 Good afternoon, everyone. Welcome back after the quick launch and break. We're going to end the recording today. We're going to switch gears a little bit and move on from all the excellent comprehensive lectures that we've been watching over the next over yesterday and today, we're going to move on to the point of care ultrasound, incorporating both transtheraistic modalities and the incentives of the deal, and focusing not only on the heart, but also other organs that can help in the overall perioperative care of these patients, and not only in the operating room, but also in critical care units, recovery, even the words. So for this section, Dr. Marcus Alvator is going to be the moderator, and myself is the curator, and then I have the president here, and I'm a cardiologist in perioperative echo at Sonnybrook Hospital, where we also run for a point of care ultrasound fellowship program. So I'll leave it up to you, Marcus. So thanks very much, Pablo. So thank you everyone for your attention and participation over the past two days, and congratulations to Dr. Vegas for putting together another incredible conference. The amount of work that Annette and her team have put in over the past year cannot be overstated, as evidenced by the quality of the talks and discussion we've seen over the weekend. My name is Dr. Marcus Alvator, and I'm an anesthesiologist and CVSU attending here at Toronto General Hospital, and it is my honor to moderate the final session of this conference focusing on the utility and practicality of point of care ultrasound in and out of the operating room. This session was curated by my good friend and mentor, Dr. Pablo Perez-Demper, who you just met, a cardiovascular anesthesiologist at Sonnybrook Health Sciences Center here in Toronto, where he continuously champions and innovates the use of point of care ultrasound and trauma, cardiac arrest, and emergency non-cardiac surgery. He has put together an extremely impressive multidisciplinary roster of speakers from across Canada and the United States, and we will hear about POCUS from the perspective of not only the cardiac anesthesiologist, but also the disciplines of internal and emergency medicine. Our first speaker of the afternoon is Dr. Katie Wiskar, a general internist at Vancouver General Hospital. She completed a POCUS fellowship at Western University in London, Ontario, and she now leads UBC's general internal medicine POCUS fellowship program, one of only two such fellowships in the country. She currently splits her clinical time between attending on the clinical teaching unit and running the VGH internal medicine POCUS service, a clinical team which provides hospital-wide diagnostic and procedural POCUS consultations. Her POCUS passions include VEXIS and POCUS evaluations of volume status, all things echocardiography, and clinical integration of ultrasound findings. As with all prior talks, please post any questions in the Q&A and we will discuss them all during the panel discussion involving the afternoon speakers. Alright, hi everyone. My name is Katie Wiskar, and I'm really thrilled to be here today speaking to you about VEXIS for fluid tolerance. So I have no conflicts to disclose. My only disclosure as such is that I admit to feeling a little bit starstruck. VEXIS is something that I'm really passionate about, and I spend a lot of my time thinking about and reading about. But I noticed that two of the faculty member on the conference today who are actually speaking on different topics are actually two of sort of the real godfathers of VEXIS, whose work has helped really push this forward. Drs. André De Neau and William Beaubien Soulinghi. So I will say that I'm very grateful to them, to their work and to the work of others that have helped push this topic forward and allowed me to be here speaking to you today. So our objectives today, we'll talk a little bit first about the idea of fluid tolerance and how we look for this with ultrasound. We'll talk about the VEXIS exam, a little bit about how to do it, and some of the evidence behind it. And then we'll finish by talking about what the knowledge gaps are. What do we not yet know about, you know, the evidence base, the technique and how to put this into practice. So let's start off by talking about fluid tolerance. So fluid responsiveness has been talked about ad nauseam. This is a very familiar topic to everybody. Enumerable publications are written on the topic, so, you know, will someone's cardiac output increase in response to a fluid bolus? And for a long time, this was kind of a main focus when we thought about fluid therapy and hemodynamics and volume status, really this focus on the left side, the mean arterial pressure fluid responsiveness. And this is not unimportant, obviously, but I think recently we've begun to recognize that there is another side of that coin, just as important as fluid responsiveness. So might the patient benefit from fluid is this idea of fluid tolerance. So might the patient be harmed by fluid. And we all recognize the increasingly the harms of excessive fluid administration and fluid overload in multiple organ systems. So, you know, to name only a few pulmonary edema, hepatic congestion, congestive nephropathy, congestive encephalopathy, tissue edema, the list goes on. And I think, you know, for a long time we believed or we hoped that patients were essentially fluid responsive and fluid tolerant to a point, and thereafter became fluid unresponsive and fluid intolerant. And what we realize increasingly is that these are really two separate concepts that can occur at different points in the trajectory in a patient's illness and those points can actually even move as a patient moves through their illness course. And so increasingly, you know, we really want to think about these separately. And, you know, despite the fact whether or not a patient's cardiac output may or may not improve with fluid, the kind of flip side to this that we really have to think about is, is there evidence that they may be harmed by additional fluid. So this is the other piece to that kind of volume status question. So, how do we look for this with ultrasound, this is an ultrasound conference after all. So obviously we'll look at the heart, we'll look at the left heart at LVEF at diastology if that's something you're comfortable with to see if there's signs that you know the left heart may not handle this well. We'll look at the right heart obviously for signs of RV dilation pulmonary hypertension RV dysfunction etc. To look for left sided congestion. We can again look at the lungs if you look for pulmonary edema be lines plural effusions. But when it comes to looking for right sided venous congestion up until recently we didn't have a lot of tools so you know we could look at the IVC in the JVP. But, you know, we've long recognized that these are imperfect measures. They are sensitive but not specific for deleterious venous congestion. Many patients, especially patients with chronic pathology will always live at a plethora IVC. And so, you know, really, we lacked a lot of tools to help us detect this right sided congestion this venous congestion. And so this is where the idea of vexes comes about. So vexes stands for venous access ultrasound score. And again, the principle behind this is, can we take a step back farther away from the right atrium farther away from the IVC and look at other inter abdominal vessels with ultrasound to find further evidence more specific evidence perhaps of deleterious venous congestion. And it turns out so so the vexes is quite a recent concept this paper this is a seminal paper on vexes that I've shown you a graphic from is from 2020. But people have actually been looking at these waveforms in isolation for decades in some cases so this is not a new concept. But what this group did doctors Bobi Assoulini and his colleagues is put these together so they said, can we look at several of these inter abdominal vessels so namely the hepatic vein, the portal vein and the inter renal veins and use them to help us paint a picture of venous congestion. Because we know that each of these vessels has a characteristic Doppler profile with pulsemaid Doppler under normal physiologic conditions, and that profile changes predictably with increasing venous congestion. And so again what we can do is look for signs of congestion in multiple waveforms because each waveform has sort of its nuances and its pitfalls. But if we see evidence of congestion in several waveforms that paints a strong picture really suggestive of organ damaging venous congestion. So I won't go through the details of how to do this in the interest of time, but very briefly this is sort of what this looks like. So your first point is always the IVC the IVC is your entry point to congestion. If you don't have a congested IVC do not do not pass go do not collect $200 you know you stop there. The other thing I'll say about examining the IVC is in the paper they used a diameter cutoff of two centimeters. And I know because I've spoken to several of the authors about this in person that they actually wish they'd also been able to include some data on the short axis of the IVC. So there's some evidence to support the fact that a really spherical round plethoric IVC is actually a better correlate, rather than the diameter or the or the collapsibility alone. So adding a short axis can help here, help you detect whether or not an IVC is truly plethoric. If you find a plethoric IVC you're going to go ahead and examine the intropodominal vessels where possible. So starting with the hepatic vein. This is usually easy to identify in B mode, either in a subzyphoid view or in a trans hepatic lateral approach, either with a phased array probe or a curvilinear probe. You'll see it in 2d you'll see it draining into the IVC, you can throw color on to confirm that you have a nice Doppler signal. And then with pulse wave Doppler, you'll put your your pulse wave on and you'll get a nice spectral waveform tracing. And then I won't go into too many of the details of this, but the waveform I've shown you here is abnormal so normally a hepatic vein should have two primary components that are below the baseline, indicating blood flow down the hepatic vein towards the heart that s and a d wave insistently and diastole. And as you get increasing and especially severe congestion we can actually see reversal of that s wave above the baseline as is demonstrated here. Next you'll go ahead and find the portal vein. So again looking in the liver typically from a trans hepatic lateral approach. The portal vein is usually quite easily identified it has bright hypercoic walls in 2d and with color Doppler you should see that nice red pathopetal flow. Again with pulse wave Doppler, you'll get a spectral waveform, which normally should be continuous low grade flow. And here I've shown you an abnormal waveform that we see as quite pulsatile with a lot of variability. Finally you can look at the kidneys. The kidneys are always the toughest. The vessels are very small because you're looking for the intra renal vessels. Ideally a vessel that is actually in the renal cortex or at the cortico medullary junction. So color is really necessary here to help you pick up those vessels. And then again with spectral Doppler you'll get a waveform. Sometimes you'll actually see the arterial waveform above the baseline and the venous waveform below the baseline. Here we just see a venous waveform which is abnormal. Again normal flow is continuous low grade flow and here we have highly abnormal what's called monophasic flow present only in diastole. So that's kind of the gist of how you do it. Coming back to the original Vexus paper very briefly this is sort of what they looked at. So this was a cardiac surgery, a post cardiac surgery population. And what they did is they took patients on admission to the CVICU did a Vexus score on them and then look to see did their Vexus score correlate with subsequent development of acute kidney injury. Now in the table on the left here, you can see a lot of different grading so you have Vexus A, B, C, which is somewhat irrelevant. Essentially the authors were playing with different permutations that made up the Vexus grading system. The one that was sort of settled on is this Vexus 3 grading system, which means severe abnormalities in more than two waveforms. I'll also say here that increasingly so many of us use this in our practice without actually using sort of a numerical Vexus score on a daily basis but rather by examining the waveforms and describing quantitatively or qualitatively what we see. Because this allows you to use these waveforms even if all of them aren't available, which can often be the case and sometimes gives a bit more nuance. But regardless we can see that here in this paper what they found is that patients with severe congestion so a Vexus of three severe congestion had a higher incidence of developing acute kidney injury compared to those who didn't. What we see here in the leaf plot on the right is actually that a positive Vexus score so again a Vexus considered consistent with severe congestion as shown in in graph a made a much more significant change in the post test probability of developing aki compared to an elevated CVP which is what you see in graph B. So this was a useful correlate for the development of adverse kidney outcomes in this population. So that was kind of the the initial seminal work again recognizing that a lot of background work had been done over many years on each of these individual waveforms. Now I'm not going to review the evidence in detail because that would be both excruciating and very long, but I'll highlight a few studies here in a couple different populations to try to give you a sense of where we're at right now in terms of the evidence base for this. So, obviously a cardiac surgery population has been studied the work of Dr. Dino and others other than that the bulk of the literature really is in heart failure populations this is where we see a lot of this work especially a lot of the background work looking at these waveforms individually. This was a really interesting quite recent study that looked at patients admitted with acute decompensated heart failure. They had a vexus score done on admission and they look to see which components of this in particular correlated with adverse outcomes and they were actually looking at death during hospitalization so a pretty significant outcome. And they found that a very abnormal intra renal venous flow IRVF so a monophasic IRVF is your most abnormal waveform was quite significantly correlated with the death during hospitalization a pretty impressive area under the curve there. Now again this is this is all correlation not causation, but some interesting food for thought. The next population here is Asia so acute coronary syndrome. This is a group where there hasn't been a lot of work yet but we're starting to see a few papers. So again, they took people coming in with acute coronary syndrome, they had a vexus score done on admission, and they look to see whether this correlated with the development of acute kidney injury during their stay. And again, they did find an association here. One thing that's interesting is that in the previous groups and generally in the heart failure population we see that it's the people with really severe congestion of vexus of three where you see that correlation. Whereas in an ACS population we actually see the association with anything more than a vexus of one so that's really any mildly abnormal waveform. And there's a few possible reasons for this. My theory is that you know in your heart failure population as we'll talk about a bit later. There's a lot of patients with really chronic pathology who probably never live at a normal vexus score right they probably always have a degree of congestion, given their chronic pathology. Whereas in an ACS population you know we do see more people come in potentially who are younger with less chronicity. And really the development of their AKI is going to be secondary to that very acute change in their myocardial contractility. So this may be why we're seeing some of an association at a lower vexus grade in this population. Finally the last paper to tell you about is this paper that was done in a general ICU population so there's been a few studies recently looking at the general critically ill population. This was the AKI vex study. It's probably the closest thing we have to sort of a randomized interventional trial in this field. So what they did is they took all commerce to an ICU. Everybody had a vexus score at admission. And then anyone who had a vexus of more than one had diuretics suggested to them. And then as an outcome they separated their groups into those whose vexus score improved during their admission versus those in whom it did not. And basically what they found is the people who improved their vexus score from that initial scan had more had better renal outcomes so more days free of renal replacement therapy than those who did not. And this you know again this is correlation this is not causation and in some ways this is perhaps unsurprising by saying okay the people who had such severe disease that we couldn't improve their congestion did worse in terms of their renal outcomes. The other thing that's interesting to point out about this population is that there's actually been some other studies that have not shown in association between vexus evidence of congestion and AKI. My theory into that is that you know in contrast to maybe hard failure or ACS populations where congestion and hemodynamics are such a big driver of their AKI. In a generalized view population you have so many other potential factors right people may have, you know they may be in hemorrhagic shock they may have ATM they may have sepsis induced micro vascular dysfunction, toxin mediate interferopathy a whole host of things. So I wonder if that's why in some of the papers that we've seen we haven't really seen as much of a correlation in those patients. So as a summary to all of that this table is not really meant to be read this table for those who are interested is from a recent very comprehensive review that basically looked at all of the evidence behind each of the individual waveforms and the vexus score. And you can sort of see which populations these were in and what was shown. But to summarize the evidence still the bulk of this, you know dating back is still for individual waveforms, although we're seeing more and more evidence for kind of this combination. Most of this is still in heart failure populations, although as I've tried to highlight we are starting to see evidence in different patient populations. And most of this is related to renal outcomes. Although we are starting to see things again things like mortality things like delirium in one when one population. So we're seeing other outcomes but most consistently, it's renal outcomes that have been looked at with this. And then probably lastly the biggest thing to highlight is as of yet we still don't have any prospective randomized controlled study of this to guide treatment so we have no study yet that says, if we take people coming in and they get a vexus compared to those who don't compare to those who just get usual care. They do better they have better renal outcomes they have better mortality better length of stay what have you that does not exist yet. Alright so finishing off with what do we still what do we still not know in this in this population in this field. So in terms of technique. Again I haven't gone into too many of the details of techniques. This is an advanced technique. You know it can be taught and we got residents on our ultrasound rotation and by the end of a month. Most of them can can reasonably get sort of a portal vein in particular, but it is a tricky technique. A lot of the evidence and things that we the papers we've talked about today are performed by a small number of expert scanners and doing all of the scanning. So it's kind of yet to be seen how this would perform in a more sort of widespread population with more widespread adoption. The availability of Doppler ultrasound especially in handheld is still varying although I think that's increasing. In terms of the evidence so many populations are still unstudied as I mentioned most of this is still in heart failure although we are starting to branch out. There's also some populations that have been almost systematically excluded from a lot of studies so especially things like cirrhosis pulmonary hypertension sometimes valve disease sometimes evidence of increased intribdominal pressure. There's a few populations where we really don't have a lot of evidence for this technique yet. And finally the biggest thing as I've just pointed out is that, again, we don't yet have any good interventional data to say that this technique results in a difference compared to the standard of care. And now this is this is an opinion and this is my opinion and clearly I'm biased because I'm here talking about vexus. But I don't think this is a reason not to use this because I think it's worth thinking about what the alternative is right. The alternative for detecting this kind of right sided venous congestion is not great. We can look at the JVP, we can look at the IVC, we can squeeze the legs for pulmonary edema. We can look at labs for congestive hepatopathy or congestive nephropathy. But it's not great we don't have a lot of other great tools to find this and so I think, you know, as this evidence base grows will will see more that perhaps will lend more comfort to using this but to me, this is a reason to not yet adopt this. Okay, and finally the clinical integration and translation to practice what are the unknowns here. So, as we talked about at the beginning you know I think the we are we are increasingly recognizing the importance of venous congestion of this fluid tolerance concept. I think that that is becoming increasingly accepted but but that is still growing. The evidence base is still an evolution there will there will always be those who don't want to jump in and adopt a new technique until there is more evidence there is sort of interventional studies. I've already I've already said my piece about my bias but I think this can be a reasonable addition at our present state of evidence. So what do you do with this information in practice so there is this very natural vexus for osmide reflex it's been dubbed so this natural tendency to want to diaries everybody who has an abnormal vexus or, you know, waveform suggestive of congestion. And for one, you know diuretics are not always the answer. So depending on the cause of their venous congestion of their elevated central venous pressures, sometimes things like, you know, treatment of pulmonary hypertension inhaled vasodilators treatment of PE, titration of ventilator settings, those other things may be the answer rather than diuretics so it is always patient specific. And then the other the bigger question I run into this all the time in my daily practice is how to manage these people with chronic pathology. So the patients with chronic heart failure left sided failure, right sided failure and pulmonary hypertension especially valve disease. These patients are really challenging because many of them will not necessarily live at a vexus zero right at their at their dry weight, their their chronic disease is such that they always live at a degree of congestion. And so the goal for these patients can't be to diaries them to, you know, a normal portal vein. And when we're seeing these patients, you know, once or twice, it can be really hard to determine where in their personal sort of disease spectrum they lie. And that's always a puzzle and, you know, I think that integrating with the rest of your data and examining these patients serially can help but those patients are really a challenge still. All right, so what's the bottom line here. Again, clearly I'm biased because I'm here giving you this talk, but I think that this technique can be a really valuable addition and kind of lends more specificity to this search for venous congestion because again we don't have a lot of great tools, even with ultrasound. So this can be a really valuable piece. You know, and I mentioned these waveforms can be challenging. This can be a difficult technique for me increasingly in my practice, I use the portal vein alone often when the hepatic is difficult to interpret and the renails are hard to get. So even some of this technique can be a useful addition to your practice. The evidence base as I mentioned is still growing in an in evolution and I expect we'll see a lot more in the coming years. And then finally, like all things with ultrasound and like all things with medicine right this is not the single answer in terms of how to manage patients. The last thing you want to do is is to do a vexa score or get a portal vein profile and use that to guide all your decisions to the to the ignorance of everything else right that is not the goal, especially in your complex chronic patients. Really you have to incorporate this into everything else that's going on their, their history their physical exam their labs the rest of their hemodynamic data to help you make decisions. All right, that's all I have for today. Thank you so much for having me and I think we have some time for questions at the end. Thank you again. Thanks very much, Dr. Whisker. I'm looking forward to hearing the q amp a regarding back sisters people get used to this new idea and modality of assessing volume status was something that we all struggle with, especially in the ICU population.