My name is Brandon Wiley, I'm an associate professor of medicine at Mayo Clinic in Rochester, Minnesota. I split my time between the cardiac ICU and the echocardiography laboratory, and I'm the director of point-of-care ultrasound for the Department of Cardiovascular Medicine. It's my pleasure today to talk about the use of ultrasonography in shock, and I want to thank the panel that I'm a part of, and thank the Society of Critical Care Medicine for giving me the opportunity to speak. Specifically, I'm going to talk about how we can use ultrasound to take the guesswork out of shock. So, let's start with a case that can demonstrate how important and how useful ultrasonography can be in a setting of undifferentiated shock. So, here we have a 76-year-old woman who presented with an acute stroke. Now, she had right-sided symptoms. She was within the window for lytic therapy, and so she received TPA. And then sometime later, while still in the emergency room, she became hypotensive, rapidly requiring norepinephrine. She had altered mental status and hypoxia, and then was intubated. So, what was going on? Well, if we apply bedside ultrasound, we can make a diagnosis. And what we see here quite clearly is that there is right ventricular systolic dysfunction, and the right ventricle is quite dilated. There is preservation of motion here at the apex of the right ventricle. This is the McConnell sign. And then we see in this image here really kind of the whole story. Here's the left ventricle, right ventricle here. There's a small, tiny little pericardial fusion, but we see something very, very abnormal here in the ascending aorta. And the reason this woman developed shock was because she had an aortic dissection, and that aortic dissection was the cause of her stroke. And then dissected into the right coronary artery, and she had an RV infarct. We can see in short axis here that dissection flap in the ascending aorta, which is incredibly dilated. So, I think that's a great case to show you how clinical ultrasound, also called point of care ultrasound, make critical care echo, bedside ultrasound, how the use of ultrasound can help you in the diagnosis of shock. Because with ultrasound, you're able to get not only an anatomic assessment, but a hemodynamic assessment of the situation. With ultrasound, you're able to guide therapeutics, and you're even able to provide some risk stratification. So, let's talk a little bit about the use of clinical ultrasound or point of care ultrasound in the diagnosis of shock, focusing on the anatomic assessment and Doppler hemodynamics. Now, this is a really nice paper coming from the Society of Echocardiography, the American Society of Echocardiography. And its guidelines for the use of echocardiography as a monitor for therapeutic intervention in adults. And the really nice thing it does here is it breaks down just how valuable echocardiography or ultrasound can be for the hemodynamic assessment of a patient. And this is just a small list of the hemodynamics you can get from echocardiography. I can't go through all of them, but you can really get the pressures in every chamber of the heart. You can even calculate the left ventricular stroke work index, cardiac power output. And if we see this comparison of a PA catheter versus echocardiography, we see that the advantage typically lies with echocardiography. So, you can get cardiac output with both echocardiography and a PA catheter, and they're about the same. And we'll show some studies for that. You definitely get better assessment of valvular function with echo. You can get assessment of obviously systolic and diastolic function with echo. And of course, this is non-invasive. Now I will caution that this table was written by echocardiographers, but we can see that echo and ultrasound is incredibly, incredibly helpful in this situation of caring for patients in the shock state. Now, when I think about the use of point-of-care ultrasound or clinical ultrasound in a patient with shock or hypotension, I think of a holistic approach, and that is to say a whole body or an integrated assessment of multiple organ system. And I include the cardiac, lung, abdominal, and vascular systems in this assessment. And again, ultrasound or echocardiography is non-invasive. It's readily available. You can take it right to the bedside. You can perform serial assessments. You can longitudinally monitor the patient. You can assess the patient when there's a dynamic change. And of course, it gives you anatomic and physiologic data. But I want to caution that clinical ultrasound or point-of-care ultrasound needs to be integrated into the clinical exam. The clinical presentation is important. And point-of-care ultrasound or clinical ultrasound is a goal-oriented exam, and it should be guided by the clinical presentation. And you should interpret the findings within that context of the clinical presentation. You should approach the patient with a pretest probability of what you think may be going on, and then use ultrasound to guide you in the right direction. So, when I apply this multi-organ system assessment in patients with shock or hypotension, I do it in a weighted approach. And my fundamental exam is the cardiac exam and the pulmonary exam, because this exam really defines the physiology of what I'm dealing with and directly helps guide therapy in that moment. And then my supplemental pieces in the exam are abdominal ultrasound and vascular ultrasound as guided by clinical presentation. And so, I think everyone is very familiar with this simplistic view of circulatory failure as being either normal or high output cardiac failure or low cardiac output, and then elevated filling pressures or low filling pressures. And I want to show how we can use cardiac ultrasound and pulmonary ultrasound and then vascular and limited abdominal ultrasound to solve the riddle of the patient who's presenting with circulatory failure. So, the first step, again, is using that fundamental cardiac exam, that fundamental cardiac ultrasound, to tell us something about the hemodynamics that we're dealing with. And we want to think about stroke volume. We want to think about cardiac output so that we can categorize the patient in front of us. And then, of course, we're going to focus on valvular function and biventricular size and function in this assessment. And really, the beauty of echocardiography, clinical ultrasound, is the fact that we're able to directly estimate stroke volume. And we do that using this equation. Stroke volume equals the left ventricular outflow tract cross-sectional surface area times the left ventricular outflow tract velocity times integral. Because really, what we're doing is we're saying that the heart ejects a cylinder of blood during systole. And that cylinder is defined by the cross-sectional surface area of the LVOT. And the height of the cylinder is the stroke distance. The stroke distance is the integral of the pulse wave Doppler signal in the LVOT. This is the velocity of red blood cells as they speed up during systole and then slow down before the closure of the aortic valve. So again, we can calculate stroke volume. And you can do it just like this equation, where stroke volume equals pi times the diameter of the LVOT divided by 2 squared times the LVOT VTI. This equation breaks down into 0.785 times the diameter squared. The diameter right here is 2 centimeters. And the LVOT VTI is gotten from tracing this spectral envelope, which is 20 centimeters. So in multiplying it out, we end up with about 63 milliliters. Because a milliliter is a centimeter cubed. And then our cardiac output very simply is 63 milliliters times the heart rate, which gives us a cardiac output of 5.7. And this is a nice study because it shows us that cardiac output derived by transthoracic echocardiography correlates incredibly well with cardiac output derived by a PA catheter in critically ill patients. You see a very strong R value there. And not only that, using echo to look at changes in cardiac output also correlates well with the gold standard PA catheter. So again, you can use echocardiography at the bedside in the ICU to track patients' cardiac output and to help guide you in the etiology of shock and then, of course, in therapeutic intervention. Now this study by Jake Jenser from our group at Mayo Clinic really crystallizes why I think it's so important to understand some basic Doppler hemodynamics when using ultrasound at the bedside. This is a study of over 5,000 patients that were admitted to our CICU that had a transthoracic echocardiogram, a bedside study done within 24 hours of admission. They were then classified by the sky shock stages. And what was really important coming out of the study was that it was actually the stroke volume index and the medial E over E prime ratio. So that is a marker of diastolic dysfunction and elevation in left atrial pressure. But it was these hemodynamic markers that were the most powerful predictors of in-hospital mortality. And it was not the ejection fraction. And the ejection fraction, I think, when we do point-of-care ultrasound, we eyeball and we say, well, the EF is normal or the systolic function is normal or it's 40%. What really is powerful is when we start applying Doppler hemodynamics. And it's important to understand that hemodynamics are better than the eyeball method. And when you incorporate hemodynamics into your ultrasound, you're doing a better assessment of the patient. Now, you may say that the calculation of stroke volume is somewhat complicated. Really, it's not all that complicated. And there are actually devices now that will do it for you automatically if you just enter the LVOT diameter. And then there are devices that will actually track the LVOT VTI for you and then calculate the stroke volume for you and the stroke volume index for you. But let's say you don't want to do that or you have a device where you can only do some pulse wave Doppler. Well, the thing to think about is that the cross-sectional surface area is a fixed number. The LVOT diameter is fixed. What is variable is that stroke distance or the LVOT velocity time integral. That stroke distance is your surrogate for stroke volume and is your surrogate for change in stroke volume. For example, if you have a patient that has a low LVOT VTI, that's a low stroke volume because we know normal is somewhere between 18 and 24 centimeters. Then if you take that patient and you give them dobutamine and you just track the change in their LVOT VTI, if the LVOT VTI increases from 14 to 18, and let's say the heart rate doesn't change, that's a 28% increase in your stroke volume. That's a meaningful change. That is a meaningful therapeutic intervention. You can use this for passive lay grades, for example, to assess whether or not the patient is fluid responsive. Now, we're working on a study of about 7,000 patients. What we found was in the Mayo Clinic CICU that a VTI of less than 16 was the strongest predictor in hospital mortality after a multivariable adjustment for severity of illness. That's a good number to remember. Less than 16 is not good, and the normal is around 18 to 24. Now, there are some caveats that you need to kind of think about when you start applying the use of ultrasound for the calculation of cardiac output. Remember that when you're calculating the stroke volume, we're assuming that the LVOT outflow track is circular during CICELI, which it may not be, and that that measurement of the diameter is squared. You want to measure that really well. Use a zoom mode. Zoom up on the LVOT and measure it. I tend to measure, and at the Mayo Clinic, we tend to measure right at the hinge points of the aortic valve, so we measure at the same place every time. You want to average multiple beats if there are regular rhythms. Be careful in the setting of aortic stenosis or dynamic outflow track obstruction. And then this is a key. Your pulse wave Doppler assessment of the LVOT VTI, that stroke distance, that assessment, the angle of interrogation must be parallel to flow. And so to be able to get that, you have to do an apical five chamber or an apical three chamber. So we've talked a little bit how to think about defining normal or high cardiac output versus low cardiac output. Let's talk a little bit about filling pressure, specifically the CVP and how we determine whether or not we have a low CVP or high CVP. And really what we use, or the simplest things to use, is the IVC, of course, and then also incorporating hepatic vein flow. Now, this is how we classify CVP or right atrial pressure at Mayo. And what we do is we use a combination of the IVC diameter and collapse, just as I think a lot of people do and is in the guidelines. But we also incorporate hepatic vein pulse wave Doppler flow patterns, knowing that systolic flow should be greater than diastolic flow in the setting of normal right atrial pressure. And when you incorporate your pulse wave Doppler of the hepatic veins into the typical IVC size and collapsibility, you do a much better job of correlation with right atrial pressure, much better than just using IVC size and collapse. So what does hepatic vein flow look like in a normal person? Well, here we see the hepatic vein. We see flow from the hepatic vein into the IVC in the right atrium. And this is what the flow pattern looks like using pulse wave Doppler with normal right atrial pressure. It's a systolic, greater than diastolic flow. And really what this is, this is a visualization of your CVP with your X and your Y descent, a little V wave, an A wave, C wave. So you're just visualizing the CVP using pulse wave Doppler. So again, normal is systolic, greater than diastolic flow. You need to have the ECG here to be able to look at that. Here's an A wave reversal with the P wave here on the ECG. And then abnormal, when there's elevated CVP, you see that the diastolic flow is predominant. And why do we even want to think about hepatic vein flow? Well, in the ICU, we have a lot of mechanically ventilated patients. And using the IVC collapse or distensibility, let's say, does not correlate well with mean right atrial pressure. This is a nice study that shows that. But instead, if we use the systolic flow in the hepatic vein, either the systolic flow here, velocity or time-velocity integral, which is the same thing as the velocity-time integral, that fraction, the higher that fraction is, the more forward flow there is, the more dominant this S wave is, the lower your right atrial pressure. And you see a much better correlation there with mean right atrial pressure when you incorporate hepatic vein flow in your assessment. And then finally, we can even derive SVR. Because we're able to use the IVC, again, size and collapse of the hepatic vein flow to tell us something about right atrial pressure, we're able to directly calculate the cardiac output. Of course, the mean arterial pressure, we can get either non-invasively or with an arterial line. And so then we can get our SVR. So now we've talked a little bit on how to use some hemodynamics or Doppler hemodynamics to assess cardiac output and assess CVP. Let's talk about how we can use ultrasound algorithms for undifferentiated shock, again, going back to our somewhat pyramid approach here of cardiac ultrasound, pulmonary ultrasound, and then abdominal and vascular. So let's start with distributive shock, which is normally a high cardiac output state or a normal cardiac output state, with exam findings suggestive of low systemic vascular resistance. And so again, we can use our cardiac ultrasound to tell us something about, to categorize the patient as either having normal or high cardiac output. They may have normal hyperdynamic systolic function. You may see dynamic outflow tract obstruction if the person has a severely vasoplegic state and low filling pressure. You typically have a normal to small IVC with that systolic dominant hepatic vein flow. We can pull in our pulmonary exam, either for a possible source, for example, a pneumonia, or something to tell us a little something about the patient's ability to tolerate fluid emboluses, whether or not they have an A or B line pattern. And then of course, the abdominal ultrasound can be very helpful for a possible source of infection. So now we move into circulatory failure in the setting of low cardiac output, low CVP, or hypovolemic shock. Again, we really utilize that cardiac ultrasound to define our hemodynamics, define that low cardiac output, that low LVOT-VTI, to define that low CVP. And then we incorporate our pulmonary exam and our abdominal exam to look for possible areas of fluid loss, whether or not there's free fluid in the abdomen doing a FAST exam or whether or not there could be a ruptured AAA here incorporating an abdominal aorta exam. If we move then to low cardiac output but a high CVP, we think of cardiogenic shock. So again, falling back on our cardiac ultrasound for findings, Doppler findings of low cardiac output. You know, we can use a chamber size, both left ventricular, right ventricular, and the size of the atria to tell us something about chronicity. So if someone has a very dilated left ventricle, dilated left atrium, likely they have a more chronic cardiomyopathy. We can think about valvular dysfunction. So typically it's the left side of valves we want to focus on, the aortic valve, whether or not there is aortic stenosis or severe regurgitation, mitral valve, severe regurgitation or mitral stenosis. Typically a dilated IVC telling you that there is a high central venous pressure with a dominant hepatic vein flow in the diastolic phase. And then of course we can use our pulmonary exam for supportive findings and even look at the abdomen in the setting of RV failure, that's the CSIDs. So here's a good case. 70 year old male who presented with dyspnea and hypotension had an episode of severe epigastric pain about a week and a half prior to presentation. Here's our bedside ultrasound. And we see, here's the left ventricle here in the parasternal view. You see cardiac function is not normal. There looks to be wall motion abnormality here in the inferior lateral wall. Here's an apical three chamber. We see here there really isn't thickening here of the inferior lateral wall. And in the short axis, we see again, inferior lateral, inferior wall motion abnormalities. So let's move forward. So our eyeball method showed us an EF around 45 to 50% maybe with some definite wall motion abnormalities in the inferior and inferior lateral wall. But that's our eyeball method. What we wanna do is incorporate hemodynamics. And I think the important one as we're gonna focus on again is that definition of low cardiac output. And we're gonna do that using our stroke distance which here we have an LVOT VTI of nine centimeters. If normal is greater than 18, then we're markedly reduced here. There's markedly reduced forward flow. The IVC is dilated. There's diastolic predominant hepatic vein flow. And then we have diffuse B lines that are present. So we know that the patient has got pulmonary edema and is volume overloaded. And no assessment of cardiac function is complete in a patient who is hypotensive without looking at the left-sided valves. And we do that with color. And what we see here is severe mitral regurgitation. So this is a patient who had completed an inferior-inferior lateral infarct and now has severe ischemic mitral regurgitation. And we took this patient to the cath lab for an intra-aortic balloon pump and then just shoot the coronaries. And finally, let's turn to the ultrasound assessment of obstructive shock. Low cardiac output, dilated IVC, but there are multiple etiologies. And these teasing out which etiology really requires ultrasound because you either have a pulmonary embolism and you may see RV dysfunction or dilation, dry lungs, DVT, pericardial effusion with tamponade. You could also have an aortic dissection that dissects into the pericardium and then have hemopericardium causing tamponade. You can have a pneumothorax, tension pneumothorax, or even a large pleural effusion. All of these diagnoses really require bedside ultrasound in a multi-organ integrated approach. So let's look at this case. 59 year old female with an ischemic cardiomyopathy who undergoes the placement of a defibrillator. And in the post-procedure unit, she develops significant hypotension and they bolus her fluids. Now the fellow is there, the EP fellow, and he performs a stat bedside ultrasound. And what he sees is a very dilated hypokinetic left ventricle, a dilated IVC, no pericardial effusion, because that's what they're worried about in this setting, that they perforated the right ventricle and the person's in tamponade. And then when the patient comes into the ICU, I do a quick VTI assessment and I see a very low cardiac output. So what is the etiology of the shock? Well, the fellow started dopamine because he thought that the patient was in cardiogenic shock from the underlying cardiomyopathy. And importantly, we didn't stop at just looking at the heart and looking at the VTI, but we performed that integrated multi-organ system assessment with ultrasound and got to the etiology of the patient's hypotension. And that is a hemothorax. So this patient didn't go into shock because of tamponade, didn't go into shock because of their chronic cardiomyopathy and low output state. They went into shock because there was a procedural complication with the subclavian and they ultimately had a hemothorax that caused a tension hemothorax and actually shifting the trachea over. And this had to be relieved by an emergent chest tube. Let's look at another case. Here's a 45 year old female with shortness of breath and hypotension. And let's do our ultrasound assessment. Let's do this hemodynamic assessment. We see that the patient has a dilated IVC. We see that there is a diastolic dominant flow with systolic reversals in the hepatic vein telling you that there's likely significant tricuspid regurgitation and elevated CVP. We look at the LVOT VTI, or again, our stroke distance. And it's 6.2, again, normal, somewhere around 17 or 18 to 24. So this is a very low cardiac output. And in fact, we calculate it right here, a cardiac index of 1.52. And then we integrate our cardiac and pulmonary assessment. And we see dry lungs and there is no pneumothorax. These are the lung being looked at at the apicy here, both on the right and left side. We see that A-line pattern, again, dry lungs. And then looking at the left ventricle in the parasternal view, we see the left ventricle is tiny and underfilled and a very large right ventricle. Here in the short axis, the right ventricle is enormous. And there is a D-shaped septum here telling us that there's significant pressure overload. And then the apical imaging really tells a great story. We see that there's a significantly dilated right ventricle. That right ventricle is hypokinetic. And the only function we see here, or motion of the right ventricle is at the apex. That's that, again, that McConnell sign. McConnell sign does not tell us that there is a PE, but it tells us that there is an incredibly high pulmonary vascular resistance, high afterload on the RV. And the LV is hyperdynamic and it's pulling the RV apex over, giving it that motion. Now we see that there is significant tricuspid regurgitation because the annulus of the tricuspid valve has enlarged, pulling the leaflets apart. Pulse wave Doppler of the RV outflow tract has a notch here during systole. The systolic notching tells you that there's very high EVR. And then finally, of course, we're able to calculate the RVSP, or right ventricular systolic pressure using the TR velocity. And here the TR velocity is 3.1. That gives us 38 millimeters of mercury plus the CVP. And the CVP is likely at least 15. So we have very high RVSP, we have high PVR, we have acute RV dysfunction, and we have dry lungs. This patient needs TPA because they have a significant. So we've talked through using clinical ultrasound or point of care ultrasound or critical care echocardiography for the diagnosis of shock using that integrated approach and thinking about hemodynamics and anatomic assessment and integrating that all together in determining the etiology of the shock that you're dealing with. Let's talk a little bit about therapeutic guidance and always that question of fluid. Now I can't get into all the nuances of the hemodynamics of fluid responsiveness because that is just a talk by itself. But what I can point out is how important it is to use ultrasound when you're assessing fluid responsiveness. Because with ultrasound, you're able to, well, first of all, you're able to in your mind determine what the pretest probability is that a patient may be fluid responsive. You're able to determine whether or not they have normal contractility and have a very sharp contractility curve and whether or not they're on the very steep part of the curve or the very shallow part of the curve. And that helps you with your pretest probability. You can also think about fluid tolerance. Is the patient already volume overloaded? Do they already have a CVP that puts them out here? Do they already have a lot of B-lines? Are they already congested? And then the other thing you can do is directly measure the change in stroke volume when you give fluid. For example, if you do a passive leg raise, you can track whether or not that change in preload leads to an actual increase in stroke volume. And that by definition is fluid responsiveness. And here's your passive leg raise test. Again, using the same thing we did with dobutamine, starting with your LVOT-VTI, doing the passive leg raise, and then seeing how that LVOT-VTI changes with that change in preload. You do a direct assessment of change in preload and how it affects stroke volume. An increase in stroke volume greater than 10% of the patients, greater than 12% of the spontaneous breathing patient, that patient is gonna be fluid responsive. Now I wanna highlight this paper from some of our colleagues at the SCCM because I think it's so smart. They really do a great job of simplifying the assessment of patients with septic shock while still doing a multi-organ system integrated approach. And what they did was they classified patients based on three different phenotypes, either empty or normal hearts, left or biventricular systolic dysfunction, and then isolated right ventricular systolic dysfunction. And they use really one view. So they use the subcostal view to look at the heart and the IVC, and then they look at the lungs. And they're using just an A pattern to say that the lungs are dry and B pattern or B-line pattern or interstitial pattern to say that the lungs are wet. And so then what they do is they say, if you're in cluster one, so you have normal systolic function on the left side of the heart, if you have a flat IVC and you have an A-line pattern and you have septic shock, then you can give those patients volume, challenge them with fluid. And if the IVC becomes plethoric or they start to B out, they start to develop B-lines, back off and start using pressors. And we can see here in patients in cluster two, so those are patients with either left ventricular systolic dysfunction or biventricular systolic dysfunction. These are patients that you're gonna be much more cautious with, with your fluid challenge. You're gonna be more likely to use vasopressors such as norepinephrine or vasopressin or even inotropic agents. But again, if they have a flat IVC and they're dry and they're in septic shock, you can give them that fluid challenge, but again, you're gonna be somewhat conservative. And the IVC is big and they have B-lines, you're going to use vasoactive agents. And then in that cluster three, patients with isolated right ventricular systolic dysfunction. In those patients that they have a large IVC, they already have B-lines, you wanna diurese those patients, you wanna remove fluid. This is a nice way of thinking through what you're gonna do with the patients in front of you based on ventricular function, based on volume status using the IVC and the lungs and just using your subcostal view and your lung ultrasound. So we can think of this as a POCUS guided fluid management strategy. You're at the bedside, you're using ultrasound and you can use simple things. Patient comes in and they're hypotensive, the IVC collapsibility index is greater than 80%. They have normal biventricular function, they have A-lines, give them fluid. They can tolerate the fluid, they may benefit from the fluid. And let's say they stabilize, again, they become hypotensive. Now there's less collapsibility of the IVC, still LV and RV systolic function appear normal. So you do a passive leg raise. You do a dynamic challenge. And what you see is that increase in stroke volume, this patient likes the fluid. Cardiac output's gonna go up, so you give more fluid. Then they're stable again, finally they become hypotensive and now the IVC is not collapsing. LV and RV are still normal. They are not responding to the passive leg raise with an increase in stroke volume and they've developed a B-line pattern. This patient cannot tolerate more fluid. They're not gonna do better with more fluid. You need to start vasopressors in that setting. So finally, let's just talk a little bit about wrist stratification. Let's talk about using that ultrasound probe and not the traditional PA catheter to wrist stratify using hemodynamics. So we already talked about this study, which again showed us that using echocardiography using critical echocardiography to define stroke volume index and your E over E prime ratio, which again tells you about diastolic dysfunction and tells you about left atrial pressure. These metrics were the most significant predictors of in-hospital mortality. And they were much better than that eyeball method just thinking about the LVEF. What about cardiac power output? Which I think is a great invasive number and something that has been touted more recently with the use of Impella devices. And this again is a study from the Mayo Group looking at using echo to calculate cardiac power output. And we see using echo in this group of over 5,000 patients. Over 5,000 patients that a CPO of less than 0.6 is where you see that inflection point for increased CICU mortality and hospital mortality. And you see that just that calculation of cardiac power output, and this was done at the time of admission tells you something about one year survival. So not only can you wrist stratify patients for their mortality in the ICU and in the hospital, but you can wrist stratify them for survival for up to one year. And we can see right there that that cutoff of 0.6, that's where mortality really goes up 20%. When you have a cardiac power output of greater than one, mortality only five. And what about the Forrester classification? The very classic cold and wet, warm and wet, warm and dry, cold and dry, that square of where you fit patients in presenting with decompensated heart failure. Well, we looked at that using ultrasound, using echocardiography in the CICU. 4,000 patients had an echo within 24 hours of admission. Again, using that E over E prime to reflect the pulmonary artery capillary wedge pressure. And we see that using ultrasound, using echocardiography gives us the exact same findings as using a PA catheter. We see that patients that are cold and wet, that is defined as having a cardiac index of less than 2.2 by echo, and an elevated pulmonary capillary wedge pressure as defined by an E over E prime of greater than 14, they had the highest one-year mortality and the highest hospital mortality. And then we can see that patients that are warm and dry, they do the best. So again, we can wrist stratify patients just like you would with a classic PA catheter using critical care echocardiography. So now I've shown you some data about how you can use a Doppler assessment of the left side of the heart, either stroke volume, cardiac output, cardiac power output, markers of LV filling pressure, your E over E prime, which reflects your mean left atrial pressure, and how you can use that to wrist stratify your patients. Well, now let's focus on the right side of the heart. Let's think about RV to PA coupling. And we looked at that using echocardiography again in the CICU in over 4,000 patients. And we see that patients that have evidence of discoupling of the right ventricular systolic function and the RVSP by echo, those patients that demonstrate discoupling have very high observed hospital mortality, no matter why they are admitted, whether it's sepsis, respiratory failure, cardiogenic shock, or ACS. So again, you can wrist stratify patients, not just based on hemodynamics of the left side of the heart, but you can wrist stratify patients using integrative hemodynamics on the right side of the heart. So I hope in conclusion that I've demonstrated how important ultrasound is in the assessment of circulatory failure, and how using a holistic whole body approach, integrating a multi-organ system assessment is incredibly important in understanding the etiology of shock, as it provides for you anatomic and physiologic assessment at that moment with the patient that is dynamic. But you need to interpret these findings within the context of the clinical presentation. The clinical exam is still important, and it sets the framework for what you find with ultrasound. I tend to focus on the cardiopulmonary exam as my core assessment, and of course, adding on to that abdominal and vascular ultrasound. And then again, I want to ensure that I drill down on the fact that Doppler hemodynamics are incredibly important. And they're not terribly difficult. A lot of machines now are doing that for you. So you need to move away from the eyeball assessment and start to incorporate your Doppler hemodynamics. Again, that tells you something about physiology, tells you how to assess therapeutic interventions, and it tells you a lot about wrist stratification.

ultrasound

shock

hemodynamics

fluid responsiveness

Doppler

diagnosis

management

integrated approach