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2: Cardiopulmonary Point-of-Care Ultrasound (Brand ...
2: Cardiopulmonary Point-of-Care Ultrasound (Brandon M. Wiley, MD, MS, FASE, FACC)
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This talk is going to focus on cardiopulmonary point-of-care ultrasound in the care of critically ill patients. My name is Brandon Wiley. I'm a cardiologist and critical care physician and the chair of the Mayo Enterprise point-of-care ultrasound work group at Mayo Clinic in Rochester, Minnesota. I have no disclosures related to the contents of this presentation. After a brief introduction describing the holistic approach to bedside ultrasound in the ICU, we will focus on cardiopulmonary ultrasound, break it down into pulmonary ultrasound, and then combine pulmonary ultrasound with cardiac ultrasound in the setting of hypotension and circulatory failure. Let's begin with a brief case. This is a 55-year-old male who suffered a VFVT arrest and was found to have an inferior STEMI on his ECG. He was taken emergently to the catheterization lab where he underwent PCI to the circumflex and RCA. During the PCI, he had multiple VFVT arrests requiring CPR and defibrillation. And then upon presentation to the cardiac ICU, he was in shock on multiple vasopressors and hypoxic on the ventilator requiring 100% FiO2 to maintain SATs in the AEDs. The patient arrived to the cardiac ICU just a change of shift when I was coming on for the evening shift, and the daytime fellow had ordered a STAT echocardiogram to be performed due to the hypoxia and hypotension. And what we see with the echocardiogram here, this is the male format with the right ventricle on the right. The right ventricle is dilated and hypokinetic. And here in the subcostal view, that free wall of the right ventricle is rather achinetic and hypokinetic, consistent with an RV impact in the setting of the patient's RCA STEMI. Here though, the left ventricle is quite hyperdynamic. And given these findings, it didn't totally explain the patient's presentation of profound hypoxia and hypotension. So given the fact that the echocardiogram didn't tell the whole story, I performed a quick bedside lung ultrasound. And what I was looking for initially was just lung sliding to make sure that there was no pneumothorax in the setting of CPR. And we see on the right side here, the lung is up and there's lung sliding with a couple of B lines. And on the left side of the screen here, corresponding to the patient's right side, we see actually the pleural line is right here. And what we see here is a large heterogeneous mass in the thorax with compression of the lung. So what that bedside lung ultrasound did for us was allow us to diagnose at the bedside rapidly the underlying etiology of the patient's presentation of hypotension and hypoxia. And that's this large interporeal hematoma. We see it here compressing the lung. And this is the CT scan done later that shows us that it was a result of the rib fracture. And so again, this is a nice case illustrating how a combination and integration of lung ultrasound and cardiac ultrasound allows us to make a rapid diagnosis of the underlying etiology of a patient's critical illness or decompensation at the bedside. And what that case allows us to do is step into this concept of a holistic scheme to bedside ultrasound in critical illness. This holistic approach to point-of-care ultrasound in the ICU has also been referred to as the whole-body approach to point-of-care ultrasound. And it refers to an integration of ultrasound assessment of multiple organ systems and using that assessment and tying it together to be able to diagnose the underlying pathology of the patient. This holistic approach or whole-body approach to point-of-care ultrasound in the ICU was nicely reviewed in this paper in CHEST by Paul Mayer and colleagues. And as they say, point-of-care ultrasound is often compartmentalized such that the clinician will focus on one body system while performing the critical care ultrasonography exam. But they're suggesting, and I'm suggesting, a change in this compartmentalized approach to a systematic whole-body ultrasound approach. And again, point-of-care ultrasound is defined in the sense that it's performed by the primary provider, the provider taking care of the patient. And what we're going to do is talk about that integrated approach. And so this holistic approach in the ICU can cover cardiac ultrasound, evaluating the pericardium, Doppler hemodynamics, the lung ultrasound or pulmonary ultrasound, and then, as needed, integration of a focused abdominal ultrasound and then a vascular ultrasound as well. And I do have a second disclosure for this talk. I am an absolute advocate for point-of-care ultrasound in the ICU. I think it should be used by everyone and we should develop robust training programs for fellows, residents, and attending providers. But I do want to note that point-of-care ultrasound should be interpreted within the context of the clinical presentation, and the clinical presentation is important. You do need to lay hands on the patient. So for example, we can use this integrated approach in a patient that presents with hypoxia and hypotension and do a cardiac ultrasound demonstrating a dilated RB. We can do a lung ultrasound that demonstrates lung sliding and dry lungs with an A-line pattern. And then we can do a quick compression ultrasound that demonstrates a DVT in the femoral vein and diagnose a PE right at the bedside, again, using the clinical presentation to guide our approach with the ultrasound. And now that we've covered the philosophy of using a holistic approach to point-of-care ultrasound at the bedside and incorporating our ultrasound findings within the clinical presentation and using the clinical presentation to guide our ultrasound, we're going to focus this talk on cardiopulmonary ultrasound. Cardiac ultrasound and pulmonary ultrasound are incredibly important in the ICU. As respiratory pathology and circulatory pathology drive the predominant number of ICU admissions. And so incorporating cardiac ultrasound and pulmonary ultrasound into a cardiopulmonary ultrasound makes sense. Also on the physiologic level in the sense that the heart and lungs are in circuit. So let's break this down and start with pulmonary ultrasound and review some of the cardinal findings. Now lung ultrasound is a mature field, and there are two experts that have some wonderful reviews in the literature. What I'm going to do is break down a simplified approach that I use at the bedside in the ICU, and I have it broken up into three basic categories. And I move in my assessment from the pleural line, I do that first, and I assess the morphology and the motion of the pleural line. Then I move to the aeration pattern in the lung, and I'm looking for normal or abnormally aerated lung. And then finally, I look at the pleural space. I begin the assessment of each intercostal space or lung zone with an evaluation of the pleural line. And what I want to see is a very thin, uniform appearing, hyper bright, reflective pleural line that's not lumpy, bumpy, or irregular, and that demonstrates normal sliding or motion with respiration. Now again, the pleural line is a hyper bright reflector and everything distal to that is artifact. On this side, we see that hyper bright pleural line, but there is no sliding there. This could signify the presence of a pneumothorax where there's loss of opposition of the pleural layers. This is a sensitive finding for pneumothorax, but it's not specific. Now we are teaching lung ultrasound to the sonographers in the echo lab at the Mayo Clinic and incorporating it with our echocardiograms. And one of the sonographers paged me after performing an echocardiogram on this post cardiac surgical patient because she said there were these really weird findings with the lung ultrasound. And I told her what she did was incredible because she picked up bilateral pneumothoraces. And what we see here on the right side of the lung, we see that there is no lung sliding, actually in both areas. Now we have the sonographers put a marker where they are so we know anatomically where they're imaging. I think she imaged just a little apical in this view as well, but we see no lung sliding. And importantly, we see no B lines. If there are B lines in the presence of no lung sliding, there is no pneumothorax. On this side, we see the very nice example of a pathopneumonic finding for a pneumothorax. That's a lung point. We see here that lung point. As the patient breathes, the lung inflates and slides into view. Of course, here we see normal lung sliding. And there are two pneumothoraces on the chest x-ray. So after I assess the pleural line, I move on to assess the aeration pattern of the lung. And of course, with this, we're talking about artifacts. So assessing the aeration pattern of the lung, in a normally aerated lung, we get this image here. Again, we see the pleural line with pleural sliding. And then distal to that, we see nothing. And that's because the ultrasound is attenuated in the setting of this very aerated lung. What we do see is this reverberation artifact of the pleural line. This is an A line. It is a horizontal reverberation artifact. Now when the lung becomes more dense in the area that you're interrogating with ultrasound probe, we begin to see a different artifact form. And these artifacts are B lines. We see there's these vertical spotlight artifacts that extend all the way down to the end of the ultrasound screen. And they move with the pleural line. See how they're moving with the pleural line. And this is an interstitial pattern, an ultrasound interstitial pattern. And it occurs in the setting of abnormal aeration or increased lung density. So again, B lines indicate an interstitial process, and they indicate abnormal aeration. And they occur when there's increased lung density. And that increased lung density or decreased aeration can be due to either fluid, such as extravascular lung water or pulmonary edema, inflammation, or fibrosis. So there's a differential to B lines. So again, in thinking about this aeration pattern, when you go from a high air to lung ratio or normally aerated lung to a low air to lung ratio or abnormally aerated lung, you go from this normal pattern here with the A line reflecting that pleural line to an interstitial pattern with B lines. And the more abnormally aerated you are, the more B lines you get until you get true consolidation of the lung, where the lung is actually consolidated. And here you can actually see the lung. This is not artifact. B lines, of course, are artifact. The most abnormal aeration pattern you can see with ultrasound is consolidation. The lung is so dense, it takes on a tissue-like echo texture, so-called hepatization of the lung. The lung appears to look like the liver. Now it's important to note that you will only be able to see subpleural consolidations with ultrasound. You will not be able to see deep consolidations that do not abut the pleura. But you can even see with ultrasound these very even fine, small subpleural consolidations that are often seen along the pleura. And then, of course, consolidation in the setting of an effusion. And so after assessing the pleural line of our image, the aeration pattern, we're finally going to look at the pleural space. A good place to look for an effusion is at the posterior axillary line, along this line here. And we see two different examples of effusions. One is an effusion with associated consolidated lung, and the other is a rather large effusion with some increased echogenicity. So now that we've gone over some of the basic findings with lung ultrasound, let's talk about some respiratory failure protocols that utilize a pulmonary ultrasound. The BLU protocol is an example of a pulmonary ultrasound-centric approach to respiratory failure in the ICU. It was developed by Lichtenstein, who is really one of the pioneers of lung ultrasound. And it's a nice, simplified approach, using the same findings that we have discussed, A-lines, A-lines, or normally aerated lung, consolidation, and lung sliding. And it approaches it using a nice, simplified exam, using two zones on either side of the anterior chest, and then an additional zone that is in the posterior axillary line that is just transverse to this zone here. And we're looking at regionality. Is it a bilateral process or a unilateral process? For example, starting with lung sliding, the lungs are up, they're sliding. If there is a unilateral process, so that is to say, A-lines or normally aerated lung on one side of the chest, B-lines or abnormally aerated lung or consolidation on the other side of the chest, that's most likely to be pneumonia. That's a focal process. Whereas you have lung sliding and B-lines on both sides of the chest, that's a diffuse process. That's pulmonary edema. If you have lung sliding and normally aerated lungs, but the patient is short of breath, then he incorporates a compression ultrasound to look for a DVT, suggestive of pulmonary embolism being the underlying cause. At Mayo Clinic, for each interrogated lung zone or intercostal space, we apply a simplified aeration pattern assessment that is built off of Lichtenstein's findings. We always, again, start with lung sliding. If there is no lung sliding and no B-lines, then we are concerned about a pneumothorax. If there is no lung sliding and B-lines, there can't be a pneumothorax. And then we define that as an abnormal aeration pattern. If there is lung sliding and B-lines, again, that's an abnormal aeration pattern. And then what we do is grade the pattern that's present based on the number of B-lines. If we're able to count them, for example, one to three, or if they become confluent where we just can't count them, they're greater than 50% of the region of interest. And we call that white lung. And then the most, again, abnormal aeration pattern is consolidation. And a simplified way of using those abnormal aeration pattern, focusing on the interstitial pattern of B-lines, is to look at the regionality of those findings. So for example, if we only see B-lines that are localized to an area of the chest, then this is a focal process, more likely to be a pneumonia, for example, an infarct or a process like that. Whereas if we see abnormal aeration defined by a B-line or interstitial pattern that is on both sides of the chest, then we're looking at a more diffuse process. And once we get into that diffuse sort of B-line or abnormal aeration process, then we're going to look at the pattern that exists. Is it a homogeneous pattern, that is to say the B-lines are sort of spread out everywhere on the chest, maybe more in the dependent areas? The pleural line is normal, and ideally there's two small pleural effusions. Well, then that's cardiogenic pulmonary edema, this is a non-inflammatory process. It is a process that does not affect the lung sliding or the pleura, the pleura is moving normally, and you have a nice diffuse spread of B-lines. However, if you're looking and scanning the chest and you see a patchy spread of B-lines, so areas where you see B-lines, areas where you don't see B-lines, there's these spared areas, it is non-homogeneous. And maybe you add to that an abnormal pleural line or decreased lung sliding in areas, subpleural consolidations. Well, this is less likely to be cardiogenic pulmonary edema, and more likely to be an inflammatory process such as ARDS, or maybe intrinsic lung disease such as fibrosis, depending of course on the presentation of the patient. So let's build on this simplified concept of using B-lines or an interstitial pattern, and then the spread of that pattern across the chest to make a diagnosis. So this is a patient, 59-year-olds with MSSA bacteremia that experienced respiratory failure on the floor, and that was emergently sent to the CCU. And then when we did the lung ultrasound on this patient, what we saw was lung sliding in all of the zones that we interrogated, and then B-lines diffusely, B-lines everywhere. In fact, so many B-lines that became confluent. And so this is a patient who had pulmonary edema due to severe mitral regurgitation. They'd actually had a flail posterior leaflet from endocarditis. And again, this very diffuse bilateral homogenous B-line pattern. Now let's contrast that with this patient who was sent to us from the ED, a 78-year-old ischemic cardiomyopathy on BiPAP. Now I would say that the fellow did evaluate this patient and said, yeah, this patient has heart failure, needs to come to us. For educational purposes, we performed a lung ultrasound. And what we see on the left side of the chest here is lung sliding, and really no B-lines at all, right? This is fairly normal aerated lung. But on the right side of the chest, as we move down to this zone here, we start to see a lot of B-lines, in fact, very dense B-lines. And then just moving down a little lower to that from there, we see a large consolidation here. So this is a focal process. This is not cardiogenic pulmonary edema, this is a patient with a pneumonia. Now we've talked about using pulmonary ultrasound to diagnose the etiology of respiratory failure. And I want to point out this study because it really lends credence to the use of lung ultrasound in the ICU for this indication. So this was a study by Dave Tierney, published in Critical Care Medicine 2020, and it's a really nice study. It looked at 67 patients that were intubated for respiratory failure, and they underwent a nine-point lung ultrasound. Now, this was meant to be a lung ultrasound that was more anatomic, that covered the right middle lobe, superior, inferior, left superior, and inferior. And they compared the lung ultrasound findings versus chest x-ray using a CT that was performed just afterwards as a gold standard. And what we see here is that lung ultrasound was incredibly good at correlating with the CT findings. Importantly, it was much better than chest x-ray. And I think this is a well-known finding, that chest x-ray is just not as good as lung ultrasound, and we really should be moving towards using more lung ultrasound in the ICU to evaluate our patients. And now as a bridge towards the next part of the talk, where we focus on cardiac ultrasound, and then the integration of cardiac ultrasound and pulmonary ultrasound into that holistic cardiopulmonary ultrasound, I wanted to present this study of the combination of heart and lung ultrasound for determining the etiology of shortness of breath in the ED. And they looked at over 2,000 patients. Now, each patient had their vitals, HNP, and ECG done. And then a group of ED physicians did an isolated point-of-care ultrasound study, very simplistic heart exam, looking at biventricular function in the IBC, and then a lung exam. And then based on that point-of-care ultrasound and the vitals and HNP, again, incorporating the clinical presentation with the ultrasound findings, that group of ED physicians came up with a diagnosis. Each of these patients had their comprehensive exam done, including CTs and ECHOs and labs, and they looked at the correlation here. And what they found was just the clinical presentation and the simplified combined cardiopulmonary ultrasound was incredibly effective at determining the etiology of shortness of breath. It was actually more effective in determining the presence of heart failure. POCUS exam didn't work quite as well, was in COPD and asthma and PE. Perhaps the COPD and asthma, it was the effect of nebulized therapies improving the patient that helped with the comprehensive exam performance. And of course, there was no vascular ultrasound to look for DVT, so maybe that played a role in the point-of-care ultrasound being not as sensitive for PE. But what I wanna point out, probably most importantly, was this time to diagnosis. We see how effective and efficient is this point-of-care exam was to making a diagnosis compared to how long it took and probably how expensive it was for that comprehensive assessment. So moving from that emergency room study that demonstrated the potential of combined cardiac and pulmonary ultrasound, let's move into a cardiopulmonary exam. And what we'll focus on is the use of this exam in hypotension and shock. Now, I believe that cardiopulmonary ultrasound is the fundamental exam in patients who present with hypotension and shock. Cardiac ultrasound in particular allows us to assess hemodynamics at the bedside in a non-invasive manner. However, in keeping with this concept of a holistic approach to bedside in the ICU, we want to add abdominal imaging and vascular imaging as guided by the clinical presentation, again, to form a very comprehensive approach at the patient. What we will focus on, particularly though, is this cardiac ultrasound and how to think about hemodynamics. So let's talk a little bit about bedside echohemodynamics and how they can be very helpful in the ICU. Now, I'm sure that everyone is very familiar with this presentation of the hemodynamic phenotypes of circulatory failure. And it is this structure or framework that we're gonna use to perform a systematic, non-invasive, ultrasound-based assessment of patients that present with hypotension. Now, in breaking down circulatory failure, we again, of course, divide them up into two phenotypes. One has normal or high output. The other is low cardiac output. And what we're able to do at the bedside with cardiac ultrasound is determine the cardiac output or specifically the stroke volume and allow us to differentiate these patients. Now, there is really a plethora of data supporting the use of echocardiographic derived cardiac output in correlation with PA catheter derived cardiac output. This study here focused on critically ill patients. These were mechanically ventilated patients without arrhythmias. And what this showed was, again, a very strong correlation between echocardiographic defined cardiac output, PA defined cardiac output, and even was able to show that correlation when there's a change in cardiac output. So now let's review how we calculate stroke volume using echocardiography or ultrasound at the bedside of a critically ill patient. And it's fairly simplistic. It only requires a couple of basic views of the heart and a couple of basic measurements. We start with measuring the left ventricular outflow track diameter, and that's measured at the hinge points of the aortic valve leaflets. Now, we want this measurement because the outflow track during systole is basically a circle. And if it's a circle and blood is ejected during systole, then that ejection of blood really takes the shape of a cylinder. And if we're able to measure this distance here, this diameter of the outflow track, we can then measure the cross-sectional surface area of the cylinder. Now, what we're left with is the length of the cylinder or height of the cylinder. How do we calculate that? Well, we calculate that by using pulse wave Doppler here in a five-chamber view, or alternatively in a three-chamber view to place a sample volume right at the level of where we measure the diameter of the left ventricular outflow track. And we measure the velocity. We pulse the outflow track and measure the velocity of the red blood cells as they exit the heart during systole. And what we end up with is this spectral Doppler profile. These are the velocities of the red blood cells as they speed up and peak and then decelerate during systole. And if we integrate this profile, we are left with a value in meters or centimeters. We're left with the distance because the x-axis is time and the y-axis is velocity. And that distance or length is our height of the cylinder. And if we multiply that velocity time integral by the cross-sectional surface area, we get the volume of the cylinder. We get centimeters cubed, which is milliliters. And then we can even simplify that calculation of stroke volume based on the fact that the cross-sectional surface area or base of that cylinder is pi r squared, but we measure the diameter here. So this equation breaks down to 0.785 times the diameter squared. And we multiply that by the LVOT velocity time integral. Again, the pulse wave Doppler spectral profile integrated, which is 20. This can be traced on almost all ultrasound machines. And then if we multiply these together, we end up with a stroke volume of about 63 milliliters. And then the stroke volume times the heart rate gives us a cardiac output of 5.7 meters per minute. As you begin to incorporate stroke volume calculation using echocardiography into your practice, it's important to note a couple of things. The first is that you should use a zoomed up view of the LVOT to measure that diameter because that result is squared and that can lead to significant error in your calculation. In the setting of irregular rhythms, make sure you average multiple beats. If there's flow acceleration in the outflow track, for example, in the setting of dynamic outflow track obstruction or even in your stenosis, be careful where you place your Doppler cursor as this can lead to overestimation of stroke volume. And then of course, you wanna have your pulse wave Doppler cursor aligned as parallel as possible to flow to reduce your underestimation of the LVOT VTF. So you may have asked yourself, why focus on this Doppler-derived stroke volume in critically ill patients? Why not just talk about the squeeze of the left ventricle or the ejection fraction? Well, the reason I'm focusing on this Doppler-derived stroke volume is because it is a really, really important risk stratifier in critically ill patients. And in fact, in this study that we did of over 7,000 patients in our CCU, looking at all the echo-derived variable, what we found was that the most important predictor of outcomes of mortality was that stroke volume index derived by Doppler echocardiography. In fact, it was more important than LVEF and the ejection fraction when adjusted for relevant echocardiographic and clinical variables was actually not a significant predictor of mortality, whereas the VTI was. And the only other variable that was important was the E over E prime ratio, which again is another Doppler-derived chemodynamic variable of left ventricular filling pressure. So what I'm trying to say here is that we need to kind of move past just the eyeball method of assessment of patients in the ICU and begin to focus more on non-invasive chemodynamics. Now, after showing you how important the Doppler-derived stroke volume is in the assessment of critically ill patients, I'm gonna show you how to simplify its assessment so it can be more easily used at the bedside in the ICU. And that simplification is based on the fact that the LVOT diameter, which we use to calculate the cross-sectional surface area, is a fixed number. It's fixed in every patient. The only dynamic variable is the LVOT VTI. That's what changes. That's your stroke distance. And so when the patient comes in and is hypotensive and has an LVOT VTI of 13.6, and we know that normal is somewhere between 18 to 22, that patient has low stroke volume. And we can use that number, that baseline number, to monitor our interventions with the patient to see if we're improving stroke volume. If we give fluid, did that LVOT VTI increase? Or for example, in this patient with an LVOT VTI of 14 and starting dobutamine, it increases to 18. That's a 28% increase in stroke volume. We've seen the benefit of our therapy as an increase in stroke volume. And if you give fluid, you could do the same thing. So I would suggest that you check the LVOT VTI in every patient that comes into the unit that is hypotensive, and then that's your baseline, and you can use it to judge how efficacious your interventions are. So now we've talked about how to calculate cardiac output using Doppler-derived stroke volume. So staying along this framework of circulatory failure, let's talk about how we define low and high central venous pressure, because that helps, again, direct us towards the etiology of the circulatory failure. Now, I'm sure everyone is familiar with using the IVC to estimate right atrial pressure or central venous pressure, and this can be very helpful and an easy way to estimate right atrial pressure and guide you in your therapy. But we need to be somewhat careful, and I wanna make a couple of key points. The first is that these guidelines, this reference, was based on spontaneously breathing patients who just perform a bit of a sniff. It's not a large inspiratory breath, for example, that you'll see in a patient with a lactic acidosis who's taking huge tidal volumes. That will throw off the amount of collapse that is there. The other thing is how the patient's position is important. The IVC is smallest when the patient is in the left lateral position and largest when it's in the right lateral position. And then, of course, this estimation of right atrial pressure, this size and collapse with sniff, does not apply in the setting of PEEP. Another important thing I wanna say is that you should assess the collapse of the IVC in two different views, both longitudinally here and in short axis here. Now, this case reinforces why I stress that we should evaluate the IVC both in long axis and in short axis. We see here in long axis that the IVC measures relatively normal and it appears to have relatively normal collapse, suggesting this patient has normal right atrial pressure. However, if we look closely, we see that the hepatic vein is somewhat dilated here, which is a clue that something else could be going on. We look here at short axis and we see that in short axis, the IVC is actually not collapsing very well. And if we scan down and look at the confluence of the hepatic veins, we see that all the hepatic veins are quite dilated. This patient has very high right atrial pressure and we were thrown off by this long axis view. And again, that's because we're cutting just the edge of the IVC here, we're not down the center of the IVC in the long axis view. So again, focus on looking at the IVC in two views, both long axis and short axis to confirm your estimation of right atrial pressure. Now, if you wanna be more accurate with your estimation of right atrial pressure or central venous pressure, you can incorporate hepatic vein flow. Hepatic vein flow is assessed using pulse wave Doppler of one of the hepatic veins. And what you're doing is you're looking at the direction and velocity of flow into the right atrium. And what you get is this spectral Doppler profile here and normal is more flow in systole or systolic dominant flow. And if you were to look at this and superimpose the JVP tracings, you would see that all we are doing is actually visualizing the JVP with the X and Y descent, the V wave, the C and the A wave. We'll be able to visualize that with pulse wave Doppler. So what we do at Mayo Clinic, which I think is fairly helpful, is we incorporate both the size and collapsibility of the IVC and the hepatic vein pulse wave Doppler profile to be able to fine tune the accuracy of our radial pressure measurement. So for example, in a patient who has a dilated IVC and dilated hepatic veins with literal no collapse and all diastolic flow in the hepatic veins, that patient has very high central venous pressure. Whereas a patient who has predominantly systolic flow in hepatic veins with a normal IVC and normal collapse, they have normal central venous pressure. And this integration of these two parameters actually improves our ability to better estimate right atrial pressure. So again, in the setting of normal right atrial pressure, the systolic flow into the right atrium is greater than the diastolic flow. You have to use your ECG tracing here to be able to time the flows. These are small atrial reversals. And then the setting of elevated right atrial pressure, your systolic flow into the right atrium is blunted and you have primarily diastolic flow when the tricuspid valve is open. And the reason I bring up hepatic vein flow is because in the ICU, a great number of our patients are either on mechanical ventilation or requiring noninvasive positive pressure ventilation. And we know that in those patients, the use of the IVC, either collapsibility or distensibility is quite imperfect for the estimation of central venous pressure. However, if we use hepatic vein flow and we use the ratio of the velocity of systolic flow over the sum of the velocity of systolic flow versus diastolic flow, or the velocity time integral of these to calculate a systolic forward flow fraction, we can see that if there's not a lot of forward flow and that fraction is low, then the right atrial pressure is usually high. And in vented patients, we have a very nice correlation with right atrial pressure if we just use this equation based on the systolic forward flow fraction as calculated using these calculations here. So a simplified clinical way to think about right atrial pressure is just applying a colored Doppler to the IVC or the hepatic veins. And if you see persistent forward flow into the right atrium then the right atrial pressure is low. We see that there's just blue flow. It's like a waterfall into the right atrium here. The right atrial pressure is low. And then of course, always look at your clinical scenario. So in a patient who is hypotensive in the PACU after a TAVR, if you have difficulty finding the IVC and you have to place color just to be able to see where there's flow coming from, then that patient is probably bleeding. And this patient in fact had a retroperitoneal bleed. So I've gone over some of the Doppler-derived cardiac hemodynamic indices that you can use in the setting of hypotension and shock. Let's go over some cases. And what we're gonna do is use an integration of pulmonary ultrasound, cardiac ultrasound, and at times abdominal and vascular ultrasound to be able to determine the type of shock that the patient has. So we're gonna diagnose the etiology of shock. So let's talk about distributive shock first. We're gonna use our cardiac exam to define our physiology and guide some of our therapy. And of course, our key findings are a normal to high cardiac output. And then we're gonna look at filling pressure, the normal or small IVC. We can use the hepatic vein flow in that. And then we're gonna apply our pulmonary exam to assess for possible source. And then we can even add an abdominal exam again to assess for a possible source. So let's start with our 45-year-old male with a history of colon cancer who presents with hypotension. We're first gonna calculate his cardiac output to place it into our physiologic profile. So his LVOT diameter is 2.3 centimeters. His LVOT VTI is 18.1. That gives us a stroke volume of 75 milliliters. If we multiply that by his heart rate, which is 125 beats per minute, we get a cardiac output of 9.5 and a high cardiac index. So again, he is hypotensive, but with a high cardiac output. So now we have a patient with hypotension who has high cardiac output, and we look at his right-sided filling pressures and we see a systolic predominant flow in his hepatic veins. His IVC is actually collapsed and there's blue forward flow. This patient has a low CVP and he's hypotensive. he's more likely to respond to fluid in this setting, more likely to be volume responsive based on where he is on the Starling curve. A check of his biventricular function and pericardium, there is no pericardial effusion and we see actually his right ventricle here is actually somewhat small and somewhat underfilled. And perhaps suggesting that he could tolerate and benefit from some fluid resuscitation. And now we're going to integrate our pulmonary ultrasound to identify possible source. And what we see is a patient has a consolidation here, subplural consolidation. We see this shred sign here and we see that thickened, thickened irregular plural line and the CT scan done later corroborated that the patient had a pneumonia as a source of his sepsis. So our next circulatory failure we're going to assess is hypovolemic shock. And with our cardiac exam, we're going to define our hemodynamics and those should be low cardiac output and low CVP based on our metrics. And then we're going to use our pulmonary exam and possibly our abdominal exam to look for fluid loss and a possible source to guide therapy. So here's our case, a 19-year-old assault victim, echo performed in the ultrasound performed in the ED. We see that the IVC to start with is completely collapsed and the right atrial pressure is very low. We see that persistent forward flow from the hepatic vein, that blue flow into the right atrium, signifying low right atrial pressure. And we see low stroke volume, the VTI, the LVOT VTI is 12, again, normal, somewhere between 18 and 22. We see normal biventricular cardiac function. We do not see any effusion or obstructive shock. And then in the emergency room, we can do a, add an abdominal exam, a fast exam looking for fluid in the abdomen, giving us a source of blood loss. And we see here, this line of free fluid here, just adjacent to the kidney. This was a positive fast exam and this patient went to the OR. So after seeing that trauma patient, well, let's talk about the 65-year-old patient who had an in-hospital PA arrest, underwent about 20 minutes of CPR on the floor, was transferred to the CCU and was persistently hypotensive, persistently in shock in the CCU. So we performed a quick bedside ultrasound, very, very focused exam. We see normal biventricular function here. The IVC is somewhat unhelpful. It's normal size. The hepatic vein here is somewhat dilated, sort of unclear what's going on, but of course the patient, again, is on mechanical ventilation. I don't have the left apical lung exam, but the right, it's the same as the right, which is here. Normal lung sliding. No pneumothorax. And so what we did is we moved forward and performed a focused fast exam in the CCU. And of course we see here a lot of fluid around the liver. This patient, in the setting of rather aggressive CPR, suffered a rib fracture, which led to a laceration of a hepatic artery and then a bleed. So what I want to talk about here and sort of present here is the fact that CPR is a traumatic procedure, and it's important then to think about adding on a fast exam sometimes in these patients if the clinical situation is not making a lot of sense. And let's look at this case of a 55-year-old female who is status post motor vehicle accident, went for an X lap, and then upon return from the OR is persistently hypotensive in the CCU. And so an echocardiogram is performed. And just looking at the echo images here, a cardiac focused diagnosis, and this was actually one of the things the fellow thought, was that the patient had hypertrophic cardiomyopathy because the LV appeared so thick. However, let's think more broadly and add some additional ultrasound imaging. So what we see when we look at the lung, both at the apicy here, we're looking for a pneumothorax. We see no pneumothorax. We actually see normal lung sliding. The lungs actually are normally aerated in this region. Then if we look really at that RV, look at that RV, it is a completely underfilled right atrium as well, very underfilled RV. And then the patient's on a ventilator, but a transhepatic view of the IVC demonstrates that the IVC is basically collapsed. So we have an underfilled LV and a collapsing IVC. We're thinking more about a bleed. And of course, this patient was bleeding, went back to the OR, and then after coming back from the OR was adequately resuscitated. And what we see, what happens to that hypertrophy of the ventricle, this is pseudo hypertrophy of the ventricle in the setting of hypovolemia, profound hypovolemia. We see once the patient is resuscitated, that significant hypertrophy resolves. And in fact, the right ventricle is now enlarged and full of fluid like it should be full of blood. So this is pseudo hypertrophy of the ventricle in the setting of profound hypovolemic shock. So our next physiologic phenotype of circulatory failure is going to be cardiogenic shock. And again, we're going to use our cardiac ultrasound exam to define that physiology, understand something about even the etiology of the shock. And then we're going to think about using pulmonary ultrasound to help us with volume status and even abdominal ultrasound, again, to look at volume status and even assess that right ventricle. Here's our case, a 70-year-old male who presented with shortness of breath and hypotension. And in discussion with the patient, he noted a severe episode of epigastric pain a week and a half prior to presentation. Our ultrasound demonstrates an injection fraction of around 40% to 45%. And actually, the squeeze is not bad here. There are some findings. The inferior lateral and inferior wall are achinetic. So now let's define our hemodynamics. Again, we are facing a patient with hypotension and circulatory failure. The cardiac output is going to be low. The VTI is 10, so that's a low stroke volume. And the filling pressure, the CVP, is going to be high. We see that the hepatic vein flow is isolated to just diastole. We see diastole here. And then a supportive measure for that shortness of breath is going to be the presence of diffuse B-lines with normal lung sliding. This patient has pulmonary edema. All of this consistent with a cardiogenic picture to his circulatory failure. So now we've made that diagnosis of cardiogenic shock, the setting of a very low VTI with the LVOT, congestion on lung ultrasound, high central venous pressure. But we want to move a step further here and understand something about the etiology. We noted that the injection fraction was, you know, around 40% was not terrible. But what tipped us off was that there was this inferior lateral wall motion abnormality. So what I'm going to suggest to everyone is ensure that you place color doppler over your mitral valve and your aortic valve because what you want to understand is, is there an etiology for this cardiogenic shock that is valvular? This patient has an EF of 40%, but a very low stroke volume because all that flow is going backwards. And that's important to know because it changes our plan. So we're going to take this patient to a cath lab and we're going to put in an intra-aortic balloon pump to stabilize him to improve the pulmonary edema and to improve his hemodynamics. So that case of severe mitral regurgitation causing cardiogenic shock is important because it reinforces the fact that assessment of the valves is really important in patients who present with circulatory failure, particularly the left-sided valve. And it can be helpful for etiology. For example, a patient could be presenting with endocarditis here of the aortic valve, or it can be helpful to help guide your therapy. For example, this patient here who has rheumatic heart disease and mitral stenosis, you're going to want to be careful with heart rates here. If this patient goes into atrial fibrillation at very fast ventricular rates, they're going to lose their cardiac output and they're going to develop more pulmonary edema. So now let's look at this complicated case of a 59-year-old female who was scheduled for elective repair of a right MCA aneurysm. And just five minutes after induction of general anesthesia and perioperative antibiotics, developed profound hypotension that led to a PA arrest. ROSC was achieved after 10 minutes of ACLS, and then she ended up on high-dose epi for MAP support. We can see that the EKG here shows some QT prolongation and some nonspecific ST changes, but no ST elevation to suggest an MI. And we see that even though she's mechanically ventilated, her IVC is completely collapsed. So she's at very low CVP, and she also has very low stroke volume. She has a VTI of eight. And if we were able to calculate out her cardiac output, it would be three. So we have low CVP and low stroke volume. Is this patient bleeding? And why? But then when we assess the ventricular function, parasternal long axis, we see that there is hypercontractility of the base with an akinetic or ballooning apex. And in fact, the apex of the right ventricle as well is hypokinetic. We can see it here in the subcostal view. So we have mixed physiology shock. We have a low CVP, low central venous pressure, and low cardiac output, and it's due to a decreased vascular tone from anaphylaxis, a high tryptase would cinch that, but then also superimpose the tachycebral cardiomyopathy or stress cardiomyopathy that, of course, resolves about a week later with repeat echocardiogram. And finally, we're going to look at obstructive shock, which is characterized by a low cardiac output in the setting of a high central venous pressure. And this is a really interesting hemodynamic phenotype, which allows us to incorporate a pulmonary ultrasound, vascular ultrasound, to move us in the direction of what the etiology of the shock is. So here's a 59-year-old female with a cardiomyopathy, undergoes placement of an AICD. She develops significant hypotension in the post-procedural unit, and they start running fluids. A stat echo is performed, and the EP fellow starts dopamine based on the fact that the left ventricle is incredibly hypokinetic. The patient is transferred quickly to the CCU, where she is still hypotensive, and we see the IVC is dilated here, and the RV function looks reasonable. There's no pericardial effusion. So high CVP and what looks like low cardiac output. So again, when this patient arrived to the CCU, she was still hypotensive on pretty high dose dopamine. And again, we were seeing this, what we thought was a high CVP and just low cardiac output, but it didn't make a lot of sense to us. And so what we added was a lung ultrasound. What the lung ultrasound showed in the left pleural space was a complex pleural effusion. And this is blood in the pleural space. This patient is having a large bleed, causing a tension hemothorax, actually shifting the trachea over, and needed emergent placement of a chest tube. So again, how incorporating lung ultrasound here can change the picture of cardiogenic shock to obstructive shock. And now let's shift to this 45-year-old female who presented with profound shortness of breath and hypotension. And this is a nice comprehensive look. We see that the IVC is dilated here. We see that the flow in the hepatic veins is limited to diastole with these systolic reversals. This is high central venous pressure. And if we look at the stroke volume, we see that the VTI is six. So this is profoundly low stroke volume. And in fact, the cardiac index was 1.5. So this is a patient with high CVP and very low cardiac output. And then we do a nice comprehensive lung ultrasound. And we see that there is an A-line pattern. There's no tension pneumothorax. We don't see B-lines here. The lungs are well aerated. And then the cardiac exam, of course, is incredibly telling. We see a very dilated right ventricle. Here in the parasternal long axis view. And here in the parasternal short axis view. With shift of the interventricular septum. This D-shaped ventricle consistent with pressure overload in the right ventricle. And here's our apical view. This is the male format RV on the right, LV on the left. We see that the RV is dilated, showing that prominent moderator band from the dilation. We see that the free wall is aconetic with a hyperkinetic apex. This is the McConnell sign. It's due to a hyperdynamic LV kind of pulling on that apex of the RV. This is not a specific finding for PE. This can be seen in other cases of acute increases in pulmonary vascular resistance. And again, the dilation of the RV that occurs in the setting of that acute increase in pulmonary vascular resistance leads to a dilation of the annulus and significant tricuspid regurgitation, which we saw in the form of V waves in the hepatic vein tracing. This is a pulse wave doppler of the right ventricular outflow tract. This is essentially our stroke volumes from the RV. And we see that there's notching here in systole. This occurs in the setting of high PVR. And then, of course, we have an increased TR velocity, which calculates to 33 millimeters of mercury. If we add the right atrial pressure of at least 20, then that gets us up to 53 millimeters of mercury for the estimated right ventricular systolic pressure. So putting this all together, we have shock and shortness of breath, RV dysfunction, an A-line pattern, so normally aerated lungs, a high CVP, a high PVR. This is TPA or a PE. So now we've comprehensively gone through the different physiologic phenotypes of circulatory failure and seen how we can use the cardiac ultrasound and pulmonary ultrasound as a fundamental or core exam cardiopulmonary ultrasound to assess these patients in circulatory failure with the addition of limited abdominal imaging and vascular imaging when clinically indicated. So I just want to conclude with a brief comment about the use of cardiopulmonary ultrasound in a therapeutic management and volume responsiveness assessment of shock patients. I wanted to highlight this paper by a couple of our colleagues at the SCCM because I think they did a really nice job of showing how we can integrate cardiac ultrasound and pulmonary ultrasound, use cardiopulmonary ultrasound to guide therapy for septic shock patients. And what they did was they created these phenotypic clusters based on ventricular function, IVC or central venous pressure, and then lung ultrasound. Cluster one are our normal hearts that have low filling pressure. Cluster two is a left or biventricular systolic dysfunction. These are patients with high CVP and pulmonary edema. And then finally, cluster three are patients with isolated right ventricular systolic dysfunction. And either those patients that have chronic pulmonary hypertension, so RVH, or patients that have RV dilation with no RVH, so patients that have more acute RV dysfunction. So what the authors recommend is that you tailor your therapeutic intervention, either volume or basal active medication, based on your findings with your cardiopulmonary ultrasound. So for example, if you place a patient in cluster one, that is to say they have normal left ventricular systolic function, if they are dry, have low central venous pressure, have a smaller flat IVC and dry lungs and A-line pattern, you're going to give them volume. And if they develop B-lines, evidence of pulmonary vascular congestion, you're going to switch to vasopressors. If they already have pulmonary vascular congestion or pulmonary edema or a dilated IVC, you're just going to use vasopressors in this setting. In those patients with isolated left ventricular systolic dysfunction or biventricular systolic dysfunction, you may try a fluid challenge, less fluid than you give those with a normal left ventricular systolic function. In those patients that have a normal central venous pressure, as denoted by a smaller collapsing IVC, and then dry lungs and A-line pattern. However, if the patients are already demonstrating evidence of elevated CVP, a dilated IVC, or pulmonary vascular congestion, pulmonary edema, you're going to focus on vasoactive medications and not give volume to those patients. And then finally, in those patients that you've diagnosed with right ventricular systolic dysfunction, your decision to give fluid or remove fluid can be based on how elevated the right atrial pressure is, how elevated the right ventricular filling pressure is. And so those patients with very elevated right atrial pressure, they may need volume removal. And you're going to make that diagnosis based on the presence of a dilated IVC, or even using, as they've noted here, a shift of the atrial septum, or the systolic to diastolic ratio in the hepatic veins, more diastolic flow than systolic flow, as we talked about before. In summary, an integrated holistic or whole body approach to point of care ultrasound in the ICU is really important. And we need to judge the findings within the clinical presentation of the patient. A step rise cardiopulmonary exam and hypotension and shock that focuses on hemodynamics, I think it's really beneficial. And don't forget to add limited abdominal ultrasound or vascular ultrasound as indicated. And don't forget to use colored Doppler on those left-sided valves in patients with cardiogenic shock so that you don't miss valvular pathology that could be driving the clinical presentation. And finally, again, hemodynamics are important. It's not just about the squeeze of the ventricles. It's about the actual stroke volume. And that stroke distance at LVO BTI is a powerful, powerful clinical indicator for outcomes. If you have any questions, please email me at brandon.wiley.mayo.edu. And I'm on Twitter at CICU underscore ECHO.
Video Summary
The talk focuses on cardiopulmonary point-of-care ultrasound in the care of critically ill patients. The speaker discusses the holistic approach to bedside ultrasound in the ICU, with a focus on cardiopulmonary ultrasound, including pulmonary ultrasound and cardiac ultrasound. The speaker highlights the importance of integrating lung ultrasound and cardiac ultrasound to make a rapid diagnosis of the underlying etiology of a patient's critical illness or decompensation at the bedside. The speaker provides examples of cases where cardiopulmonary ultrasound was used to diagnose specific conditions, such as a patient with an RV infarct, a patient with pneumonia, a patient with hypovolemic shock, a patient with anaphylaxis and stress cardiomyopathy, and a patient with a tension pneumothorax. The speaker emphasizes the importance of understanding hemodynamics, such as cardiac output and central venous pressure, in guiding the management of shock patients. The speaker also discusses the use of Doppler-derived stroke volume to assess cardiac output, as well as the use of abdominal and vascular ultrasound to assess volume status and potential sources of bleeding. Overall, the talk highlights the value of cardiopulmonary ultrasound in the ICU and encourages its integration into clinical practice.
Keywords
cardiopulmonary ultrasound
bedside ultrasound
ICU
rapid diagnosis
hemodynamics
shock patients
Doppler-derived stroke volume
volume status
clinical practice
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