. This is a short axis view of the aortic valve. What does it show? Is it a bicuspid aortic valve, a Lambel's expressions, a fibroelastoma of the non-coronary cusp, or a fibroelastoma of the left coronary cusp? So knowing the cusp of the aortic valve both in TE and non-TE views is extremely important. That's a very nice thing to test on. And your answer is non-coronary. Excellent. Very good. That's exactly right. Your marker is the intraatrial septum that you're looking at there. That's the marker of the non. The left is to the right of that. You can see the LID coming off of it. And then the right is on the bottom here on TE. Everything is flipped on non-TE views and is the opposite. So remember that as well. Very good. Fibroelastoma are very small, round things that are on the cusp. It looks very different. The bicuspid would not have this nice three-leaflet that you're seeing here. And a Lambel's expression is like fibers coming off the aorta, normally seen in a short axis view. So it looks very different than this round fibroelastoma. Very good. Just to show you which one's which. Okay. Another case. This is a young woman in her 40s who came in saying that she was short of breath, that she had palpitations all the time, and that she felt a rumbling when she lied in certain positions in her chest. It was very uncomfortable. It was making her feel weird. And it had come on gradually over time. So this is a POCUS surface echo. Go through the different views. Which of the following statements are correct? It is the most common benign tumor of the heart. It's usually attached to the intraatrial septum. A, surgery is treatment of this choice, or D, all of the above. Good, excellent, it's a left atrial myxoma. Classic for being in the left atrium like that, it's usually attached to the septum. It's the most common benign tumor of the heart, and surgery is the treatment of choice. Very good. Usually present with palpitations, shortness of breath when they have some heart failure from it, or this rumble feeling when it moves around when they're lying in certain positions. Okay, next question. Can't even see it, sorry. A patient with a membranous VSD presents with infective endocarditis. So it's a membranous VSD. Where is the vegetation arising from the jet lesion most likely to be located? Is it the mitral valve, the left ventricular outflow tract, the septal lifted of the tricuspid valve, the aortic valve, or the pulmonic valve? It's a membranous VSD, and it's a jet lesion coming back from it. What would it hit is the question. So the answer is septal, leftover, tricuspid valve. Knowing where membranous lesions are located is the key anatomy here that you're looking at. Knowing the difference here, this is a muscular VSD, is the body of the intraventricular septum. An inlet VSD is right at the point where the crux is, where the valves connect to it. And then a perimembranous VSD is right here. So you could see how it would hit the septal leaflet of the tricuspid valve right there, as it hits there. You're gonna see different names for these in different books. Perimembranous is one place, and somewhere else it's called something else. It's very confusing. But if you know the basic anatomy of where they are, then you should be able to get questions that are based upon this. All right, this is a calculation question. I'll give you a few minutes. 25-year-old female has a secundum ASD. She's being evaluated for closure. She has no pulmonic stenosis. She has mild TR. And you're looking for the shunt, the pulmonary, the QPQS, the pulmonary as compared to the ratio of the systolic. I'm giving you all of this information, and I'm asking you to calculate the QPQS. So I will give you a few minutes to try and work out this calculation, and then we'll go through how to do it. I think this is good practice, and if you're not finished, don't stress. This comes with practice and time. Definitely get a question book and go through all of this again, and 1.5 to 1 is the answer that you guys came up with. Let's go through it quickly. So it's ASD with a left-to-right shunt. So remembering the total system flow reaches the RA through the systemic veins. So the sum of QS and the shunt flow is the pulmonary blood flow. So let's go through the calculation. So you're going to calculate the RVOT flow, and then you're going to calculate the LVOT flow. So the RVOT flow is pi R squared. So the radius of the RVOT was 2.6. You're going to half that, square it, multiply by pi, and then multiply by the RVOT VTI, which will give you 11.9 on the right side. The left side, you're going to do the same thing, pi R squared. You're going to have your LVOT diameter is 2. You're going to divide that in half and get the radius, which is 1 squared times pi times the LVOT VTI, which is 20. And then you're going to multiply by the heart rate if you wanted to to get the cardiac output to get your total LVOT flow of 4.7 liters per minute. So you have both flows, and the shunt fraction is 2.5 to 1. So it's 11.9 to 4.7. Does everyone understand that? You'll have these slides. You can go over it again and just know how to do those calculations. That's a basic flow equation, just understanding how the ratio is calculated. Okay. Okay. Let's go to this one. This is another congenital one. I know that it's torture. I'm sorry. The congenital stuff is very difficult. Two-week newborn being evaluated for cyanosis and a murmur. The echo is performed as shown below. A diagnosis of congenital heart disease is made. What is the best guess of right ventricular systolic pressure? Is it half of systemic pressure, three-quarters of systemic pressure, near systemic pressure, or supra-systemic pressure? Let me get this out of your way so you can see it. This is a congenital defect that you need to know for sure. Okay, we're split between systemic and supersystemic. So this is Tetralogy of Fallot. It's right ventricular hypertrophy, a VSD, and overriding aorta and pulmonic stenosis. It's large, it's non-restrictive. You get equalization of pressure between the ventricles, and I'll go back. You can see there's a very large VSD right here, and there's equalization of pressures between right and left. So it's systemic pressure that you're looking at. The left ventricle is systemic pressure, and that's the same pressure that you get in the right ventricle with Tetralogy of Fallot. That's something that you should definitely recognize, that VSD that's present, the right ventricular hypertrophy, you can see the thickened walls, and the overriding aorta. Can I add? Yeah, sure, of course, please do. Could you go back one slide to that color? The other thing that you see is, if it's such a large defect, I mean, you can see it really obviously on the 2D image, right? And so then in the color map, you see almost no aliasing. So that kind of tells you that the pressure difference between these two chambers can't be very large, because otherwise that flow would be squeezed through that VSD and become turbulent as it enters the RV. So that's another kind of like pointer, that these have to be fairly equal in that there can't be much of a gradient between these two chambers. Thank you. Can I ask a question? So for suprasystemic, does that mean the RV pressure will be higher than the aortic? Correct. And how would that- That may happen over many years for this patient, right? They'll get Isenmenger syndrome, and the RV will get conditioned, and they'll have very high pressures on the right side. But it wouldn't happen at two weeks time. And how will that flow look like here? It would be backwards, the flow. It'll go in the other direction. Okay. Good question. All right, next question. Another congenital question. 12-year-old boy was sent to the clinic for shortness of breath with exertion. The echo is represented by the following image. The most diagnostic echo feature of this condition is a displacement index of greater than eight, a sail-like anterior tricuspid leaflet, posterior tethering to the RV free wall, a dilated valve annulus, and a right ventricular dilatation. Another nice echo to be tested on. It's a relatively common question that comes up. And I will stop the poll. OK, so there's a real mix here. So this is Epstein's anomaly, right? And the diagnostic feature is the apical displacement of the leaflet. Let me go back to show you that. You can see that the valve should be around the same area. Sometimes the tricuspid valve is slightly towards the apex. Sorry about that. You can see that there's big displacement of the valve here towards the apex. This is classic for Epstein's anomaly. And this is what's most characteristic of it. Now, all of the other things can be true. There is a sail-like leaflet, anterior leaflet, that can be posterior tethering. And you can have a dilated tricuspid annulus. And you can have RV dilation over time. But the most characteristic thing here is the displacement index. OK, this image represents what type of VSD? Is it membranous, inlet, super crystal, or muscular? It's really just a memorization one, looking to see where you're located. This is the short axis one, and you're split between inlet and membranous, I see. This gets really confusing. So this is really perimembranous versus membranous versus outlet versus inlet. I would say in the short axis view is the most important place at the aortic valve level and at the short axis midventricular level where you're looking here are the two most important places to look, and that's where you're going to differentiate between them, between perimembranous and inlet. And that was perimembranous that you're looking at, the membranous that you're looking at here. All right, I think this is the last case, 44-year-old female, dyspnea on exertion, occasional chest pain. EKG shows LVH, and she gets an echo. The LV ejection fraction is 65%. The intraventricular septal thickness is 18 millimeters. The posterior wall thickness is 13 millimeters. Based upon the Doppler image presented, which of the following is true? Here's your Doppler image, I'm gonna put this on the side so you can see this. Based on the Doppler image presented, which of the following is true? There is an LVOT gradient of approximately 60. There is an LVOT gradient of approximately 100. The tissue Doppler measurements are expected to be within normal limits, or there is a delayed aortic valve closure expected. So you have two curves here, you have a late peaking one and you have another one. One is 3.76 and the other one peaks at 4.97. And there's a good split. So the patient has HOCUM with asymmetrical septal hypertrophy. There's an LVOT obstruction. The LVOT gradient is around 60 because the peak LVOT velocity is 3.76, right? So the gradient comes out to 60 when you do 4V squared. The B choice uses the velocity of the MR jet, which is higher and not the LVOT jet. It starts at the onset of left ventricular contraction and it goes beyond the aortic valve closure. That's how you know that it's the MR jet. The LVOT jet is the dagger-shaped late systolic peak velocity. You would see diastolic dysfunction, you would expect. And you would, with SAM and LVOT obstruction, you might see premature aortic valve closure. So the answer is choice, choice, let me go back, what was the answer? So the LVOT gradient is 60 is the answer. So look at those Doppler curves, know what those double shadows are, what you're looking at and what you would expect to see. This is a nice simple curve ball, I think to end the night. What is the estimated pulmonary artery systolic pressure? You're given a peak velocity through the tricuspid valve, CW, and you're given a CVP pressure. Didn't see what the poll closed at. Okay, so the people who chose 57 didn't add the CVP pressure of 10 to the equation of 4V squared. And the people who chose 77, I'm not sure, but it's 4 times 3.78 squared plus 10. And you get 57 plus 10, which is 67. Questions about that? Okay. Seems to be more. This is an apical ballooning pattern. It is not playing, so I apologize about that. And we just want to know what vessel is the culprit vessel. Is it the RCA, the LAD, the OM? Or is it both LAD and left circumflex territory? Apical ballooning pattern. Yep, it's both. Hopefully you got that and see the poll. Good, excellent. Most of you did. It's 50-50, actually. The LAD would really be just an interlateral wall. Here you have both walls being affected, and it's apical ballooning. It's not fair because I didn't show it to you. But really know this diagram really well and know that in that four-chamber view, when both the septum and the interlateral wall are out, that you have both territories. The videos are not playing tonight. What is the name of this sign? And we're looking at the RV at apex. Is it the McIntyre sign, the myocardial performance index, the McConnell sign, or the RV contractility index? Should be hopefully simple. Good, final sign, excellent. Again, our sign of RV strain doesn't really tell you if it's an RV infarct or a PE or what's causing the strain, it's just a sign of RV strain. Excellent. Okay, last one, this test showed up, this question showed up for me in many places, I won't say where. So I want you to get this because it's not something that you would normally look to study. So I'm throwing it in there for that reason. The structure at the area of the asterix is most likely the right atrial appendage, the right atrium, the superior vena cava or the inferior vena cava. Joanna, just put the results above the pole and then I'll move forward. Okay, so this is the RV inflow view, remembering that this is the right atrium down here, the right ventricle here. So remembering that, this is the anatomy that you're gonna find in this view. The IVC comes in right here to the right atrium, the SVC leaves right here. This is the posterior tricuspid leaflet, the anterior tricuspid leaflet, and the RV down here. So remember that RV inflow view, I got tricked by it. So just wanted to show it to you guys. All right, so I have a couple of questions around some of the heart-lung interaction stuff that we had spoken to. And because this exam does ask clinical questions related to heart-lung interactions, I thought we'd start with a couple of questions related to that. So here's a echo of a 41-year-old woman who has ARDS and is intubated. There's worsening oxygenation, so you increase the PEEP from 8 to 14. And on these settings, plateau pressure is 33, and AVG shows hypercapnia. Following the increase in PEEP, her norepinephrine dose has increased to maintain a mean arterial pressure of 65, and hence you're doing this echo. So I'll give you a minute to look at the images. And then here's your question, and you can put your answer in the chat since we're not using the poll for this section. So what does the imaging show? What diagnosis do you think we're looking at? Is it acute corpulmonalis, fluid overload, constrictive pericarditis, or ACS? Okay, so we have a couple of answers for A. Yeah, so this looks like, if we go back to the image here, you can see that what we're showing here is basically the IVC, the right atrium, the IVC is dilated, plump, not really varying with any of the respiration, and then a four-chamber apical view with a clearly dilated RV with showing corpulmonalia, and especially in the setting of ARDS, that's something that you have to think about in these patients. All right, moving on, so the next question. So in this patient, raising the PEEP from 8 to 14 was likely associated with which of the following effects on RV end-diastolic volume? Did the RV end-diastolic volume increase from 180 to 200 cc? Was there no change, or would you expect a decrease from 180 to 165 ml? So go ahead and put your answers in the chat again. So we have a couple of things for C. So let's go back to, if you recall the lecture on heart-lung interactions, the increase in PEEP in patients with ARDS, what the studies show that when we put echoes on these patients, the RV end-diastolic volume actually increases. And that increase in RV end-diastolic volumes is thought to be due to the increase in RV afterload. And so in this patient requiring higher norepinephrine and showing the effects of RV end-diastolic size increase, the increase in PEEP was likely related to or likely associated with an increase in RV end-diastolic volume. So answer A would be what you would expect. And this is kind of different. We know that PEEP falls, but oftentimes we think of it as a reduction in the venous return, whereas studies show that that's probably not the case in patients with severe ARDS. There it's more likely due to an increase in RV afterload. And then lastly, based on the echo findings that we've seen so far, what is the next best step for this patient? Do you want to lower tidal volumes to 4 cc per kg? Do you want to cancel the ECMO service? Do you want to do prone ventilation? Do you want to start a bi-carb drip? Again, go ahead and put your answers in the chat. Okay, so we have someone wants to cancel the ECMO service. Okay, so diuresis, yeah. So I think, so this one's kind of one of those things, right? You do a lot of different things at the bedside. One of the things to keep in mind, again, is that we know that when you place patients prone, it can have a protective effect on the RV. And it does tend to normalize the RV-LV ratios. And it does tend to reduce the pulmonary vascular resistance in these patients as well. So probably prone ventilation is where you would start. And then certainly if the patient's still not improving and still having issues, then ECMO is appropriate. Certainly diuresing them, provided they're otherwise volume resuscitated, is appropriate. Lowering the tidal volume, probably not, given how severely acidemic the patient already is. So I encourage you all to read about some of these heart-lung interactions. And just because it is kind of tricky, especially some of the changes that occur with severe ARDS. All right, so I'll go through. We'll take maybe half an hour and go through a few cases. Some of these we've already talked about, at least in passing with some of our other faculty. And so we'll try and get through a few of these just so that you can see some repetitions and kind of get used to seeing these images. So here's your first case. This is a 54-year-old who's got pneumococcal pneumonia and is now much more hypotensive, requiring escalating doses of pressors. That's her blood pressure. Those are her vital signs as well as the ventilator settings. And so a bedside echo is performed. And so here's a past and a long axis view and some color Doppler for you. I'll let you look at that. And then let me show you some more views. So an apical four chamber and then a zoomed in apical four as well. And a three chamber with some color. All right, so based on these images, what do you want to do next? Joanna, how many answers do we have? We've got about three. Oh, here we go, five so far. OK, all right, we can go ahead and stop the poll. OK, so kind of a little bit of a variation. And we'll go through some of these. I'll show you a few more views and a few more or give you a little more data. And then we'll come back to all of these. I think stopping epinephrine and additionally more data, probably both appropriate in the setting that we're seeing. And so here's a CW through the left ventricle. So the question is asking if the CW profile is normal. Joanna, you can start the next poll. OK, I apologize. I don't have this one. No worries. Y'all can go ahead and put it in the chat. What do you think, is this normal or is this not normal? So we have a few people saying, yeah, this doesn't look normal, right? So you can see that there's a late peaking profile of the CW through the LVOT. It really should be a lot smoother. And you should not have this late peaking profile here. So that suggests that there's something the matter here. And so what is the cause for the high velocity? We'll have to use the chat for this one as well. OK, no worries. So do you think that the velocity we are seeing, as well as the late peaking profile, is this due to aortic stenosis, mitral stenosis, HOCUM, or dynamic LVOT obstruction? Great, wonderful. So this is an area that's tested fairly frequently. And it's fairly common in critically ill patients. So get used to seeing the velocity profiles for dynamic LVOT obstruction. And also get used to seeing what it looks like on 2D images. So here's the profile again. Again, this late peaking profile that occurs as the LVOT sort of gets obstructed during late systole. And Dr. Millington showed earlier that that was due to the redundant tissue in the valves. This is a slightly different reason. And we'll talk about why. So here's the, we're showing you some of the profile and then the velocity, which is 689 centimeters per second. And so what is the pressure gradient through the LVOT? Joanna, should we use the chat? Yes, sorry, my numbers are all. No worries. So go ahead and put in what you think in the chat. Again, these are calculations that once you get used to, you can do quickly. And so get used to sort of knowing some of these frequently asked ones. Okay, so instead of calculating it out, why does someone put in the chat what you're actually looking at? So what are we calculating? Put in the formula. So I see someone saying D, which is 190 millimeters of mercury. Yeah, so you're doing 4v squared, right? So keep in mind that the 4v squared is, when you're using this, make sure that you keep track of the units, which should be in meters per second. The number I gave you was in centimeters per second. So it's 4 times 6.89 squared, and that's going to work out to 190 millimeters of mercury. I've gotten confused a few times when I was preparing for this test between the centimeters per second and meters per second. So just kind of keep your units similar. All right, so here's the pressure gradient that we calculated out, and so does this patient have aortic stenosis, based on what we know so far? So we know that the velocity through the LVOT that we calculated, or that we measured, was 6.89 meters per second, and that the gradient is 190 millimeters. So based on that, does this patient have aortic stenosis? Joanna, we can stop the poll. Okay, so about half and half. So let's look at what, let's go back to this. Now, what is this high velocity from? We are measuring this through the LVOT, but what is it from? What does the shape of this tell you as to the etiology of this velocity? And you all said earlier in one of the questions that this appears to be dynamic LVOT obstruction, right? And so when it's someone that has dynamic LVOT obstruction, that's going to occur below the level of the aortic valve, and you're going to measure whatever velocity is highest along the system. And based on what we know currently, there's no way to know whether there's aortic stenosis hiding under here as well. You would have to fix the problem of the LVOT obstruction, or the dynamic LVOT obstruction, and remeasure it to be able to say whether or not there's aortic stenosis underlying here. Based on the information we have currently, you do not know whether this patient has aortic stenosis or not. All right, so what's the next best step in the management of this patient? Do you want to start to butamine, stop epinephrine and start IV fluids, start beta blockers, or place an intra-aortic balloon pump? Joanna, we can stop the poll. Okay, great. And so I think, you know, going back to what we think this patient has, which is dynamic LVOT obstruction, I think stopping epinephrine or stopping anything that's going to increase contractility is appropriate and volume resuscitating these patients. Starting beta blockers is not wrong, but keep in mind that if someone's on triple pressers, it's going to be challenging to start any kind of beta blocker in that moment. So you usually have to get them tanked up, get their volume status a little better, and then potentially as the presser requirements come down, potentially start them on beta blockers, and preferentially something that's short-acting like Asmolol might be preferred. And so let's look through some of these in more detail. So the parasternal long axis is oftentimes the view in which you'll start to think about LVOT obstruction. And one of the clues, even sort of looking just at the 2D image, is that the valve itself, and I'm just going to try and do this sort of this way, where you see that the valve leaflet actually gets pulled into the LVOT during systole causing SAM. The other clue that you can have is like Dr. Millington mentioned, where you get this Y shape, where you get some amount of turbulence in the aortic outflow tract or in the LVOT outflow tract, but you also get mitral regurgitation as a result of that anterior leaflet being pulled away. And so in patients in septic shock, oftentimes the type of SAM that you will see is the variant where the anterior leaflet gets pulled into the LVOT and then potentially causes mitral regurgitation as well. And so here's just a slowed down image, again, just sort of showing you that that valve leaflet gets pulled into the LVOT causing the LVOT obstruction. And here's just some of the other views where you can see it as well. And so this one, I'm actually just going to run through this and show you as it sort of, and you can see that every so often that that leaflet gets pulled away when it shouldn't be, when it should be closed. And then in a three-chamber view again, sort of similar to, you'll recall that the three-chamber view is essentially just the parasternal view. And so you can really nicely see the turbulence near the LVOT as well as the mitral regurgitation coming into the left atrium as well. And then I'm just going to skip some of this. I'll skip this question, but I'll show you, this is sort of similar to what Dr. Narasimhan had shown earlier. Be careful about catching the MR jet in the same plane. And so you can see that there is a late peaking jet here, but we are also catching part of the MR jet. And so you can get confused. So when you measure the velocity, in order to calculate the gradient, make sure that you can identify which jet it is that you're measuring. All right. So 24 hours later, this patient's received four additional liters and then weaned off all pressors and her lactate improved, and she's looking a lot better. And here's just her repeat scans to compare. And now you can see that the valve is behaving normally. You no longer see any more of the SAM. You see that the valve is actually morphologically pretty normal itself. And then just sort of additional views for you to compare and look at. And you can now see that that turbulence is gone. The regurgitation has gone for the most part. And most of this looks normalized. She does have a plural effusion now after all of the volume that she had received. And then once the LVOT obstruction was fixed, now you can look through the aortic valve and you can look at the velocities and you can calculate the aortic valve area and it was normal. So in the presence of dynamic LVOT obstruction, you cannot comment on underlying aortic stenosis. So here's just some information. So SAM, if you go looking for it, you will find it in patients with septic shock, especially about one in four patients potentially has SAM or dynamic LVOT obstruction. And when it's present, it's associated with worse mortality. So think about this in patients who are not responding to standard therapy and start getting worse as you increase pressures or especially when you increase or add on something that increases contractility like dobutamine. An LVOT gradient of more than 30 is considered clinically significant. Look for that aliasing of systolic flow through the LVOT as well as the additional presence of MR. And then look for that late peaking flow through the LVOT. And like we've talked about, stopping inotropes, stopping anything that reduces afterload, and then using IV fluids and beta blockers if they're able to tolerate it is sort of the standard of care here. All right, before I go to the next case, does anyone have any questions? Okay, hearing none, let's go to our next case. So this is a 32-year-old, no past medical history, who was found down at home by his roommate. And he basically had a PA arrest, achieved ROSC, was intubated, transferred. He's cold, clammy, mortal extremities, tachycardic, has significant lower extremity edema, also has metabolic acidosis as well as a lactate of 13, is still hypotensive and tachycardic. He has his ventilator settings and then is on three different presses, including epinephrine. So here are some of his views. So I'll let you look at them. And then I'll show you the question, and then I'll go back to the clip so that you can look at the clips, the clips to look at. Joanna, how many answers do we have? We've got six. OK, we can stop the poll. OK, great, excellent. So you all got the fact that what we are looking at here is that rule of thirds with the RVOT, the aortic outflow, as well as the left atrium. The RV is clearly way out of proportionally enlarged. So much so that it's actually causing the LV to be hyperdynamic. And sort of similarly, on the short axis view, with the RV being giant, pressing against or causing the LV to be hyperdynamic and small in volume, as well as some flattening of the septum here. Great. Here's an apical four chamber view. And then some measurements for you. So the LVOT VTI, which is 13.4, heart rate of 108. And then Dr. Millington's favorite subject, here's some additional diastolic numbers as well. And so I'll point out the E to A ratio of 0.72. And then this is a lateral E prime of 14 centimeters per second. So what do you think is the cause for this patient's shock? Okay, Joanna, we can close the poll. All right, great, excellent. So, you know, I think a lot of times, especially test questions, sometimes give you a lot of extraneous data, and picking out the things that are the most important and that make the most clinical sense is important. And so here, clearly, the reduction in LVOT VTI is due to the fact that this gentleman's RV is really in trouble and hugely dilated. Whether or not there is some diastolic dysfunction here doesn't really factor into this, but if you were to look at this, your A is slightly higher than the E, so he has some mild diastolic dysfunction. His E prime is relatively preserved and doing okay. So at most, this is mild diastolic dysfunction and certainly not the cause of the clinical scenario that we are seeing. So put it in clinical context, kind of put your 2D image in there as well, even if you get a lot of numbers thrown at you. All right, so here's a lung ultrasound. And so why do you think that this patient is hypoxic? We can close the poll, Joanna. Okay, yeah. So I think, you know, like we said, clearly the RV is super dilated. Chances are this patient was sick before and either didn't seek care or didn't have symptoms and he's young and was able to compensate. But the pulmonary hypertension could certainly be a reason for the hypoxia, especially given the fact that he's now on positive pressure ventilation and the higher PEEP is going to adversely affect that RV as well. And then something else is possible too. So what thinking about what that something else is. So what do you want to do in addition to what we've already shown you, what else do you want to do to evaluate this hypoxia? And so you can just put in your answer into the little box there. Okay, we can close the poll, Joanna. Guess we didn't, so what else are you thinking of when you see a big RV and someone's hypoxic, what else are you thinking about? Okay, so you're thinking of a PE, certainly something that's certainly possible. What else? Is it possible that this patient could have a shunt? Yeah, so you think about some sort of a shunt, right? Do they have a PFO that opened up because now they're on positive pressure ventilation? Could they have had some sort of ASD and that's what led to the RV dilation? So all of those things, probably your next step would be at the bedside to do a bubble study to look and see if there is a shunt. You could potentially consider imaging them and sending them for a CT, but you probably want him to be a little more stable before you send him off for a road trip for the CT scan. All right, so we are at 6.02, Joanna. Should we keep going? So I guess I'll ask the attendees, would you like to do one additional case or should we call it an evening? Okay, let's do one more case. So Amit, you do have the time. I do? Yes, absolutely. Okay, cool, let's do one more case then. If I can get it to work. All right, so here's a 50-year-old woman with dermatomyositis who presented in respiratory distress, has bilateral infiltrates, is hypoxic despite being on 100% non-rebreather. And then following intubation, her SATs worsen. And when you increase the PEEP, her SATs worsen even further. And before I go any further, this is actually a case courtesy of Dr. Greg Schmidt. So thanks to him for this case. So here's some imaging for you. And this is while the patient's on some norepi as well as a PEEP of 12. And this is the S-prime looking at the tricuspid systolic velocity. All right, so what is the next best step for this patient? Joanna, do we have a poll for this, or should they use the chat? Let's use the chat. I'm still searching. OK. Yeah, so I see D, unload the RV, great. So let's go back to this and look at this a little more. Whoa, that's not what I wanted. OK, so let's look at this. So what are we looking at here? We're looking at a bubble study, and a bubble study should not look like this, right? So you should have the right side get opacified with the bubbles, and under normal circumstances, shouldn't see anything at all on the left side. Whereas here, the density of bubbles on the left side is pretty much the same as what you're seeing on the right side, which tells you that there's likely a big PFO, or a big sort of intracardiac shunt that's occurring that's likely the reason for her worsening hypoxia, especially when the PEEP was increased and the positive pressure was increased. And so trying to offload the RV and reducing the pressures on the RV and the RA would be a good next step to try and help prevent this shunt fraction from getting worse, and trying to reduce that shunt fraction as we go. So here's this patient after she was put on ipoprostanol and switched to pressure support, as well as the PEEP being reduced. And you can see that now the density of bubbles on the left, while you still see bubbles, the density of them are much, much, much lower compared to what we showed previously, telling you that the amount of blood and the amount of shunt that's coming across is a lot lower now that you've lowered the pressures on the right side. And then her RV, other measurements improve as well, with her S prime getting better, the TAPC getting better overall once the ipoprostanol was started. And then finally, with her extubated, this is a subcostal view. And again, you can see that there's a very small shunt, if at all, that you can now see with the bubble study. So keep in mind that these patients, when you intubate them with big PFOs, especially when their RV function worsens, it can make their hypoxia much, much worse. So A, you need to recognize it, and a bubble study at the bedside can be a quick, easy way to figure this out. And B, effectively lowering those right-sided pressures can really make a big difference in the amount of blood that's being shunted across and in the hypoxia that we are seeing in these patients. Amit, we had a patient today in my unit where she had a big PE, post-hip replacement, and had a stroke at the same time, and had a bubble study during that time period, which showed bubbles going across, got TPA for this PE, and the bubbles stopped going across. So very dynamic changes based on the pulmonary pressure. So good case that you have there. It was a beautiful case. Yeah, beautiful. Yeah. Yeah, and it's strange how many times we have found PFOs in these patients who are in refractory hypoxia, and then putting them on whatever you do to treat their underlying disease, how rapidly their hypoxia and their RV function actually improves. So when you start going to look, you'll be surprised how many of these you'll pick up. Yeah, yeah. All right, so just to sort of reiterate that the RV failure can occur in about 30% of patients with severe ARDS, so the cor pulmonale is fairly frequent. And so these patients who have pre-existing PFOs, when they develop cor pulmonale and they develop the increase in right-sided pressures, it can open up this PFO and cause this reversal of flow, thereby worsening the hypoxia. So kind of think about that in patients who paradoxically worsen. All right, moving on to the next case. So this is a gentleman with non-systolic heart failure who's brought in by his wife, as he's been more lethargic and encephalopathic. He's fumbling incoherently, but he's moving on his extremities. Although his extremities are cold to touch, he's hypotensive. And those are his vitals. He's got a few crackles of the base and no lower extremity edema. And here are his, I'll give you a minute to look at these. So before we go to the question, put in the chat what you think his LV function is. Is it normal? Is it mildly reduced, moderately reduced, severely reduced, hyperdynamic? Yeah, so this looks like it's pretty severely reduced, right? OK, let's go to the question. So the abnormality that's seen in the images that I showed you is associated with an increased risk of which of the following? And I'll go back to the images so you can see. Joanna, we can close the poll. Okay, excellent. And so what we're seeing on these images, and you can see it really clearly in this image down on the left, is that this patient has a spontaneous contrast and the presence of spontaneous contrast, whether in the left atrium or in the left ventricle has been shown to be associated with an increased risk of stroke. You can see it in patients who have really low flow states, like this gentleman who's got severe underlying heart failure. And so when you see it, sort of think about, depending on your patient's symptoms, think about what else it might predispose them to. So here's just more images for you to sort of... Mangala, my videos are giving me trouble too, whereas I could play them a little while back, weird. And so you can see the contrast in multiple images that, again, just speaks to the severity of the low flow state for this patient. All right, and so here's just what we talked about. Okay, so here is an LVOT VTI. So the VTI is 11.5 and you're given a heart rate. And so assuming an LVOT diameter of two centimeters, what is this patient's stroke volume and cardiac output? So again, this is a very common question. You know, shows up multiple times in multiple sort of variations. So get good at quickly doing this and plugging it into the formula. Joanna, do we have some folks who have answered? Just, oh, four so far. Okay, all right, let's close the poll. Okay, so let's go through this calculation. And we've talked about this a few different times. So stroke volume is gonna be LVOT area times the VTI. And for this patient, you're given a diameter of two centimeters, so that makes your LVOT area 3.14. Stroke volumes, that times VTI, which is 36 CCs. And then cardiac output is stroke volume times heart rate. Again, this should become second nature. These are really quick, easy ones that you can score on. And they don't take a lot of time. You will have a calculator available. So calculating it out by hand is not important, but at least writing it out so that you know the formula is important. All right, so this will be my last case. We'll have a 45-year-old with ESRD and hypertension who presents with hypertension that developed during dialysis. During the last few days, he's been having chest discomfort that he attributed to heartburn. He has also missed at least four days of antihypertensive medications. He takes a whole bunch of them, but decided that he needed to take them that morning before his hemodialysis session. And when you see him, he's diaphoretic, he's cold and clammy. He's hypotensive and he's on norepinephrine as well. And here are, you can see the question that's on here. I'll just minimize this and play these clips. All right, Joanna, let's close the poll. Okay, excellent. So let's look at this a little. So what are things that we see here? So you'll notice again that the rule of thirds seems to have been violated. So there's a dilation of the aortic or the ascending aorta, right? There definitely seems to be a pericardial effusion. You can see it here next to the left atrium, also anteriorly and kind of better seen in this view and it looks like there's probably something more than just simple fluid. And then if you look at the LV wall, the LV chamber size actually there is encystolic effacement so the LV is hyperdynamic. What this patient doesn't have is a pleural effusion. So this is an artifact. It's a mirror image that you're seeing from up top. The pleural line and the pericardium is up here. So there's no pleural effusion here. You would usually see the pericardium sort of highlighted against the thing if there is a pleural effusion present as well. So this person has aortic dilation, has hyperdynamic LV as well as a pericardial effusion. All right, so here's some additional images for you and some of these you may not have seen before. So a high parasternal long axis view is basically when you have a parasternal long axis view, moving up a space or two will give you a more detailed look at the ascending aorta itself. You don't always get this in most patients or don't get it in all patients, but sometimes you get lucky and you pick up a slightly higher view of the ascending aorta. So this is essentially the ascending aorta that we're looking at with some color thrown in. And then you have some color Doppler here with the parasternal long axis view and then the parasternal long view that we saw before. So I'll let you look at that. And what do you think may be the cause for this patient's hypotension based on what we've seen here? I'll go back to the images. Okay, Joanna, we can close the poll. All right, so most of you said aortic dissection and that is true. So if you look at the ascending aorta here, you can see that there is a little flap that's present within that ascending aorta, that the presence of some aortic regurgitation plus the more ominous presence of what appears to be clot in the pericardial space should make you think about aortic dissection. You can also see that that dissection, so this is the true lumen here and there's no flow going back into this area behind the dissection as well. So a lot of sort of very, very worrisome things on these echoclips. So, ah, well, that just showed some aortic regurgitation and unfortunately my video is not playing. And here's a aortic regurgitation Doppler measurement and it shows you the pressure halftime. So the pressure halftime is 432 milliseconds here. And so what is the severity of the aortic regurg? And you can go ahead and it's a little bit of a shame that you couldn't see the color Doppler as well, but just based on the pressure halftime, what do you think is the severity of the aortic regurgitation here? Okay, we can, great, yeah. So most of you said it was mild or moderate and we look at sort of how you can classify this. So you can use a few different things to classify the severity of aortic regurgitation. You can look at the JET versus the LVOT width, although this is probably less reliable. And if it occupies more than 65% of the LVOT diameter, then that's considered severe. This you would see in a parasternal long axis view. And then you can look at other things like how intense is the regurgitation JET itself? Does it sort of approach the same density as what the forward flow looks like? And so in severe AR, you would start to see much denser JETs. And then finally, you can look at the pressure halftime. And essentially, if your pressure halftime is more than 500 milliseconds, that's considered mild. If it's less than 200 milliseconds, that's severe. And then in the middle is moderate. So let's go back and look at what we had. So you can see that the intensity of the regurgitation JET is much less compared to the forward flow. So that's one clue that this is not super severe. And then the pressure halftime is 432. So very close to that 500. So it's in that mild-moderate range of severity of aortic regurgitation. All right, I will quickly show you this case. We won't go through the questions, but here's a young man who presented with shortness of breath for a week and plays basketball regularly and noted that he's been feeling more tired. And when he came in, he was tachycardic and then just didn't look right. And his lactate was elevated at eight. And here's his parasternal long axis view. So put in the chat what catches your eye. What catches your eye in terms of what's abnormal here? Okay, so there's a pericardial effusion. What else? What do y'all think about the size of the aortic root? So this. Yeah, so a lot of you picked up on a lot of the abnormalities here. So let's just look through them real quick. So the first thing that you see is that this aortic root is giant. Dr. Millington mentioned earlier that for males, it really ought to be three and a half centimeters. This is clearly seven or eight centimeters. And so this is markedly abnormal. The LV is severely reduced in functions. It's dilated as well as reduced. And there is a pericardial effusion here and there is a pleural effusion here. And then when you look at the short axis view at the level of the aortic valve, you can see that the aortic valve annulus is so markedly dilated that the valves don't even come together. The cusps don't come together. They don't co-act. And so this would be someone where you would expect to see very severe aortic regurgitation just by virtue of the fact that these cusps don't even co-act together. And so sure enough, there is a huge aortic regurgitation jet that's present. Amik. Yes. I have like something else that probably is not helping. And if you go back to the short axis without the closeup on the aortic valve, you can see that the left atrium is like squished by this humongous aortic root. Yeah, both in the long axis, but more distinctly, I think, even in the short axis view. So- Yeah, for sure. I would point that out. Absolutely, I think. Yeah. Go ahead. Sometimes if you have like intraatrial shunts, they will be like positional. This doesn't have anything to do with an atrial shunt, but it just brings to mind that these atria, they can be kind of like fairly dynamically changing in configuration with the interatrial septum. So in some people you have shunts that only happen when they're upright or like lying down, and they can be caused by these configuration changes. This one is more permanent, I would think, but it's still marked, I feel. Yeah, this one is probably anatomic just from the fact that the aorta is giant. So anyway, so this gentleman, after we probed a little bit, basically told us that, yeah, my brother died when he was 15, and I'm not, we don't know why. And he was six feet, nine inches. And so he actually, he ended up having an aortic root replacement, did well, got tested, and he sure enough had marfans that had not been diagnosed or picked up on. And so it was just unfortunate that he sort of presented the way that he did. But yeah, so those were my cases. Any questions about, I guess, any of my cases that I've presented or any of the ones that, any of the faculty or any other questions that may have come up before we end for the day? Mangala and Gisela, did you all have anything else to add? No, I think they've had enough for the day. I think they're exhausted and tired of us. Yeah, I bet. Yeah, thank you guys for hanging in and we appreciate it. And email us with any questions, thoughts, concerns, and we will see you next week, Thursday. Thursday. Yeah. All right, everyone have a good evening. Thank you. We'll see you soon. Bye now. Take care. Bye.

Critical Care Echocardiography Exam

medical training

echocardiography

cardiovascular conditions

LVOT obstruction

Systolic Anterior Motion

septic shock

pressure gradients

bubble studies

pulmonary hypertension

PH

RV strain

clinical decision-making

heart-lung interactions

congenital defects

prosthetic valves

Pulmonary Hypertension

PH