Yay! Hi, everybody. Thanks so much for coming to our session here today. You know, people were asking me during the Congress, what is your talk going to be about? And I said, well, something really simple, RV failure and fluid responsiveness. And now we have 15 minutes to cover it. So let's just get started. I don't have any relevant disclosures, but we are going to review how ultrasonographic evaluations of volume responsiveness have arisen, and we're going to talk about them from the perspective of the right side, all right? And we're going to assess RV function and pulmonary arterial pressures and see how to do that with ultrasound, both qualitatively and quantitatively. So when we published this piece back in 2020, we really felt like the RV and volume responsiveness for the RV deserved a whole section in this piece, because this is kind of the great unknown for us in management of patients and their volume status. And oftentimes, you'll hear about the right ventricle being called the forgotten ventricle. And the reason for that is multifactorial. But if you think about most of the fluid responsiveness techniques that we use and that you have heard about today, except for perhaps on Murad's talk just now, they have all been left ventricular-based. And if you think about the right ventricle, the right ventricle is almost like a hand, a giant hand, and it wraps around the LV. So the LV is very dependent on the right ventricle. And even though it may seem small, it's actually kind of mighty. In keeping with drawing things for you, I drew this so that you could see that the RV is a ventricle too. It's got all different kinds of walls, and you can see them differently depending on what views you look on in echocardiography. And it also deserves the same kind of attention, if not maybe more. So perhaps we should call it the people's ventricle, because without the contributions of the right ventricle, the left ventricle just cannot succeed. And we know this very clearly, because isolated RV dysfunction in septic shock is an independent predictor of worst one-year survival. That's a big deal. So despite however big and blustery the LV is, we need to pay attention to the right ventricle. So if you think about these volume assessment modalities that have been discussed today, look at this, this left ventricular end diastolic area as a suggestion of hypovolemia, or even the left ventricular outflow tract peak velocity variations that Tony talked about. These are both LV-based. So if the RV is failing and cannot push the blood forward, either because the pressures in the pulmonary vasculature are too high or the RV itself is failing, no matter what you do, the left side is going to look empty. You can get volume and volume and volume and do whatever you want, but the left side is going to look empty. And these parameters are going to look like the patient is volume responsive when in fact, it could be detrimental to the patient. Or let's think about the passive leg raise or even the mini fluid challenge. Both of these assessments are done in the left ventricular outflow tract. So these are both LV-based measurements, and they don't really have the same kind of predictive value for us in patients with RV failure. So indeed, it is the people's ventricle, because people are complicated. This is the complicated ventricle. Both hypervolumia and hypovolumia can reduce cardiac output and worsen outcomes. And there is no one size fits all optimal filling pressure. And I think you've kind of been hammered with that during this talk, but there really isn't. It really varies depending on the patient and the right heart contractility, what the afterload is, and what the underlying pathology is. So if you think about the RV and how to assess for volume responsiveness, what we actually really have to be able to do is assess RV contractility and afterload. So let's look at this first case here, this patient. Right ventricular failure. If you have RV failure with a normal afterload, you actually may need a higher preload in order to maintain cardiac output. So this patient is a classic case of that. This patient has an RV infarct. You can see the basilar to mid portions of the RV are moving well in the lateral free wall. And then there's a clear transition point. And from mid to apex, the lateral free wall of the RV is not moving well at all. So in patients who have RV infarct and normal pulmonary vascular resistance, they typically need higher preloads, higher filling pressures in order to maintain cardiac output. Now you can't translate that same sort of thinking to a patient who has RV failure with elevated or increased afterload. Because these patients, you can see here, the septum of the RV in the parasternal long axis view is just bowing down every time systole is occurring. You can see it pop down. OK, so this is a sign of pressure overload. An increased volume administration to a patient like this could be really detrimental. It's going to increase the tension on the walls in the right ventricle. It can actually cause ischemia to the myocardium. So this is not a good scenario. And Dr. Gabrielle Villa and Susanna Price published this really nice piece quite a while ago now talking about 10 situations where the inferior vena cava really failed to accurately predict fluid responsiveness. And the RV pathology kind of falls right in there. So patients who have chronic RV dysfunction and severe TR, of course their IVC is going to be dilated. Of course they're not going to have variability. That doesn't mean that they too cannot be fluid responsive. You just don't know what their baseline was, right? Like their baseline, if you think about it in CVP terms, may be 15. So if their baseline is 15 and now their CVP is 10, they're going to be fluid responsive, right? Their IVC is smaller than their baseline, they'll be fluid responsive. But it may not be small by all kind of definitions that we think of when we think of small. Or RV myocardial infarction like we just talked about. These patients typically have RV dilation and systemic venous congestion. So the IVC may be large and not collapsible. And you may think, oh, they're not going to be responsive to fluid when in fact they are. So take the IVC with a real giant grain of salt, okay? It can mislead you. So how do we actually assess the right ventricle from a qualitative way? Well, you can look at the size of the right ventricle. You can look at the lateral free wall motion and see how is it moving both at the base like a piston or at the kind of mid to apical portions, is it coming in and out? How is the free wall thickening? How does the internal area of the RV change over the cardiac cycle? And what is the septum doing? Is there intraventricular septal dependence? So if you look at this patient, you can see really clearly here is the right ventricle. It's larger than the left ventricle. The apex of the heart is being taken up by the right ventricle. You can see that this piston motion at the base is a bit depressed, that the lateral free wall doesn't really thicken or move in. And the intraventricular septum is pushed over to the left. And this patient has like all the signs of RV failure with pressure overload, okay? What about some of the other modalities? So you hear about using quantitative tools such as the TAPC, which is the tricuspid annular plane systolic excursion, to assess RV longitudinal function. There is space for this. So you would put M-mode on the lateral wall of the lateral portion of the tricuspid annulus and see how much does it move up and down like a piston. But I just told you earlier that the RV is a bit complicated. So the base may look like it's moving okay when the rest of it isn't moving that well at all. So you can't use this as like a slam dunk, right? And if you talk to cardiologists, my husband's one of them, they'll say, yeah, TAPC is crapsy. So just keep it in mind when you're thinking about this. So one of the things that you can do, even though it's still a 2D modality, is look at fractional area of change. So how much does the actual internal cavity of the RV change throughout the cardiac cycle? And that would be kind of demonstrated here. The other thing we oftentimes can look at is tissue Doppler at the lateral annulus of the tricuspid valve. This is called S-prime. And this is looking at how fast is the velocity in systole. If the velocity is really fast and the myocardium can go fast, then you would think that the RV function is relatively normal. If it's slowed down or depressed, then you would think it's abnormal. But once again, you're looking at one spot. You're looking at one place. And the other thing is all of these things that I've just mentioned, for the most part, are very load dependent. And I just told you, you have to understand the loading conditions of the RV. So this can be a bit problematic, right? So if the patient isn't loaded adequately or you may get different values. So what are some tools that we could use that are a little bit more load independent for assessing the strength of the RV? And there is this thing called the RV index of myocardial performance, or the RIMP. Some of you may have heard it called as the Tay index. This is actually not an assessment that depends on load. And it doesn't really depend on the Doppler angle. And the reason why is because instead of looking for maximal velocity, you're looking for time. How long does it take the RV to eject? And what it's actually measuring is when you put tissue Doppler on that lateral annulus of the tricuspid valve, what it's actually measuring is to say, how long does it actually take you to start the contraction? Because if it takes you much longer to start the contraction, then your strength is probably depressed. And I think of it like weightlifting. If you put a 50-pound dumbbell in my hand, besides it may be breaking my elbow. But if you put a 50-pound dumbbell in my hand and I tried, tried, tried to start the contraction, it may take me a lot longer if I'm not strong to do it. But if I was strong, let's say I was Arnold Schwarzenegger in his heyday, and I had a dumbbell in my hand, I'd just, boom, be able to lift it up. So this is kind of a measure of that time that it takes. So that's one tool that you can use. The other thing, and don't poo-poo it, because friends, it's coming for you, RV strain. So we say, oh, this is not a POCUS modality. These ultrasound companies are getting, the technology is getting bigger and faster and better, and AI is coming for us. And looking at RV longitudinal strain is here, and it's going to be at your fingertips before you know it. So I just want to tell you that it is a modality. They use it in the echo lab. It will come to point-of-care devices, I'm sure of it. And this is a way to look at speckle tracking of the walls, the wall of the RV, and points within the RV, and how they move in relationship to each other. And what we do know about this is this is a more sensitive, this is more sensitive to subtle changes in myocardial function than conventional parameters that have been used to assess RV, which I've talked about. And this is just some examples of that. You can see here, this patient had Takotsubo's cardiomyopathy. And once you got towards the apex or the mid portions, you can see that the strain changed, the pattern changed, and you can see that the RV function actually was changing. All right? So you can also use these non-invasive tools like ultrasound to measure systolic or systemic pressures in the pulmonary vascular resistance, or RVSP. So you can use it as a surrogate of PASP. So for example, if you have a tricuspid regurgitant jet, you can put continuous wave Doppler over that TR jet, take that maximal velocity, put it into the modified Bernoulli's equation, which is this change of pressure equals 4V squared, and it'll change it into a pressure gradient. So you know that if the gradient between these two chambers is X, and there is a certain underlying pressure in the right atrium, then if you add that pressure gradient to the right atrial pressure, it'll get you the pressure in the right ventricle, and that's right ventricular systolic pressure. So you can use that as a surrogate of pulmonary artery systolic pressure in patients who don't have pulmonic stenosis or strange intracardiac shunts. Okay, this is just an example of that, and you can see this maximal velocity was measured at 4 meters per second. So just as like a quick tip, any time that maximal velocity is greater than 2.8 or 2.9 meters per second, the patient has pulmonary hypertension. Okay, I mean, it's just math, right? So then the next thing we want to talk about actually is measuring mean PA pressures without a regurgitant jet. So maybe your patient doesn't have a regurgitant jet, and you still want to be able to measure PA pressures. Well, you can put pulse wave Doppler actually in the right ventricular outflow tract in, for example, the parasternal short axis at the level of the aortic valve and see how fast does it take to accelerate to maximal velocity. And you can use that acceleration time called the RV acceleration time and calculate mean PA pressure. So RVAT divided by 2 will give you this value, and then 80 minus that number will give you the mean PA pressure. So this is something that you can do at the bedside. So in conclusion, despite being the forgotten ventricle, the right ventricle is actually the people's ventricle, okay? And don't underestimate it. It's important. And it's complicated, just like people are. And it turns out that standard volume assessment modalities are not really applicable to the RV. Most of them are LV-based. And you can use qualitative tools to really understand RV contractility and afterload conditions. So the size, the lateral free wall motion, the change of the internal area, intraventricular dependence. And you can use quantitative tools, such as TAPSI, CRABSI, fractional area of change, S prime, RIMP, or right ventricular longitudinal strain. And also, you can also use these quantitative modalities for measuring afterload, which we talked about. So I want to thank you so much for your time, and I hope you have a great rest of your Congress. Thank you.

right ventricular failure

fluid responsiveness

RV evaluation

septic shock

echocardiography