SCCM Resource Library-Echocardiography for Assessment of Hemodynamics

Video Transcription

Hi, I'm Keith Walley. I'm an intense care physician and a translational scientist in Vancouver, Canada. I'm going to talk to you today about bedside echo assessment of left  ventricular systolic function and cardiac output. I have no disclosures. And what I want to talk about is first that you need a strategy for applying POCUS to assess ventricular  function. It's not good enough to take this view and that view and this measurement and that measurement. You need a way of thinking through it. The second point that I want to  make is left ventricular ejection fraction isn't a pure measure of contractility. It also depends on afterload, diastolic function, whether you're infusing inotropes, for example.  So you need to take those things into account. The ways that I'm going to tell you about to assess ventricular function are ejection fraction and then tissue Doppler indices.  I'm going to talk about a future use of speckle tracking. And then I'm going to talk about old school systolic time intervals. Then I'm going to talk about measurements of cardiac  output. They may not be that helpful in many instances, but we'll go through that. And the final point that I want to make is that you do need a very strategic approach because  the time delay you take to make a whole bunch of different measurements can adversely impact  your patient. So here's the context that I use. You can develop your own or you're certainly  welcome to use this. This is a strategic approach to figure out what the cause of shock or hemodynamic  instability is. And it's based on the red capital letters SHOCK. The first thing to do is a clinical evaluation. Is this warm, high cardiac output, distributive shock, septic  shock, for example, or is this a cold, clammy, thready pulse pressure, low stroke volume, low cardiac output shock? In that instance, POCUS, bedside echo, is enormously helpful  to decide is this an empty central circulation, which is hypovolemic shock, or a full central  circulation, which leads you to the next question, is this due to obstruction, RV for pulmonary  embolus, lungs for pneumothorax, pericardium for tamponade as the most common causes of  obstructive shock, versus is this due to decreased systolic contractility? And this is the point  of this talk, assessment of ventricular function and systole. But there's one final question  that you should ask, which is what doesn't fit, because usually in medicine things aren't  entirely straightforward. And that final question leads you to consider other rarer kinds of  shock, neurogenic shock, adrenal insufficiency, anaphylactic shock, for example, or combinations of shock, septic plus hypovolemic shock. So the point is POCUS fits into a strategic  framework. It's not the process of getting a whole bunch of interesting measurements. The next point I want to make is left ventricular ejection fraction is sensitive to a number  of different things, and it's not just a pure measure of contractility. And you can see that if you consider a left ventricular pressure volume relationship. Here's left ventricular  pressure plotted against left ventricular volume. During diastole, the ventricle fills, volume is increasing, until the ventricle contracts with the valve closed, so volume  doesn't change, until ventricular pressure exceeds aortic pressure, the ventricle ejects  and then relaxes down. That's a cardiac cycle. Interestingly, all end systolic pressure volume points lie along an end systolic pressure volume relationship. And what that means is  if afterload were higher, the ventricle couldn't eject as far. And if afterload were lower, the ventricle could eject further. But the slope of this line then becomes a measure  of contractility, because if you had an increased slope, at the same afterload, you'd be able  to eject further. In this example that I did in an Excel file, I have stroke volume divided by end diastolic volume as ejection fraction, which is 66%. And sure enough, if we were  to decrease contractility from the dashed lines, which were on the last slide, to a lower slope, then stroke volume, you can see, is decreased, and the calculated ejection  fraction is decreased. So certainly, ejection fraction reflects contractility. But remember  that if afterload were increased, the ventricle would similarly not be able to eject to as low an end systolic volume, so stroke volume would be decreased. And in this example I  chose it, so ejection fraction would similarly be decreased to 58%, with no change in contractility,  no change in slope of the end systolic pressure volume relationship. And then there's the interesting circumstance, with no change in contractility, no change in afterload,  if the ventricle is stiffer, and the same preload pressure, the ventricle wouldn't fill as much, stroke volume would be decreased, and I chose things so the ejection fraction  here is 58% again. The point is, ejection fraction is sensitive to afterload, to diastolic function, and then you have to incorporate the concept of am I infusing inotropes, for  example, to assess what's going on. So when we look at ejection fraction, you could do this a number of different ways, but at the bedside, typically it would be a short axis  view, a left parasternal short axis view, shown here, and you can see that ejection fraction is greatly reduced. Now you can't see the whole ventricle, so this is just an  estimate, we haven't taken everything into account. And from the previous discussion, you now know that obviously is due to a decrease in systolic contractility, but it could also  be contributed to by greatly increased afterload. Here, there's no difference in diastolic function,  but that was something that you had to consider, and you had to consider, was this jazzed up by the use of inotropes, and therefore, is this ventricle even worse? Now, you could  calculate ejection fraction accurately, for example, using Simpson's biplane, that's going to take a couple different views and tracing of the endocardium and the difference between  end diastolic volume and systolic volume, it's going to take way too much time. It can be done, it is done during a comprehensive echo exam, but typically not helpful at the  bedside. How else might you assess ventricular systolic function? You could do it with tissue  Doppler. You could put the tissue Doppler probe there on the lateral border of the mitral valve, for example, and look for systolic excursion, which is shown as the white trace  here, it's a Doppler, tissue Doppler trace. The maximum velocity coming towards the probe is called S prime, the peak velocity, it's a measure of systolic contractility, but you  could actually look at the integral of this whole thing, which would just be the total excursion from diastole to systole of the mitral annular plane, mitral annular plane  systolic excursion, and that would be a measure of systolic contractility, typically more  than one centimeter, for example. So tissue Doppler is a way of assessing it. In the future,  the machines are coming out with speckle tracking. They're in an early stage, not all the kinks  are worked out, but I want to point out to you why in the future this might be a useful thing for us. Instead of just looking at ejection fraction, it looks at the distance between  two points, mathematically a little bit different than that, and in this example, again, I did  an Excel file with all the calculations. The ejection fraction is reduced to 42 percent because the shortening, global longitudinal strain shortening, is reduced to 16 percent,  minus 16 percent, from a normal value of 20 percent or minus 20 percent, however you like  to talk about that. So ejection fraction and fractional shortening are related, but consider this weird concept. What I do is I just toss a blue marble into the ventricular cavity.  The ventricle here and here is doing exactly the same thing in terms of fractional shortening, but you can see that the pink blood volume, the fraction of pink blood volume ejected,  is much higher. So by just putting a blue marble in the ventricle, I increased the ejection  fraction to 72 percent, even though the ventricle is doing the same thing. Now, big jump, what  if I redistributed that blue marble as tissue edema in the ventricle myocardium or stunned myocytes, for example, in the ventricular myocardium? Now, you can see compared to the  first part of this slide, the ventricle is a little thicker. It's a little thicker, and with the same reduction in fractional shortening, the ejection fraction can be back up to 72  percent. So ejection fraction is also dependent on the myocardial properties that speckle tracking may get around in the future. Then, that was the future, how about the past? You  can think about systolic time intervals, and the interesting thing about systolic time intervals is they're really simple, they're fast, they're way more producible than any  of the other measures that I talked about here, and you can take into account heart rate dependence. And so a systolic interval is a pre-ejection period from the start of  the QRS to the start of ejection, and the left ventricular ejection time shown there from an aortic valve Doppler trace, for example, and the ratio of pre-ejection period to left  ventricular ejection time in the range of 30 to 40 percent in normal, and when decreased,  that would be decreased contractility, essentially a prolongation of the left ventricular ejection  time because of decreased contractility. So there's an interesting old-school measurement that is highly reproducible that could be considered at the bedside when the other measures  are technically difficult or unsatisfactory for whatever reason. How about cardiac output? I'd like to start off by making the point that the absolute value of cardiac output  is sometimes not that informative. It depends very much on the context of your patient. So for example, if I took a high normal range cardiac output and cardiac index, it actually  could be a patient in septic shock and indicate a low systemic vascular resistance and the  distributive shock state associated with severe sepsis. But it is just top end of normal range, so it could just be the patient sitting in bed, they're completely normal, ready for  discharge, could be a normal value. Or in a distance runner who should easily be able to take their cardiac output up to 20 liters per minute, if this is an exercise test and  that's the best cardiac output they have, this is greatly decreased systolic function. So the absolute measure of cardiac output really depends on context. How could you get it?  Well, you could look at the aortic valve Doppler and you could integrate the velocity across the aortic valve during systole times the area of the aortic valve orifice, and that  would give you stroke volume times heart rate would give you cardiac output. I suppose you could carefully measure stroke volume from, say, Simpson's end diastolic volume and end  systolic volume and get cardiac output that way, but that's going to take way too long and is not used. And really, the final point I want to make here is, I believe, an important  one, which is that the time delay that you take in doing a bedside echo could be detrimental. So think about what you're doing. And this brings me back to the original point, which  is you need a strategy that walks you quickly through the questions that you must ask and answer. So time delay is bad. Let's just look at the sepsis patients, for example. In no  POCUS study, the mortality rate was about 30%. Now, if you do a POCUS study with a bunch of measurements and stuff like that, before you really get going on your resuscitation  of patients, mortality rate jumped up to 44%. Alternatively, if you clinically assessed your patient, got started with your resuscitation, and then, once things were underway, went  back in with your POCUS exam, mortality rate does not increase, and you have more information.  But the main point here is, you don't dither around with your ultrasound probe. You need a focused approach, and you need to get on with the patient's resuscitation if you want  good outcomes. So, in summary, a point-of-care ultrasound to assess left ventricular systolic  function needs to fit into a strategy, a goal-directed approach, and I gave you a shock mnemonic  with questions to show you how that might happen. I wanted to make the point that left ventricular ejection fraction is influenced by more than just contractility. It's kind  of a dirty measurement, and so you must consider afterload, which, when elevated, would decrease  ejection fraction, which, when decreased, would artificially increase your measure of ejection fraction. You need to think about diastolic dysfunction. You need to think about  whether the drugs you're infusing could alter contractility, inotropes, and, for example, beta blockers going the other way. Then measures that are among many include these ejection  fraction tissue Doppler measurements in the future, speckle tracking, and old-school systolic time intervals. Cardiac output, a number of ways of measuring it, may not be  perfect, and the key point is the time delay that you take in making a whole bunch of weird  measurements may adversely affect your patient's outcome, so you need, once again, point number  one, to be goal-directed. You need a strategy to think through it, so thank you for your attention.  Hello, I'm Cliff Grayson. I'm Associate Professor of Medicine at the University of Colorado School of Medicine and a staff cardiologist at the Rocky Mountain Regional VA Medical  Center. I have no industry relationships to disclose. I spend a lot of time in the echo lab explaining to internists and family practitioners why they shouldn't care about  diastolic dysfunction. Generally, there's nothing they should be doing differently in  most outpatients that they wouldn't be doing anyway. Pulmonary doctors love diastolic dysfunction  because they deal with a lot of dyspnea that doesn't seem to be explained by lung disease  or can't be effectively managed using standard therapy, but for the most part, once we offer  an opinion, they pretty much ignore us anyway. Diastolic dysfunction is really interesting to cardiologists, largely because we don't know how to define it, don't yet understand  how to measure it, and still don't know what to do about it. That provides a lot of space for opinion pieces and application of what we euphemistically call clinical judgment.  Not sure we do much useful with the information. Hospitalists and critical care specialists,  though, do need to care about diastolic dysfunction or diastolic function because abnormalities  of diastolic function or normal but maladaptive responses of diastolic function arise commonly in critically ill patients. Over the next 12 to 15 minutes, I'm going to talk about  how echocardiography can provide some insight into what's going on. Assessing diastolic function in the outpatient setting and the quiet and controlled setting of the echo lab  is quite a different matter from assessing it in the ICU. In the outpatient setting, we're often trying to explain subtle signs of heart failure or dyspnea on exertion. In  the ICU, the main questions we're usually asked are, why can't my patient breathe and  why is my patient edematous? Let's deal with the second point first. You don't need echocardiography  to tell if edema is from diastolic dysfunction. Assess the central venous pressure. Look at  the jugular veins or measure it through a central line. If it's low, the edema has nothing to do with the heart. If it's high, it might be cardiogenic, but there's nothing else to  be done with cardiac imaging that can prove or disprove that. That leaves us with the one important question in the ICU related to diastolic function. Why can't my patient  breathe? Echocardiography can provide clues here, but the question that we actually can answer and that my colleagues really should be asking more often is not so much, is there  diastolic dysfunction as much as what is the left atrial pressure? That's because what we're almost invariably worried about is whether pulmonary infiltrates are cardiogenic. While  cardiogenic pulmonary edema can be caused by all sorts of cardiac abnormalities, elevated left atrial pressure is always the common final denominator. Direct assessment of left  atrial pressure, for example, using a pulmonary catheter, may be required for definitive diagnosis,  but echocardiography can provide clues. Because left atrial pressure is the central question for the rest of this talk, we're going to be focusing on the left atrium more than on  the left ventricle. So let's go back to first-year medical school. There are a number of related  but different ways to think about LV and LA function. We can describe it in terms of changes in pressure, flow, size, shape, and movement. Pressure measurements have been central to  evaluating diastolic function since the beginning of cardiac physiology. Left ventricular pressure  and left atrial pressure look something like this in the top tracing. You have an increase in pressure over a short period of time, ejection, rapid relaxation, atrial kick,  and then now the cycle begins. The rate of relaxation of LV pressure, the so-called tau, between the two vertical black lines, is an index of early diastolic function, but it's  actually not all that helpful in identifying the cause of pulmonary edema and can't be used to reliably estimate left atrial pressure. What we really want to know is the actual  left atrial pressure in the bottom tracing. Notice it doesn't actually change very much. Unfortunately, unless we put catheters into the LV and the left atrium or measure it through  the pulmonary circulation, we can't measure it directly. From the echocardiographer's point of view, one thing that we can measure is LV filling, which you see now in the lowest  tracing here. Let's take a closer look at LV filling. In this diagram, we're looking at LV volume, not pressure. Immediately after the mitral valve opens, there's this rapid  inrush of blood, the so-called early rapid filling phase. There's usually a period of slow filling after that while blood flow continues from the pulmonary veins through the open  mitral valve called diastasis. There's a little kick from atrial contraction if the patient is in sinus rhythm. Velocity of blood flow is one of the things we can directly measure  using echocardiography. Because the volume is changing quickly in early diastole, the velocity of inflow is also rapid. In most cases, atrial kick isn't all that important,  leading to a smaller change in ventricular volume and a smaller inflow velocity. That's the A wave. If left atrial pressure is low, that early inrush of blood will be relatively  slow, leading to a low E wave. High atrial pressure causes more rapid filling and hence  higher velocity inflow. That's why early diastolic inflow, or E wave velocity, is a crude estimator  of left atrial pressure. Here's what it actually looks like in practice. You can see the initiation  of systole with the QRS complex down below, then end of systole at the end of T wave, then early rapid filling represented by the E wave, and late atrial filling represented  by the A wave. It's actually usually possible to make these measurements even in sick patients  in the intensive care unit. The other thing we can assess is myocardial motion. This is where tissue Doppler comes in. Tissue Doppler is really nothing more than looking at muscle  movement. During contraction and systolic ejection, the mitral annular plane moves towards the apex. We used to call this the descent of the base. Focus in on the part  of the tracing right after the mitral valve opens, marked by the vertical red bar. During relaxation, simultaneous with LV filling, the annular plane, mitral annular plane, moves  back upward. To assess movement, we use tissue Doppler, which is just using different settings  on the echo machine, that allow us to measure the lower velocity movements in myocardium. As a point of reference, blood typically moves at around 100 centimeters per second, while  the mitral annulus here is moving at 13 centimeters per second. A generally useful measurement,  as we'll look at in a moment, is of the mitral annular plane. Here we're measuring the E  prime, or early mitral plane diastolic movement, and the A prime, or the mitral plane movement  related to atrial contraction. This is more or less the same way we would measure TAPSY for RV function, but here we're measuring velocity of movement, not excursion or distance.  Fast-moving tissue is usually healthy tissue, and slow-moving tissue tends to be sick, which  is why low E prime, or at least E prime that's low in comparison with blood flow velocity, is a marker for relaxation abnormalities. You can see the relationship between both  of these here. This shows the timing relationship between early mitral inflow and the upward  movement of the mitral annulus. You won't be surprised to hear there's a strong relationship  between these two signals, because healthy hearts have high E prime, i.e. the heart relaxes  quickly, and don't have high left atrial pressure, i.e. the E wave is low. A low E to E prime,  here it's marked EA, now we call it E prime, is an indication that left atrial pressure is probably low. There are even more complex ways of assessing movement and atrial function  that seem to perform better in some studies. Contraction of the atrial wall, quantified by longitudinal percentage and change in length, known as strain, can be quantified  if you can obtain adequate views and if you have speckle tracking software. But this can be quite difficult and unreliable in a critical care setting, and it's also not helpful at  all in patients with atrial fibrillation or significant mitral valve disease. While there's a great deal of focus in the echo community on various indices of blood movement, let's  not forget that echocardiography started off as a means of measuring shape and size. Atria that are exposed to chronically elevated pressure tend to dilate, so the first clue  that we might be dealing with a problem of left atrial pressure is that the left atrium is enlarged. The easiest and most reliable way to measure that in the ICU is with simple  linear dimensions. This can be done both by M mode, and yes that is still a thing, or 2D. As a rule of thumb, if the left atrium looks bigger than the aortic root, you may  have a dilated left atrium. Current guidelines emphasize atrial volume, ideally indexed to  body size. If you can make these measurements in the ICU, you should, but they require better  imaging than commonly can be obtained in critically ill patients. For the measurements to be meaningful, you need pretty good imaging. Garbage in, garbage out  becomes a bigger problem the more complicated the measurements and calculations are. In particular, since volume measurements are related to the cube of the distance measurements,  small errors in measurement lead to big errors in calculated volume. By the way, take a look at  what's being measured here. Just like they taught you in kindergarten, it's important not to draw  outside the lines and don't include anything beyond the mitral annulus. Many, many sonographers trace the mitral leaflets, leading to significant overestimation of atrial size.  I told you we can't measure absolute pressure with echocardiography directly, but acceleration of blood across an orifice is related to the pressure difference between the  separated chambers. That's the basis using the Bernoulli equation for estimating RV pressure  from tricuspid regurgitation jet velocity, shown here. Elevated RV pressure comes from either abnormalities of the pulmonary circulation or from elevations in left atrial pressure.  If there's no pulmonary disease, we can assume that pulmonary hypertension is due to high left  atrial pressure. Unfortunately for most patients in the ICU, we're worried about respiratory failure.  We can't reliably distinguish between these, so TR velocity is not a reliable indicator of left  atrial pressure in patients with respiratory failure. In fact, the guidelines explicitly say TR jet velocity should not be used in patients with significant lung disease.  So just to review, what echo can measure is dimension, tissue movement, and flow velocity.  That's it. It can't measure left atrial pressure directly, and in the settings that we're generally  interested, the pressure measurements it can make actually aren't all that useful. That pretty much  leaves us with just a few measurements that actually are useful. Basically, mitral inflow  velocities and atrial size. Now, if both of these things are normal, we are pretty much done. We can say it's unlikely that significantly elevated left atrial pressure is the major  cause of respiratory failure in this patient. If either of them is abnormal, if there are other  strong reasons to suspect significant diastolic dysfunction despite these, such as severe  hypertrophic cardiomyopathy, we can move on to the next step. Once we've concluded we might be  dealing with left atrial pressure that's high, we can try to confirm or refute it. This shows the  contemporary recommended algorithm for how to estimate LD filling pressure in the echo lab  in outpatients. The evidence is reasonable that most patients with very low E to A ratio have low  left atrial pressure, and patients with very high E to A ratio have high left atrial pressure.  Unfortunately, a large number of patients fall into an intermediate category. Despite this being  a guideline recommendation, actually, there's not very much data to show that it actually works too  well. Another problem with the guidelines is that there's no guidance as to how to resolve conflicting data. For example, to get to this point in the algorithm in the first place,  we should already have evidence of left atrial pressure overload. In critically ill patients,  that's probably going to be because the E to E prime ratio is high. And how often would we see  a high E to E prime ratio and a low E to A ratio? Not often. So it's actually not all that clear  that adding E to A to the E to E prime actually gives better estimates, because most of the time  there's going to be concordance between them. Fortunately for patients with reduced LD function,  a very high E to E prime or high E to A are strongly supportive of abnormally elevated left  atrial pressure. And conversely, we almost never see high left atrial pressure with very low E to E  prime or E to A reversal. For patients with normal LD function, E to E prime and E to A correlate  with left atrial pressure a little bit, but not nearly as well. So how well do these all actually  correlate? Here are data from the original publication by Ominet-Al, where they actually  directly measured LD diastolic filling pressure with a catheter and compared it to the E to E  prime ratio. And you can see there's pretty good reliability for patients with reduced EF,  the open circles, for very low on the left or very high on the right E to E prime. For patients with  normal EF, the relationship is less robust, but there's still one. In the middle, not so much.  There have been a number of subsequent studies that have done direct catheter assessment of  pressure versus these various indices, but there isn't really any that shifted the needle on this  very much. Now, unfortunately, none of the other measurements really work. You can see the correctly classified patients is somewhere hovering around 50%, which is basically a flip  of the coin. All right, assuming we've determined that left atrial pressure is high, the second most  common question that we're trying to answer using a non-invasive method is, what will happen if I  increase or decrease the left atrial pressure? Depending on where we are on the LD pressure  volume curve, an increase or a decrease in left ventricular volume might lead to a large or a  small increase in left atrial pressure, but might not lead to a meaningful change in cardiac output.  These questions relate to fluid responsiveness, and they are directly tied to diastolic function.  That's because the shape and position of the diastolic function curve directly affect whether  there's going to be fluid responsiveness. Of course, that's assuming that the fluid we might  give can get to the left side of the heart. On the normal curve in the right panel, V, assuming we're  starting at a normal filling pressure on the left side of that curve, a large increase in end-diastolic  volume will increase cardiac output with only a small increment in left atrial pressure, but if  we're already high up on the normal curve, or if we're moderately to the right on the heart failure  curve in panel A, there may be very limited ability to enhance cardiac output using an increase in volume because it'll lead to a large increase in left atrial pressure and cause  pulmonary edema. An important point here is that it doesn't really matter whether there's some  intrinsic diastolic dysfunction or not, regardless of whether we're on a heart failure curve or a  normal curve. If we're too far along on the curve, there's going to be minimal benefit to increasing  volume in terms of increasing cardiac output. Echocardiography can be useful for assessing fluid  responsiveness. The main technique is to use changes in the left ventricular outflow tract  velocity time integral, or VTI, to assess the response to a fluid challenge. The VTI basically  tells us how much fluid is being injected on each beat, and because dimensions of the heart don't  change appreciably between the measurements, you actually don't need to measure LVOT diameter.  Measure the VTI, then either give a small rapid bolus of fluid or simulate a fluid bolus with a  positional change that enhances venous return. This could be a passive leg lift or shifting into  Trendelenburg. Then measure the VTI immediately after. You do need excellent imaging and clear  Doppler recordings for this to be useful. Of course, fluid responsiveness also depends on the RB and pulmonary circulation, but echocardiography will provide some clues about  whether right heart failure or pulmonary hypertension might be confounding the measurements.  So in summary, the main role for echocardiography in assessing the impact of diastolic dysfunction  in critically ill patients is estimation of left atrial pressure. Findings that suggest  that left atrial pressure is abnormally elevated include left atrial enlargement, elevated RV pressure in the absence of primary lung abnormalities, low mitral annulus velocity,  or high early mitral inflow velocity. But remember the Doppler indices do not make the diagnosis.  You still have to use what you know about your patient. If you're in an intermediate zone and  aren't sure if diastolic dysfunction might be hurting you, echocardiographic assessment of  fluid responsiveness may be helpful. Hi, I'm Steve Hollenberg from Hackensack Meridian School  of Medicine. And if you'll indulge me, I'm going to be pinch hitting for Dr. Monet. So I'm actually  sharing my screen in a Zoom setting. This is actually live, and I'm hoping this works out.  And I'm going to talk about imaging the right ventricle. I have no disclosures with respect to  this talk. So with respect to RV imaging by echocardiography, we'll talk about modalities,  and we'll talk a little bit about the information that you can obtain. And the echocardiographic  modalities to be discussed are two-dimensional echocardiography, Doppler echocardiography,  and then a little bit about three-dimensional echocardiography. And what you get is information about structure, size, mass, geometry, and interactions between the right and left  ventricle, and also about function, right ventricular systolic function, and also the coupling of the right ventricle to the pulmonary circulation, and to some extent to the left  ventricle. So the right ventricle goes back a long way. Those of you who recognize mirror handwriting  will recognize that this is Leonardo da Vinci, and the first drawings and descriptions of the  right ventricle came out of da Vinci's notebooks. And what da Vinci recognized, and which I'm sure  you all know, is that the right ventricle is a complicated structure, and it has three portions.  It has an inflow tract, it has an apical portion, and it has an infundibulum, and the blood flows  from the tricuspid valve through the inflow tract into the apex and out through the infundibulum,  and the pulmonic valve. So it's a complicated geometry, as you can see on this slide. This is a  view of the left and right ventricle, and you can see that the right ventricle is thinner than the  left ventricle. It is more trabeculated than the right ventricle. That MB there is the moderator  band, and it is, at least in that cross-sectional view, it's crescentic. So whereas the left  ventricle is, it looks more or less like a bullet, right ventricular shape is much more complicated,  and this poses challenges in estimating size and function of the right ventricle.  So here's the old school view. So the old school is that the right ventricle shouldn't look bigger  than the left ventricle in two out of three views, and you look at the radial and longitudinal motion,  and you say, what does the right ventricle look like, and we're done. Yeah, the right ventricle  is kind of the right size, and its function is normal, or it's somewhat dilated, and the function  is a little down. So this is a little bit like characterizing things in broad categories.  Here we have small, medium, or large, and I think it's pretty clear that the large is bigger than  the small, and the medium is somewhere in between, but it doesn't allow for a lot of distinction in  between, and this is kind of what you get with mild, moderate, or severe. Severe is worse than  mild. Moderate is somewhere in between, but it doesn't really allow for much distinction, and in particular, it is really challenging when you start talking about changes over time  in the individual patient. Is there a better way to do this? Well, I think so, and I'm going to  try to take you through some of those measures. Many of this comes from Guidelines for Echocardiographic  Assessment of the Right Heart in Adults. This is the American Society of Echocardiography, along  with the European Association of Echocardiography, and this publication was out in 2010. There's an  update of chamber quantitation in 2015. So let's talk about measuring right ventricular size.  Up on the top, you see the three dimensions in diagrammatic form and then in an image. You have  the right ventricular dimension at the valve orifice. You have mid-ventricular right ventricular dimension, RVD2, and you have the longitudinal dimension of the right ventricle.  So down on the left, what you can see is that, at least in that short axis, in that parasternal  short axis view, what you get, the impression you get of the right ventricle is very determined,  very much determined by the plane that you're cutting through the right ventricle, and what you  can see on the bottom is when, if you cut through three different planes, you get three different  impressions of the size of the right ventricle, and this really poses challenge for figuring out  how big the right ventricle really is. On the right, what you see is the usual apical four-chamber  view on the bottom, and what you'd really like to get is what's called an RV-focused apical  four-chamber. You want to open it up a little bit, you want to get a better assessment of true right  ventricular dimensions. The bottom line is that this isn't so easy to do, and it takes a little  bit of practice and a little bit of experience to get it right. Here are the right ventricular  dimensions from that diagram in 2010 and updated in 2015. What you see is there are all sorts of  dimensions that you can look at, etc., etc. Simplified, there are really four that you that you might want to know. The basal diameter at the base where the valve greater than 42  millimeters is abnormal, the mid-cavity diameter greater than 35 is abnormal, the length greater  than 86 millimeters is abnormal, and RV wall thickness greater than 5 millimeters is abnormal.  You should recognize that these values are not indexed to body size, so you might have to be careful when looking at patients with different body habitus. There's also ventricular  interdependence, as you know. Here's a normal heart on the left with a normal RV and LV pressure, and  what you see on the right is that as RV pressure increases, that pressure pushes against the septum  and it flattens the septum. Interestingly enough, it also increases, it compresses the LV and can  increase LV diastolic pressure from this example from 8 up to 18, but you get a flattening of the  septum with right ventricular pressure overload. You can actually quantitate that by something  called an eccentricity index, and this is an eccentricity index of the left ventricle, and you  have the anterior-posterior dimension and the septolateral dimension, and as you can see, normally  those are usually about the same. The left ventricle in this view is circular, but as you get a  D-shaped septum, as you push that septum toward the left ventricle, then you get the AP diameter is greater than the septolateral diameter, and you get a different ratio in  pulmonary hypertension. You could use the ratio as a number, although it's usually pretty obvious when  you see a D-shaped septum. Now there are a number of ways of evaluating right ventricular function  by echocardiography and methods of quantitating as opposed to just eyeballing. There's fractional  area change, there's the tissue Doppler S wave, there's a tricuspid annular plane systolic  excursion. I spelled it out on the slide so I can remember what it was. Everybody, including myself,  knows it is TAPSE, and there's the right ventricular myocardial performance index, which is a time  interval as Dr. Wally alluded to in his talk. There are also newer modalities that we're going  to mention, three-dimensional echo ejection fraction, right ventricular strain imaging, you  heard a little bit about left ventricular strain imaging, and you also heard a little bit about  spectacle tracking. So here is TAPSE, and this is basically the movement of the annular plane  toward the apex with right ventricular contraction. It's longitudinal motion of the right  ventricle, and what you can see on the M mode there is that you can measure the TAPSE, and normal  is greater than something along the lines of 20 millimeters. And when the right ventricle doesn't  contract quite so well, the longitudinal motion is decreased, and on the right you see a reduced  TAPSE. This is actually predictive of mortality. You see a paper out of Paul Forfia in 2006 looking at an overall cohort of patients with pulmonary arterial hypertension,  and what you can see is that a cutoff value of 18 millimeters of 1.8 centimeters of TAPSE distinguished patients with good survival from patients with worse survival in this study.  There's also myocardial strain. On the left is the definition of strain, and a shortening muscle  has a negative strain. That is the shortened length minus the resting length is a negative  number, and this can be measured in a number of directions, longitudinal, rotational, and radial,  and circumferential, and a normal value strain is negative 20 percent, and basically anything  less negative than minus 16 is abnormal in a number of contexts. It's a little complicated  with different software, but we're going to leave it at that. So here's a measure of myocardial  strain on the left, and what you can do is the strain packages are basically built for the left  ventricle, and what you can do is essentially draw the right ventricle instead of the left  ventricle and fool the software into thinking it's looking at the left ventricle and measuring  that as strain. The problem with strain is that it's load sensitive. Reproducibility is very much  an issue. You see these sort of squiggly lines on the right, and it's not immediately obvious where to measure them. It's less well validated, certainly on the right side than left,  and another challenge is that different vendors use slightly different methods, and they get  slightly different cutoffs, and so while in a particular lab that's relatively consistent using different vendors or even different machines, and some labs have two different  machines, can get you two slightly different values. All that said, right ventricular strain does  seem to correlate with prognosis here. There's a proportion of with strain less than 12.5,  there was more symptom progression, there was more edema despite loop diuretics, there were higher  loop diuretic doses, and there was lower survival at follow-up. Now probably the best way to get  right ventricular volumes and ejection fraction is by three-dimensional echo. It's pretty difficult  to do with a two-dimensional echo. You can do it in a number of planes, but because of the complicated  shape of the right ventricle, it's crescentic in some views, it's circular, it's elliptical in other  views, it's pretty hard to do. Three-dimensional echo is the way of trying to measure all that  without making geometric assumptions. All that said, it's a lot harder to do this in the right  ventricle than it is in the left ventricle. I'd like to talk a little bit about pressure and function coupling, and this is a diagram of coupling between the right ventricle and the  pulmonary artery. What you can see is as pulmonary artery pressure in the green  rises, cardiac output stays the same for a while, and then eventually the right ventricle decompensates.  As the right ventricle decompensates, eventually cardiac output drops off, and when cardiac output  drops off, pulmonary artery pressure drops off. You can imagine you could be at the same pulmonary  artery pressure and not know whether you're on the ascending loop of this curve or on the  descending loop where you're in big trouble if you're just looking at pressure without relating  that to right ventricular function. There is something called the TAPC pulmonary artery  systolic pressure ratio, and if you think about it, TAPC is a measure of right ventricular systolic  performance and pulmonary artery pressure, so if the performance is good and the pressure is low,  then that number is high and that's good. If the performance is bad and the pressure is high,  then that number is low and that's bad, and as you can see, as this ratio goes less than 0.36 in this  study, then prognosis in terms of survival worsens. Another way of doing it, and a more elegant way of doing it, is actually to look at notching of the right ventricular outflow  tract tracing. So this is the tracing in the outflow tract across the pulmonic valve. You get  an envelope, a flow envelope, just like you do through the aortic valve, and normally this is a  parabolic envelope. It's a laminar envelope and you can see two examples of normal envelopes in A  and B on the left. When you have pulmonary arterial wave reflection, that is when pulmonary artery  pressure is high, you get wave reflection in the middle of ejection and that notches the way,  notches the outflow tract tracing, and you can see that in the arrow A and B on the right. This suggests poor vascular compliance and increased pulmonary vascular resistance. Again,  a measure of high pulmonary artery pressure. So you can sort of make a little bit of a two-by-two  table. What is TAPSE and whether there's right ventricular outflow notching. If you don't have  a notch and your TAPSE is normal, then you're in the green zone, everything is fine. If you don't  have a notch but your TAPSE is low, then your pulmonary pressure is okay, but your right ventricle  is dysfunctional. If you have a normal TAPSE, that is normal function, but you have notching,  then you have afterload mismatch, that is you have elevated pulmonary pressure but your ventricle is  still hanging in there. And if you have notching and low TAPSE, now you have both RV dysfunction  and afterload mismatch. So probably the best way to look at right ventricular function is by cardiac  MRI. And I know this is an echo talk, but I thought I'd at least mention the role of cardiac MRI.  It gives you a good look at right ventricular function and morphology. You can look at pulmonary  artery flow and to some extent angiography in some context. You can do tissue characterization  with specialized techniques. You can look at perfusion, but you can also look at late gandolinium enhancement and myocardial fibrosis with cardiac MRI. In terms of just  right ventricular performance per se, cardiac MRI is the gold standard for right ventricular volumes,  fractional area change, and right ventricular ejection fraction. It's more reproducible. It measures not only longitudinal shortening, but also transverse shortening of the right  ventricle. Remember, TAPSE only measures longitudinal shortening, not transverse shortening. And there are no, at least very fewer issues with poor windows. And so it's a more  precise and better way to assess treatment efficacy. So it's promising. Techniques are  evolving to assess exercise responsive strain and to characterize tissue more precisely. However,  most of the data are derived from cohorts that are enriched in pulmonary hypertension. Most of the  data are based on right ventricular remodeling and thus advanced pulmonary hypertension. It's pretty  hard to do in an ICU patient road tripping a guy on a ventilator into an MRI and worrying that you  don't have any magnetic devices. And it's unproven in a certain number of contexts, screening early  disease, group two pulmonary hypertension, and yes, sort of unproven in the ICU as well. So in  summary, you can go with small, medium, and large, mild, moderate, and severe. But as your practice  evolves, you're probably better to try to get yourself into familiarity at least with more  sophisticated ways of assessing right ventricular function, looking at things like TAPSE, looking at  three-dimensional studies, trying to do speckle tracking or strain imaging to assess right  ventricular performance in a more sensitive fashion. So you want to quantify right ventricular  size. You probably want to get into the habit of doing routine TAPSE and right ventricular  tissue Doppler. Three-dimensional echo may be better for volumes and ejection and traction.  MRI is the most precise way to assess right ventricular performance, but it's not always easy  to do. Strain responses and exercise responses may be more sensitive for subclinical or more  subtle right ventricular dysfunction. And whatever you do, you want to immigrate imaging with physiology.  So to conclude, I hope you're thinking something like this. This is a quote from Enrico Fermi,  one of my favorites. Before I came here, I was confused about this subject. Having listened to  your lecture, I am still confused, but on a higher level. So I hope your confusion is on a slightly higher level. Thank you very much.  Jose, you want to introduce yourself? All right. So, my name is Jose Diaz Gomez, as many of you know, I'm the Congress co-chair.  I have this immense privilege to be part of this moderation, and let's try to celebrate something right now. This is for all membership.  Right now, you have this group of individuals, which are, half of them are cardiology-trained  imaging specialists, and you have the other half, including myself, who are not primarily imaging specialists.  But we all share something, which is, we take care of critically ill patients. So, I really believe this is a unique session, and it is my pleasure to have Dr. Hollenberg  as the main driver of this session. And my two colleagues are Dr. Hernandez and Dr. Hsu, both of them have been in leadership  positions within SCCM, and they are very well-respected individuals in critical care ultrasonography. So, hopefully, people will ask questions.  I thought I would start by asking both Dr. Wally and Dr. Grayson, you have cardiology backgrounds, but also critical care backgrounds.  So, I wonder if you could talk a little bit about differences in echocardiographic assessment  in a classic coronary care unit setting with cardiac patients from a general ICU setting. Cliff, you want to go first?  Yeah, I think it's really, really hard to do quantitative echocardiography in the intensive care unit. It's really, really hard in the outpatient echocardiography laboratory.  Many of our patients in the VA Medical Center have lung disease, they're obese, they're having positioning problems, they have bad lung windows, bad acoustic windows, and making  even basic measurements can be very, very difficult. And to assess diastolic dysfunction, even in the outpatient setting, requires excellent  imaging and excellent Doppler measurements. And those things are often difficult or impossible to do in the intensive care unit.  So, I think that we really need to focus on what's germane to the immediate problems that we're dealing with in the intensive care unit.  And for the most part, we're trying to find, in terms of diastolic dysfunction, we're trying to understand what the left atrial pressure is, and we really don't care about the more  subtle grades of diastolic dysfunction, for example. We're really looking for basic stuff that we can do in sick patients who may be on ventilators  or dyspneic, they may be in atrial fibrillation with high heart rates, all the things that make the more quantitative measurements difficult or impossible.  So I think focusing on what you can do reliably is key. Yeah, I agree completely with that. For me, there are two very separate interventions.  One is a bedside echo, which is a question and answering process, and then there's a comprehensive echo. And look, I use them both.  To me, the bedside echo, you have to have a specific question and you go and answer it. And it's a clinical question. Your question could be, is my patient hypovolemic or not?  And there are a whole bunch of approaches. You can look at the IVC, but it depends on whether the patient's breathing spontaneously or not.  Hey, Dr. Grayson pointed out, you can examine the jugular veins. This is actually really important.  And you can look at the size of the ventricles to get a sense, is this patient empty or full? But the point there was you had a specific question.  Another specific question could be, is the ventricle functioning normally? And again, we went through a whole bunch of different ways you could look at that.  You probably want quite a simple way and answer that question. It's very important that you have a question and answering structure for bedside echo.  And it's very important that you get good at what you use a lot. So for example, you say, hey, maybe this guy has some aortic stenosis and you're sitting  there in the ICU and you put a measure of velocity across the aortic valve. Well, it could give you a hint.  But if you're no good at it, if you haven't done it all the time, it's going to be pretty close to hopeless information. And what you need then is a comprehensive echo.  So that's a completely different tool and it has a different use.  Yes, you can direct questions to the echocardiographer who does it. But they're going to go through a little bit of a stereotyped exam.  And for example, they will look at the aortic valve velocity and they will look at it from three different windows.  And in some instances, they'll use a CW probe, you know, supersternal notch, to get it right. That's something that very few of us would be able to do properly.  So there are two different tools. Bedside echo is a question answering device. And a comprehensive echo is to give you a much broader understanding of everything that's going on.  You've got to get good at what you're going to use because, you know, measuring things that you're not good at is not going to be helpful for your decision making or for your  patient.  Yeah, I'm going to inject just a little bit of bias and with a little bit of pedantry here. My own preferred term is focused echocardiography.  Because, I mean, you know, bedside is where the echo is done pretty much all the time. Patients usually aren't standing up, right?  So I like the term focused echocardiography to make precisely the point that you made, Dr. Wally, which is that you're focusing on a clinical question.  And as you both said, there is a time urgency. You need to know the answer to this question now so that you can treat your patient.  If you don't and you can wait for a comprehensive echo or the question would take a comprehensive echo to answer, then you ought to get a comprehensive echo.  I don't know any doctors at all who are as good as any of the echo techs I know at doing echocardiography.  And I'm sure that no Dr. Wally will agree because he knows a couple of very good echo techs. Jose. I raise my hand. I love this starting point.  You just said focused echocardiography and comprehensive echocardiography. An hour ago, we have our wonderful Dr. Hernandez mentioning something that's called limited  echocardiography. Would you welcome that term? And if so, I will allow Dr. Hernandez to give his input in that regard. Well, this sounds like a good debate.  I'll take one side and then I'll be shown to be completely wrong. And I'm totally fine with that. I've lived my life being completely wrong. I don't think it's a limited echo.  It's goal-directed. You have to have a question. You've got to answer the question. And if you order a comprehensive echo, it won't meet the needs at the bedside in the  emergency department of answering the clinical question. Why? It's going to take half an hour for the echo tech to come down and all that kind of stuff to get a comprehensive echo.  So it's not limited. It's focused on a specific question and an answer. It never attempts to give a comprehensive evaluation. And so I argue it's not limited, it's very focused.  So your society, our society actually, and fellow of that society as well, the American Society of Echocardiography, came out with that paper making a specific definition of  focused cardio-ultrasound. They make a contrast between focused cardio-ultrasound, limited trans-thoracic echo, and comprehensive echo. And that's what I was alluding to.  So what it takes, the difference between limited trans-thoracic echo and comprehensive echo is only the fact that you are making the same diagnosis with lower number of views.  So that implies that the person who is doing a limited TTE doesn't mean it's less skillful. Actually it has to be more skillful because it has to make the call with less views.  And that's kind of the world that we live in the ICU at 3 a.m. in the morning where the comprehensive echo is not practical for critical care in America.  And that's the reason we try to be something in between. Of course, a person like you will be our leader that we should follow work for comprehensive echo.  But from the practical standpoint, we need that presence of that skillset in a 24-7 basis at the bedside. Dr. Hernandez, I don't know if you want to mention anything about it.  So I agree with Dr. Wally's comments in that you just want to answer a question. You know, the whole comprehensive nature of the exam is valuable, but probably not practical  in that setting.  I would say that I do ask, so the National Board of Echocardiography has opened this critical care echocardiography pathway. And so now there's all these terms, right?  It's like we're all, there's this like word soup and nobody really knows what, you know, is it POCUS? Is it, what is it?  So it's confusing, but I would say that at least for intensivists, and I made a comment about this earlier, is that if you can, some institutions, and I would say ours is not  different. Ours is trying to change it a little bit. So if you can hold a probe, people are going to start doing these exams.  And so I do ask that they share some quantitative analysis because I have had people try to initiate therapies on patients for an IBC exam when the patient was in a chair because  they're oligarchic. I'm like, hold on here. That's not how the authors did the trial. Well, you know, you have to assume the exact same conditions the authors did if you want  to get the same result. It's like baking a cake. You need the same exact ingredients. So I do encourage them.  In fact, I request like, if you're going to do this, show me some quantitative analysis.  It doesn't have to be big, but something that's going to convince somebody else to say, yeah, you probably know what you're doing.  You know, even if it's basic, because otherwise we're sort of just having to go on the honor system and I think our patients deserve more than that.  So Dr. Hollenberg, in your opinion as our expert, and Dr. Grayson, Dr. Wiley, in which specific settings, in which specific medical conditions would you advise to any intensivist  in this country that they should order a comprehensive echo instead of a focused cardiac ultrasound?  Well, so, you know, to me, to me, the answer is how quickly do you have to answer the question?  So to me, focused echocardiography is I need an answer to a specific question and I need it faster than I can get an echo tech here, because I know the echo tech study is going  to be better. And frankly, the echo tech is coming to my unit with me standing there telling them what I want.  And I guess my definition of limited echo is, okay, don't spend half an hour looking at the pulmonic valve velocities. I don't care about that.  I want to know is the LV pumping, is the RV pumping, you know, get me a stroke volume across the aortic valve, whatever.  So to me, that's a limited echo as opposed to a protocolized comprehensive echo reporting 28 things with an echo tech. So and I guess my bias is sort of colored by my practice.  As I get better at looking at echocardiography and I learn what sort of things that I can get out of it, then I want more comprehensive echo.  And at least with respect to my talk, I hope one of the points is that the right ventricle is hard.  And so, you know, I think particularly for point of care, I can't get anywhere with a probe in the right ventricle.  I think you ought to be really cautious about interpreting a focused echocardiography that purports to say a lot about a right ventricle other than that it's enormous and it doesn't  pump at all or it's normal size and pumps okay. In between, there's a lot of room and if you really need to know that subtly, then  you need a comprehensive or an ultrasound tech style echo. With other things, you can see a big pericardial effusion.  I think it is really useful to see whether the left ventricle is filled or whether it's big and dysfunctional. There are an awful lot of uses.  I also would say that point of care ultrasound, I think it's slightly different from point of care echocardiography.  Point of care ultrasound says I can take my probe and I can look at other things.  I can look at lungs. I can figure out whether I got pulmonary edema. I can look at ascites, et cetera, et cetera. That's an ultrasound test. I can do that.  My echo tech can't do that. Point of care ultrasound is okay and that includes focused echocardiography if that makes any sense. That's great. Basically, we are coming together now.  We know we need to distinguish those. Basically the time is defining everything. I like that starting point. Let me ask you this.  There are a few units in the country that actually have established the presence of a cardiac sonographer in the ICU. What do you think of that model?  In order to gain more quantification, quantitation in the records in the ICU or you will invest more in the skill set making the critical care workforce be more skillful obtaining  the measurements when it's needed? I have an answer, but go for it, Cliff. I was going to say there are probably units that can justify having a dedicated sonographer.  If you can, great. Through all of this, I think it's really important to understand what the limitations of the  technique are. Coming back to what Keith said, going into this with a specific question, because there  are things that you simply are not going to be able to adequately answer with a focused or limited or less than comprehensive echo.  If your question is, does somebody have severe or moderate mitral regurgitation, hey, if  there were easy ways for us to make that diagnosis with a limited number of views, we'd be doing it already.  Just because it's being done in the intensive care unit doesn't mean that you can now do it.  No matter how skilled you are, there's a reason that you need a comprehensive exam to figure out whether somebody has moderate or severe MR or moderate or severe AS.  Those are questions that you are not going to be able to answer with limited skill sets and point of care or focused ultrasound.  The presence or absence of a large pericardial effusion is something, yes, that you can probably do.  But you need to have an ultrasonographer dedicated to the unit to answer that question. If you're in a CCU and you've got a lot of valvular heart disease coming in, maybe you  can justify it and maybe you need it. But I think you probably don't need that for the most part in the intensive care unit where  these are not the kinds of questions that you need to answer at the bedside. Thank you. So one of the things we've done in our ICU is make it a teaching issue for our residents  and typically our fellows. So we've been lucky, and this has sort of worked out, every month we have another fellow.  They're often anesthesia fellows, sometimes surgery, sometimes medicine. And the way we've formalized it is we kind of hired one of the echo techs from the echo  lab for two days a week. And she is a teacher then of the whole group, I mean, of the fellow, but also of us.  We have several of the attending physicians who are a little bit more expert, I would say, at echo than just average.  So there's a teaching group related to echo focus or focus in the ICU, and they go on rounds with us.  So at the bedside, yeah, we still look at the chest x-ray, the chest CT, but we also look at the cardiac ultrasound and the rest of the focus exam, which goes beyond ART.  That's worked out well for us, but we had to push that to make it work. Well, thank you. I'm going to let Dr. Hernandez get in there, and then I'd like to get some questions to  the audience. So Dr. Hernandez, you had a comment? Very briefly, when we started doing bedside ultrasound in the ICU, we had a communication  with our cardiology department, and there was some anxiety over it. But what I propose is that our approach would lead to more appropriate consultations.  And in fact, what ended up happening was that they had to hire another sonographer, because we were finding things, right?  We were finding things that nobody expected, and then there were more appropriate exams. And so it ended up being a really good synergistic relationship that ultimately ended up for  the betterment of the patients. All right. So we have a question out there about VEXUS scoring for assessing volume status.  I'm going to take the first crack at that and say it's not a cardiology thing. It's an ED thing. So any opinions from people who are cardiologists on VEXUS scoring?  No. Okay. Next question. How quickly would you expect E to E prime to change with changes in volume status? Well, I can take a crack at that.  I think it would change immediately, because the E wave velocity is directly related to the filling velocity, and if the volume status changes, that's going to change right away.  The E prime, which is more a characteristic of the quality of the myocardium, probably is not going to change much ever if you're not giving a patient inotropic agents, which  can quicken it or increase it. So I wouldn't expect changes in volume status to affect the E prime, but the E most certainly should be pretty quick. So minutes, probably. Yep.  I agree with that. There are a couple more questions on diastolic dysfunction. Two things. Actually, I think you're going to have an answer for both of these.  The first says that once diastolic dysfunction is found in a critically ill patient, are there any data that treating it improves outcomes?  Well, we don't know how to treat diastolic dysfunction, per se, if it's not being caused by something else. For example, ischemic heart disease causes diastolic dysfunction.  So if a patient is ischemic and they have diastolic dysfunction because of that, you treat the ischemia, but we'd be doing that anyway.  If a patient has hypertensive emergency, that's going to create diastolic dysfunction. And as I think I alluded to in the talk, this whole concept about diastolic dysfunction,  it really is more a matter of where you are on the diastolic filling curve. So if you have diastolic dysfunction because you're grossly volume overloaded, you're going  to reduce your volume and then you're going to be treating your diastolic dysfunction. So yes, you need to treat the things that are causing the diastolic dysfunction, but  we don't have a way to treat diastolic dysfunction, per se. Just a little bit. I absolutely agree with everything you said.  But just as a reminder, this steps a little outside of just an echo, but just a reminder  for everyone, if you are worried about diastolic filling of the LV impairing how your patient is doing, you do need to look at ventilator pressures and reduce those if possible.  You do need to look to see if there are big pleural effusions that might be contributing. You do need to think about intra-abdominal pressure and how you might position your patient  to reduce that. So these are outside of the realm, but there are a few things you still need to think about. All right. I'm afraid that we are out of time. One minute. Okay. Yeah.  So I would like to wrap up by thanking Dr. Wally and Dr. Grayson for the great talks. Thank you, Dr. Hernandez, Dr. Hsu, and Dr. Diaz-Gomez for being along.  There are ways to ask questions in the course of the meeting. There must be some way to do that. I'm not very technical, but I think it was a really interesting session.  I'd like to thank you all for participating, including the audience. Have a great rest of the day. Thank you. One last thing.  The last paper by James Kirkpatrick demonstrated how the ECHOLabs are supporting better intensivies in the United States.  This is all about collaboration. I just leave that message there. We need to come up together. I'm pretending to say that in five years we'll be in a better place. Thank you.  Very good.

Video Summary

The video discusses the challenges in assessing right ventricular (RV) function using echocardiography. It proposes more precise measures for evaluating RV size and function and explains various measurements that can be used. The importance of assessing RV interdependence and its impact on left ventricular function is highlighted. The presenters discuss different methods of quantitating RV function, including fractional area change, tissue Doppler S wave, and tricuspid annular plane systolic excursion (TAPSE). They also mention newer modalities such as three-dimensional echo ejection fraction and right ventricular strain imaging. The challenges of assessing RV function in the intensive care unit (ICU) are discussed, and the use of focused echocardiography in this setting is suggested. The benefits of having a dedicated cardiac sonographer in the ICU and the importance of collaboration between cardiology and critical care are also mentioned. Overall, the video provides insights into the assessment of RV function using echocardiography, particularly in the ICU setting.

Asset Subtitle

Procedures, Cardiovascular, 2021

Asset Caption

The Society of Critical Care Medicine's Critical Care Congress features internationally renowned faculty and content sessions highlighting the most up-to-date, evidence-based developments in critical care medicine. This is a presentation from the 2021 Critical Care Congress held virtually from January 31-February 12, 2021.

Learning Objectives

Recognize the complexity of echocardiographic assessment of cardiac performance
Discover the degree to which technical skill and advanced Doppler echocardiographic techniques are useful in achieving optimal evaluation of left and right systolic and diastolic dysfunction
Apply echocardiographic measurements to the formulation of therapeutic plans in different clinical situations, particular those with a degree of hemodynamic complexity

Left Ventricular Function and Cardiac Output
Keith R. Walley

Diastolic Performance
Cliff Greyson

Right Ventricular Performance
Steven M. Hollenberg

Meta Tag

Content Type Presentation

Knowledge Area Procedures

Knowledge Area Cardiovascular

Knowledge Level Advanced

Learning Pathway Cardiothoracic Critical Care

Membership Level Select

Tag Echocardiography

Tag Point of Care

Tag Ventricular Function

Tag Cardiothoracic Critical Care

Year 2021

Keywords

RV function

echocardiography

RV size

RV interdependence

left ventricular function

fractional area change

tissue Doppler S wave

tricuspid annular plane systolic excursion

three-dimensional echo ejection fraction

right ventricular strain imaging

intensive care unit

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