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Echocardiography as a "Biomarker": Echocardiograph ...
Echocardiography as a "Biomarker": Echocardiographic-Driven Approach to Characterization of Cardiovascular Phenotypes
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Video Transcription
Thank you for this beautiful introduction. Yeah, I've been knowing Alexi for a long time. I don't want to say how many years, but. So I have, let me just start here. I have no disclosures. So I'll talk today mainly about how to characterize cardiovascular phenotypes utilizing point of care ultrasound based on a single view. And that will entail subcostal short axis, long axis and IVC and lungs, so three systems. All right, so we'll start with our typical case. I'm in the OR and then this patient showed up with an encephalic shock with perforated viscous and the pressure is 70 over 60. The patient is right in front of me and I'm wondering how am I gonna start managing this patient. I need to stabilize him then anesthetize him. And the first three buttons they have to push is fluids, vasopressors or inotropes. So we know from the hemodynamics of septic shock that septic shock starts with capillary leak and this will lead to hypovolemia together with increased venodilation and arterial dilation. So that will also cause relative hypovolemia. After some time, the myocardial muscle get also affected and you need to get septic cardiomyopathy and then because of ARDS, the pulmonary vascular resistance also will increase and cause sometimes isolated right ventricular dysfunction. And many of these patients will have arrhythmias especially atrial fibrillations. So the surviving substance guidelines 2018, the recommendation was to promptly within one hour infuse 30 mLs per kilogram IV fluids, give pressors and inotropes if pressors doesn't work. But this probably is not going to work for everyone because we know that septic shock has many flavors. Could be hypovolemic, maldistributive, obstructive, pump failure, could be a mix. And we would like to treat the cause. For instance, blood pressure is cardiac output times stroke SVR. If there is cardiac output is heart rate times stroke volume, if there is a problem with heart rate, we need to fix it. And then if there is a problem with preload, we need to give volume. SVR corrected with vasopressors and inotropes should be for pump failure. We tried static measures to differentiate between these kinds and like right atrial pressure, left atrial pressure, they failed us miserably. So in 2021 guidelines, the recommendation continued to be fluids, vasopressors and inotropes. But how there was a little tweak. The giving 30 mils per kilogram to everyone was downgraded from strong to weak evidence. And they recommended the utilization of dynamic measures. So dynamic measures is echocardiography, could be, but it seems very complicated. In 2004, the FATE protocol was published. 97% of the time the intensivists after training were able to identify, to get good images of the heart. And then more than one fourth of them have made decisive decisions based on point of chiral tracel. But the problem I tried to train my faculty on FATE, it's kind of complicated and difficult. And it takes, it took our residents 18 minutes to complete. How about if we look only at the subcostal view? So if we only focus on the inferior vena cava and subcostal area, then we can still gather a lot of information and we know during extreme situations like cardiac arrest, this is probably the only window which is available. So we have experience with it and it's very informative. So we compared the FATE exam for all chambers to only subcostal view. We published this in the Canadian Journal of Anesthesiology. We made a simple comparison, only is there any significant pericardial effusion? How about the RV size and function, LV size and function? And it's all based on pattern recognition and whether there's severe dysfunction or not. And then volume status based on the inferior vena cava. And in 102 patients, our residents were able to get good images in 82. And the subcostal view took only four minutes compared to the full FATE. And then there was substantial agreement in the RV size, LV size and contractility, almost perfect agreement in the presence of pericardial effusion, RV contractility and septal motion. The least agreed upon was the RV size. And this is because you can see here based on the axis you cut the RV, it can actually, the size can vary. So we can underestimate the RV. For this reason, when you do a subcostal, you need to align the tricuspid and mitral valves. So now we know ultrasounds are becoming more accessible. They're smaller, they're cheaper. You can actually replace the stethoscope and place it around your neck. Also, the public knows about that. Last year, the New Yorker published that with the handheld, with the AI being spread, the public starts to expect us to use ultrasound as well. And I like the frame of work of EyeAIM very much because it actually gets us to the point where first we need to use the point of care ultrasound for a specific question that we cannot wait for it to answer. And then the acquisition, we need to optimize the patient position for subcostal patient laying on the back. And then utilize the correct probe. And then you need to have a protocol in mind. And then after that, the interpretation, you need to look at the image quality, recognize structures and patterns. And then the most difficult part is relate the information to the clinical context. That's where you need to still be a physician. And there's a lot of, you need to relate the finding to the patient's complex situation. So for instance, here, subcostal long axis, you can see pericardium, the ventricles are contracting very well, almost hyperdynamic. And then you see the inferior vena cava is smaller. So this patient's probably in hypovolemic slash or maybe distributive shock. Six hours later, you can see that the LV now is not contracting very well. The IVC is plethoric. And because probably we gave a little bit too much fluid, now we have high pressure pulmonary edema, septic cardiomyopathy. So now if we try to simplify the process and utilize ultrasound as a qualitative tool to assist these patients, maybe we can streamline and maybe start introducing ultrasound. So we published the classification of phenotypes for, we separated the hearts into clusters and phenotypes based on the subcostal view. And basically we classified them in three clusters. Cluster one basically stems on normal ventricular function. Cluster two is left ventricular systolic dysfunction. Cluster three is isolated right ventricular dysfunction. So for instance, when the ventricles are small and hyperdynamic and the inferior vena cava is flat, that's a phenotype one, that's probably hypovolemia, especially if the abdomen is soft and there's no increased abdominal pressure, it would be safe to say that this patient can utilize volume. And this situation here in cluster two, left ventricular systolic dysfunction, you don't need to do a lot of measurements to notice that this ventricle is not getting smaller during systole. The anterior mitral leaflet is not hitting the septum and then there isn't much of motion at the mitral annulus. So we can safely say, especially when you link that to the inferior vena cava, that's basically a pump failure. And this situation probably will need some sort of inotropes after optimizing the volume. Here, anytime the RV gets bigger than the LV causing septal shift toward the LV with the plethoric IVC to demonstrate obstructive physiology, that's acute or acute on chronic corpulmonale. In this situation, we definitely need to be very careful of fluid. So is this patient hypovolemic or no? I mean, the ventricle is full, not contracting really very well, but one system is not enough. Now looking at the inferior vena cava here, you can see that this patient, despite having severe systolic dysfunction, is dry and the treatment, the correct management here is giving fluid. This patient basically has a baseline of cardiomyopathy with ejection fraction of 20% and now having sepsis. So probably his ejection fraction is a little bit better than the baseline, but we don't know the baseline. So underlying chronic disease and sepsis is a problem. For instance, in this patient here with the 62 with small bowel obstruction, hypotensive, you can see here the LV cavity is very thick. I mean, the LV walls are thick and the cavity is small. Placed an NG tube for this patient, 1.3 liters came out. And yeah. In this situation, is the patient dry? There's a small cavity, but this patient has baseline dystoic dysfunction. So you cannot really look at the cavity as an indication of how much volume status is. Normal heart basically contracts actively and pulls blood in, but patients with dystoic dysfunction, that doesn't really work. Lysotropy is a problem, which is ATP consuming process, and you need to have a higher preloads and filling pressures to fill these ventricles. If you give volume, you need to keep it at tight range because if you give too much volume, you'll end up with pulmonary edema. So you have to pay special attention to patients who have chronic disease. In this situation, your question should be, is my patient hypovolumic or not? That shouldn't be the question. The question should be, is my patient volume responsive or not? This, we can actually integrate measures like pulse pressure variation, because that patient is in a very good condition, circumstances where he is totally paralyzed in the OR. The ventilation is controlled. We changed the tidal volume to 600 mLs. So it's a bigger tidal volume. And then we looked at the variation. So there isn't much of variation compared here. This patient's probably volume responsive, here he's not. So now we know that patient was hypotensive in 100 of microfenylephrine. We maintained that we didn't give more fluid. And then is my patient fluid tolerant or no? Before extubation, you just look at the upper lungs and you look at the pattern. There was no B lines indicating pulmonary edema. So we were able to extubate him without any problems. Now, signs of chronic disease could be tricky. This patient had right atrian enlargement, RV hypertrophy. There is some asides. This is a falsiform ligament, so asides. It's very difficult to assess the signs of chronic disease when the patient is in the gray zone. That means when the patient is not hypotensive. So this is the same case. Basically, the IVC was smaller. So he received some fluid and then he got induced. And then when he became hypotensive after induction, now you see the obstructive physiology, how the LV cavity is getting obliterated. The IVC is becoming plethoric. During cardiac arrest, you can see here how collapsed the LV. That's why it's an obstructive shock. So it's easier to apply point-of-care ultrasound in extreme situations. In cardiac arrest, everything, the pathology is very clear. When they're hypotensive, it is clear, but when they are not hypotensive, they're not clear. That's why I caution using ultrasound for operative clearance. Point of care ultrasound should be to answer a question that you cannot have an answer unless, like you cannot delay the answer. So in our clusters and phenotypes, we figured that we should really include signs of chronic disease because it changes management. So phenotype three in cluster one includes thick ventricles, enlarged, thick LV, enlarged LA, and usually it's associated to these problems or chronic diseases. When there is systolic dysfunction, there are, we need to assist for these problems, and then if there's an RV hypertrophy and RA enlargement, then we need to, especially with this history, we need to do a complete critical care echocardiography, and Sarah will be talking about the STARS-FRAG protocol where any time you identify chronic, signs of chronic disease, we need to go and do more testing or complete critical care echocardiography. So both your hands are gonna sit on the left-hand side of this one. You're gonna walk out, both your arms. You're gonna push with your right and pull with your left. Focus on that front side tip. Now if you want, on this 44 Magnum, you can shoot in single action. And then push with your ball. Did you mean to do that? Yeah. So we just give a full day course on how to utilize the subcostal view in patients with sepsis as a pre-course and at this SCCM meeting. And I felt like all my students at the end of the day felt like they know everything and they felt their confidence levels was here. What I wanna caution them, then they will discover that there's a lot that they don't know, and then they need experience in filling the gap. So for this reason, the workflow should always have a mechanism for quality assurance. So always we need to save the patient's information, utilize DICOM-compatible machine. It takes a minute because I made it as much as possible it could be because our residents are very not lazy, like everywhere. And then utilization of the scanning ultrasound is the scanning should not be, should be take place without any interpretation. So this is one of the students during pre-rounds scanning the subcostal long axis, then the IVC, then the aorta to differentiate it from the IVC, then look at the subcostal short axis view, and then ended up with a lung examination. So this is only acquisition time, which takes few minutes, no interpretation here. And guess what? If she didn't save the images, we cannot interpret anything, only black screen. So now by utilizing the phenotyping of and clustering of these characters of the patients, we can talk about, we can comment on the image quality. This would be done under the supervision of attending during rounds. So we assess, there is a sound here. So this would probably be closer to a phenotype three, the left ventricular hypertrophy. We also have the pre-work IVC, and then, and then we had definitely a lot of B-lines. So we utilize the same concept and we test it out during COVID. During COVID, our hospital in New York got hit like all other hospitals. We had too many patients that the critical care team couldn't manage. So we start creating teams, utilizing anesthesiologists, and this is a surgical resident who got one day training in how to obtain subcostal view. And basically pre-rounds, they would go to the rooms and they would scan the patients every day. Anytime there is a hypotension or emergency, they would go in and do a subcostal view. So this patient is hypotensive, and you can see that the ventricles are contracting very well. The IVC is full. How can I advance without? Can you do the next arrow? Click, okay. So we saw that the ventricles were contracting well, but the IVC was full and the patient, like any other ARDS patient with COVID, have lots of B-lines, so they're not fluid tolerant. But given that, this situation tells me that this is more of a distributive shock rather than hypovolemic. So the treatment was, clicks please, the inotropes. I mean, vasopressors with some inotropic activity because of sepsis. Now, the entire exams took around like four minutes. And then in 80s, anytime there is signs of chronic disease or the images were not clear, I had to go back after rounds and do a full critical care echocardiography, the STARS-CRASH protocol. And to be honest, we're publishing this in Critical Care Exploration this month. I entered the room only 13% of the time. 87% of the time, the images were sufficient. So if we can move, I'll share with you a few cases. All right, so this patient, 50-year-old, COVID, PF ratio is really low. Received two liters in the last 24 hours on norepinephrine, vasopressin, lactate is four. So upper lungs, we have B-lines. There's good contractility and the IVC is flat. Now, hypovolemic shock. When we are looking at the aorta, we discovered that there's a lot of stuff here in the gastric area. So we placed an NG tube and 1.8 liter came out. So all the fluids was third spacing. Then we gave multiple boluses and we continue to follow the inferior vena cava and we got off pressors, lactate normalized. This is another one with some chronic disease. We didn't have any baseline echo, but you can see here the ventricles. I mean, this is not the most beautiful picture that I would send to New England Journal of Medicine, but still you can tell that the ventricle is not really doing a lot of contraction. And the IVC is full and the lungs are, like everyone else has B-lines as indication for mixed, probably high and low pressure pulmonary edema. So this is cluster two, boy ventricular function is phenotype five. The treatment was to titrate norepinephrine and then added low dose epinephrine. We have basically management cards based on the phenotypes and clusters to facilitate communication with trainees and to get everybody in the same page. Here, the RV is much bigger than the LV with a septal shift toward the LV. So this is acute on chronic corpulmonary. I had all my resident, they need to save the aorta and the IVC because I want to show you how similar both they look like. So you can not really confirm that this is the IVC without also saving the aorta. B-lines, so vasopressin and epinephrine. We pronged the patient, we started removing volume. So with cluster three treatment, basically based on optimizing filling pressures and then pump supports after load reduction and then pulmonary vasodilator. I'm going to share with you a patient who has signs of chronic disease. Too many videos, I guess. Okay, well, that's it then. Thank you. Five minutes? All right, because I have, I'll keep going. I have a few more cases, but I placed the cases at the end. So in case of, if Alexi says I stopped, then I'll stop. Not here, go to, let me see. Yeah, that's fine. Yeah, that's good. Perfect, all right, let's pray that it goes. Okay, so this patient showed signs of chronic disease. Basically the LV was thick and there's a little bit of thickening here at the aortic valve. The IVC was, despite being hyperdynamic, the IVC also was full. But because of the signs of chronic disease, I really cannot utilize the IVC to optimize my volume. So basically we did the critical care echocardiography. We diagnosed severe AS and then we used diastology to optimize volume. And I hope the others work better. Okay, oh, we have no videos now. Okay. This is probably a sign for me to stop. Anyways, this patient, we optimized volume based on the IVC for extubation, based on the subcostal view and the patient was extubated successfully. You can see here, there were bilateral B lines, but after diuresis, some A lines started to show up here. So once you do this every day on every patient, you start to see trends and it becomes dynamic measure. And this patient has very thick ventricle, very small cavity with a subcostal short axis. Only if the videos would work, flat IVC, bilateral B lines. So it was hypovolemic. We gave volume and then pre-round, the residents will text me the patient's phenotypes. And we noticed that on day five, the RV started to get dilated. So now it was time to actually prone the patient. So the phenotyping is dynamic based on the patient's hemodynamic activity. All right. Yeah, I think the publication and the critical care exploration is not out yet. It's but final revision. So maybe next week or so it will be out, it will have all the patients. We discovered early that patients have, that are hypercoagulable because this patient has good mechanics, was in PSV, good lung mechanics, and the PF ratio was low. And there is some RV dilation that was not noticed the day before. So we did ultrasound of the femoral veins and there were bilateral DVTs which start the therapeutic habit. That was an indication because the RV wasn't that dilated the day before. And those were sudden and there was no, there is the mechanics of the lungs. It was, there is no decreased compliance. This patient coded and after RASC, we placed an ECMO. This is the surgical residents confirming the ECMO position, cannulation position. And by the time we'd done with the examination, maybe an hour later, the cardiac, the ecotech showed up. And at this time we knew that the RV is decompressed. And so the LV is, the function was improving and the surgeon was comfortable to go home. So final message is you need to save the images and the only way to figure out if, the only way to progress because point-of-care ultrasound acquisition is not a problem. It's easy. The problem is interpretation and relating information to the patient. So to tackle this, you always need to save your images and always needed to be reviewed with an expert. So this could be achieved with a team based approach where you can have a lot of, in our institution, many of the resident students, even nurses are scanning and saving the images but nobody's allowed doing interpretation unless an attending is involved. How am I doing with the time? Thank you very much.
Video Summary
The presentation provided an in-depth overview of using point-of-care ultrasound (POCUS) to characterize cardiovascular phenotypes, particularly in cases of septic shock. The speaker, familiar with Alexi, discussed strategies to stabilize a patient in shock through fluids, vasopressors, or inotropes, acknowledging that static measures like atrial pressure are often insufficient. Recent guidelines have shifted towards dynamic measures, such as echocardiography, to address septic shock's nuanced presentations. The subcostal view was emphasized as a less complex, time-efficient alternative to comprehensive exams like the FATE protocol, demonstrating strong agreement in assessing cardiac function and volume status. Real-world applications were highlighted through case studies, illustrating how POCUS informs management decisions, including fluid administration, identifying obstructive physiology, and recognizing signs of chronic disease. The talk underscored the importance of saving images for quality assurance and learning, advocating for a team-based approach to interpretation.
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Two-Hour Concurrent Session | Be FOCUSED: Ultrasound Support for Resuscitation of Patients With Sepsis and Septic Shock
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2024
Keywords
point-of-care ultrasound
cardiovascular phenotypes
septic shock
echocardiography
subcostal view
fluid management
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