[SPEAKER_02]: We spend a disproportionate amount of time in medicine and inganizing over decisions to give or remove fluids with either fluids or dioretics.
[SPEAKER_02]: Every low urine output prompts kind of this discussion about should we be giving this patient fluids.
[SPEAKER_02]: And if we actually think about it at kind of the most in the level, IV fluids are just salt and water.
[SPEAKER_02]: salt water hasn't and never will be the treatment for so many diseases.
[SPEAKER_02]: So I guess I just hope that in 2025 and beyond we can stop, kind of overestimating the perceived benefit of slew it and maybe just kind of focus more on the core things like, have we addressed the underlying processes?
[SPEAKER_00]: That's Dr. Ross Pager, an intensiveist and scientist who taught me a ton in this interview about the new advancements in assessing a patient's fluid status.
[SPEAKER_00]: Something I know plagues a lot of us, and I was actually surprised to understand just how relevant Venus congestion can be for anyone who takes care of patients in any setting not just the ICU, and of course, definitely motivate me to up my ultrasound skills.
[SPEAKER_00]: So let's start with what is Venus congestion?
[SPEAKER_00]: What does that actually mean?
[SPEAKER_02]: At the most core level, we've seen its conditions when high back pressure or high actually reversal flow from the right-each and goes to the end organs.
[SPEAKER_02]: For example, kidneys, liver, brain, the bowel even, and causes congestive organ injury.
[SPEAKER_02]: Now, this is a little bit different than volume overload, where there's too much actual physical, extracellular or interstitial volume on the patient that could be manifesting as peripheral edema, plural effusions, and just kind of general puffiness.
[SPEAKER_02]: The reason why this distinction is important is that patients can have severe venous congestion without volume overload.
[SPEAKER_02]: And in fact, some conditions like paracritial effusions,
[SPEAKER_02]: I think it's probably also just worth mentioning the other term that gets thrown around volume status, which, to be quite honest, means a lot of different things to a lot of different people.
[SPEAKER_02]: I think that for people use it as, do I need to die?
[SPEAKER_02]: Rest the patient, give them fluids or do nothing, and it's kind of this holistic term, but because it means different things to different people, it's not particularly precise.
[SPEAKER_02]: And so I prefer more specific questions contained within that.
[SPEAKER_02]: For example, to start off, does this patient have microcirculatory organ dysfunction?
[SPEAKER_02]: Do they have signs of endorphin dysfunction and high-volt perfusion?
[SPEAKER_02]: Does this patient have clinical features of volume overload?
[SPEAKER_02]: Does this patient have Venus congestion?
[SPEAKER_02]: And is that congestion on the left of the right side?
[SPEAKER_02]: Are they fluid tolerant?
[SPEAKER_02]: And fluid tolerance is the concept with fluids and giving fluids to that patient actually harm them through the... Sure.
[SPEAKER_02]: You'll ask chronic homervidities.
[SPEAKER_02]: And then, do they have low stroke volume?
[SPEAKER_02]: And if that low stroke volume going to be responsible to fluids, or potentially even vasopressors.
[SPEAKER_02]: And so when you break down a generic trend like volume status into these sub components, you can start having their precise conversations and weighing their risks and benefits of fluids or at least it's or any other team of dynamic intervention you might use.
[SPEAKER_00]: Yeah, absolutely.
[SPEAKER_00]: And so just to kind of like say that loud, what is the badness that happens, you know, what is the complication?
[SPEAKER_00]: Why do we not want this?
[SPEAKER_02]: Every organ has a profusion pressure.
[SPEAKER_02]: And in interim, as we talk a little about cerebral profusion pressure, particularly in the end of the series, that we know that arterial pressure is minus that intercranial pressure.
[SPEAKER_02]: And patients with low cerebral profusion pressures might have iPops who can just keep
[SPEAKER_02]: Well, it turns out that every organ actually has a profusion pressure.
[SPEAKER_02]: The kidney, for example, has a renal profusion pressure, which can be approximated as kind of the inflow pressure or your mean arterial pressure and the venous pressure or central venous pressure.
[SPEAKER_02]: And this is why, actually, when a patient's central venous pressure goes up, it's associated with adverse outcomes.
[SPEAKER_02]: So the problem is,
[SPEAKER_02]: elevated central venous pressure for an individual patient in front of us doesn't have very strong predictives to see a predicting adverse outpost and there's a standing eye reasons for that.
[SPEAKER_02]: One might be that the pressure at the right-eat streamer's central venous pressure does not actually reflect the pressure that's being felt by the organs which are obviously distilled to it.
[SPEAKER_02]: There's other factor in drug thoracic pressure, interoptional pressure, compliance of the venous system.
[SPEAKER_02]: But perhaps we are importantly, and what we're starting to really think is that it's less about pressure and more about flow, and that it perhaps is more of this retrograde flow that people experience during being as congestion that might drive the organism dysfunction.
[SPEAKER_00]: Yeah, that's interesting.
[SPEAKER_00]: How do you distinguish like it's not the pressure as much as the flow?
[SPEAKER_00]: Can you help me help cement that in my head?
[SPEAKER_02]: But yeah, I think the first thing is that there's been a lot of studies that have associated elevated venous pressures with adverse outcomes like acute kidney injury, particularly opatients, patients with sepsis, but it turns out when in the same study, when you actually look at end organs, all clear markers of congestion that actually detect the flow abnormalities in the kidney or the liver, those are even more correlated with adverse outcomes.
[SPEAKER_02]: for patients with sepsis, for example, venous congestions associated with an increased hazard for requiring renal replacement therapy or death.
[SPEAKER_02]: For patients who are in failure, at least associated with acute kidney injury, but then also heart failure hospitalization and cardiac death.
[SPEAKER_02]: And then for patients with ATI that already have established acute kidney injury, venous congestions highly associated with mortality.
[SPEAKER_02]: And so really the causal pathway for these patients is that Venus congestion seems to cause multi-organ dysfunction that contributes to increase need for organ support and then had superior unit and then ultimately mortality.
[SPEAKER_00]: Yeah, absolutely.
[SPEAKER_00]: Can you ground us in like what are the painful situations where you're like I am so glad we have Doppler, Vaxis,
[SPEAKER_02]: I think that my favorite use case for Venus Condition Dolls Blur and Venus Condition Assessments is a cute kidney injury.
[SPEAKER_02]: Patients for you're not sure whether or not the secret dynamic acute kidney injury is because they're actually have a leemic or they're actually congested.
[SPEAKER_02]: And now, I think in an ideal world on the textbook, it's always easy to distinguish, but we know from real life it could actually be incredibly difficult to distinguish these patients.
[SPEAKER_02]: And having a starting point that said that patients
[SPEAKER_02]: diet is incredibly valuable.
[SPEAKER_02]: Also for patients with acute canandry, with cardiovascular cardiorenal syndrome, you think that they're congested.
[SPEAKER_02]: You start direasing them.
[SPEAKER_02]: At some point, somebody is going to inevitably ask that they be intravascularly dry.
[SPEAKER_02]: It's the sodium's climbing a little bit, and try to determine when you actually stop the congesting patient.
[SPEAKER_02]: Having baseline and then trended markers of congestion is incredibly valuable.
[SPEAKER_02]: For patients with acute sepsis or even just acute shock in general, lenus congestion can also be quite helpful to assess.
[SPEAKER_02]: And so, for example, in our local devins after the shock, 20% of patients when they're admitted to the ICU have severe venus congestion with septage shock.
[SPEAKER_02]: Um, and they're overly on in their course.
[SPEAKER_02]: These patients actually are usually could be harmed by additional IV fluids.
[SPEAKER_02]: So many of them have RV dysfunction and vibe-intricular failure.
[SPEAKER_02]: And perhaps the treatment for these patients is actually not more fluids, but a fluid or strokes is dropped G, potentially even LASICs.
[SPEAKER_02]: D congestion with ionic tropes and vasopreciers.
[SPEAKER_02]: And that's what we're really interested in.
[SPEAKER_02]: Is how can we sub-vino-type these patients with septage shock, for example?
[SPEAKER_00]: And we'll just, because that, how do we so surprise to hear this being involved for patients, or step-to-step?
[SPEAKER_00]: Because you know, you think of them as like, give them fluids.
[SPEAKER_00]: They have infection.
[SPEAKER_00]: But in these patients, as of shock-lifts severe congestion, is it they always have some type of RV dysfunction that's causing that or is it something with a milieu of whatever here in the military response?
[SPEAKER_02]: That's such a good question.
[SPEAKER_02]: I think this is the most important taken point probably for Venus congestion.
[SPEAKER_02]: Venus congestion is not just related to volume.
[SPEAKER_02]: Venus congestion is really the interplay between cardiac function and the loading conditions for the right side.
[SPEAKER_02]: And let's just think about it from the left side of the heart.
[SPEAKER_02]: And we're very familiar with this.
[SPEAKER_02]: We have patients in the community with EFs of 10% who are walking around who have no pulmonary congestion at all.
[SPEAKER_02]: They're dry.
[SPEAKER_02]: It's the way I work to function, but because their pre-load condition is optimized through diuretics and heart failure therapy, they don't have commonary congestion.
[SPEAKER_02]: Yeah, when that patient comes to hospital a sepsis and gets three liters of fluid empirically, now suddenly they're in fluoropominaridema.
[SPEAKER_02]: They have the substrate for congestion, which is now manifested after receiving IV fluid.
[SPEAKER_02]: The same thing happens on the right side.
[SPEAKER_02]: You have a patient with the substrate for developing Venus congestion.
[SPEAKER_02]: Maybe that's RV systolic, where I've installed this function, elevated PE pressures, or cardiovascular diseases, or paracarticocusions, right-cuspid re-gurge,
[SPEAKER_02]: and then interplaying in with their acute illness and the volume and resuscitation they get for that, they now manifest or in this function and be in this congestion on the rights.
[SPEAKER_02]: And there's a lot of different causes of venous congestion, it's not just cardiac either.
[SPEAKER_02]: So for example, we know that patient cycle on higher peak on the ventilator can develop rights-heavy congestion if they're over-distended.
[SPEAKER_02]: And in fact, titrating peak can actually help improve renal function for those patients.
[SPEAKER_02]: We know that patients with large plural of fusions can have severe renaissance congestion.
[SPEAKER_02]: And I think back to a case that we had where patient was really, really bad, greenal failure in this massive right-sided plural of fusion.
[SPEAKER_02]: But they weren't on much oxygen.
[SPEAKER_02]: We put a chest to change and drain that plural of fusion, and immediately saw improvement of the severe real congestion, and improvement of the continued kidney injury, just from draining that plural of fusion.
[SPEAKER_02]: We know how interesting.
[SPEAKER_02]: How can have elevated intramural pressure and elevated intramural pressure, intramural hypertension, also cause renal dysfunction?
[SPEAKER_02]: And we've seen also patients that have IVC stenosis, for example, post-libertranspite, that have severe renal congestion.
[SPEAKER_02]: And it's not at all related to the heart at this point.
[SPEAKER_02]: Is due to a proximal upstream occlusion from a thrombus?
[SPEAKER_02]: And so we saw this thrombus on ultrasound, actually in the patient went back to the OR for
[SPEAKER_00]: So, thank you for clarifying, you know, the pain points where we are, maybe invoking some type of Venus congestion.
[SPEAKER_00]: So, how does one measure Venus congestion and what in the world is sex?
[SPEAKER_02]: Yeah, and I think it's even helpful just to take a set back from that.
[SPEAKER_02]: So, we are so familiar with left-sided physiology.
[SPEAKER_02]: We think about all the time on medicine, so let's start there.
[SPEAKER_02]: When you have a patient with elevated left-age trope fracture, that gets transmitted retrograde into the lungs, it causes calmer edema, and we can detect that on ultrasound with the lungs, wrong chest X-ray, curly joint, backwing all the normal stuff.
[SPEAKER_02]: Turns out this is very similar to the right-sided top physiology, elevated bread to bread to bread to real pressure.
[SPEAKER_02]: It's transmitted retrograde causes organ level congestion, but the organs we're talking about now are the brain, ow, the liver and the kidney for the most tart.
[SPEAKER_02]: This can be detected by Doppler after those organs.
[SPEAKER_02]: It's a traditional tools to quantify this congestion like central Venus pressure measurement.
[SPEAKER_02]: Oh, the examination of the JVP are really really limited because those are pressure estimates.
[SPEAKER_02]: And we've just talked about how slow is probably more important than pressure.
[SPEAKER_02]: And then, also, even if you are looking at them as actor metrics, there's a lot of variability.
[SPEAKER_02]: Even for CVP, which is something that we assume is very repeatable, you just transduced.
[SPEAKER_02]: There's a lot of interator reliability issues there.
[SPEAKER_02]: And similarly for JDP, and we know that there's so it's such a thing that it is with intrarator reliability for JDP.
[SPEAKER_00]: And do we have an understanding of what type of Haitians might have a more compliant Venus system versus a more tight one?
[SPEAKER_02]: Yeah, so that's a really good question.
[SPEAKER_02]: So that's actually a little bit where the IVC measurement comes in to play.
[SPEAKER_02]: Because if your IVC is super distant, you have, by definition, not a very compliant system anymore, because it's already full and stretched to kind of the maximum.
[SPEAKER_02]: Past versus if you have a totally collapsed IVC, that may be a patient that has some more compliance.
[SPEAKER_02]: And if you fill up more kind of,
[SPEAKER_02]: I think we're going in there, and if the pressure is higher, it might not be transmitted retrograde, which is a great segue into how do we actually measure it now on ultrasound.
[SPEAKER_02]: And so initially, Venus congestion was quantified using individual Doppler markers.
[SPEAKER_02]: So for example, after cardiac surgery, the group in Montreal, on the Denose, in Bolbia, Slovenia, they looked at patients with postcardia surgery and examined their portal veins.
[SPEAKER_02]: And they found that portal vein possibility was associated with versus outcomes, particularly acute kidney injury, but also delirium and congestive and cephalopathy, following surgery.
[SPEAKER_02]: in the heart failure population, a lot of the early work was done looking at intra-renal venous doppelts.
[SPEAKER_02]: It's actually looking at the kidney and looking at these tiny little inter-lobular vessels because the artery and the vein they run right together.
[SPEAKER_02]: And you can throw them all away with doppelts or these vessels that run together and look at the flow abnormalities there.
[SPEAKER_02]: And then in acute kidney injury, we've looked at it using multiple different metrics.
[SPEAKER_02]: Hepatophane, Fortaline, and Introrenal Venus Doppler.
[SPEAKER_02]: But the problem is that each of these in isolation have some limitations.
[SPEAKER_02]: There are certain conditions that over exaggerate some Doppler markers, and actually there's other conditions that dampen some of the others.
[SPEAKER_02]: And so, in 2020, Dr. Boggia Solini and Dr. De Nau in Montreal, they said, well, how could we combine multiple different measurements into one kind of scoring system?
[SPEAKER_02]: And they took the interview in Kiva, a padded vein, portal vein, and interreal beta stockler.
[SPEAKER_02]: And they put it into something called a vexist score that that's become quite popular in most recent years.
[SPEAKER_02]: And it's a score that ranges from 0 to 3, with scores of 2 or 3 representing kind of moderate to severe congestion.
[SPEAKER_02]: and this was derived and validated postcardi-excergery.
[SPEAKER_02]: And what they found was that compared with central venous pressure and compared with any of the individual dogler markers by themselves, there was improved predictive accuracy to predict the future canyandry.
[SPEAKER_02]: know, how that they choose the thresholds of portal names, including abnormalities.
[SPEAKER_02]: You got to start somewhere.
[SPEAKER_02]: So they just picked reasonable numbers and looked at their data and picked reasonable numbers.
[SPEAKER_02]: And so actually in my practice, I don't use the Vexus4 at all in a research or in Pettamy Assessment because it was derived in one population.
[SPEAKER_02]: We're studying a different population.
[SPEAKER_02]: It was derived in post-critic surgery population.
[SPEAKER_02]: And so we're interested in Sepsis, who is to say that the thresholds of congestion in Sepsis are the same as in cardiac surgery.
[SPEAKER_02]: So for our large international prospective study that we're just wrapping up right now, we're actually revalidating to look at for each of these markers, what is the threshold that causes congestion in this population?
[SPEAKER_02]: And we actually need all these different components, or maybe the portal vein is one vein to rule them all, so to speak.
[SPEAKER_02]: And we'll actually have the same predictive accuracy as a more comprehensive score, and as much easier to do for example than
[SPEAKER_00]: So it sounds like there are four main components that we're gonna be assessing.
[SPEAKER_00]: The IVC, the hepatic vein, the portal vein, and the intra-renal venous congestion.
[SPEAKER_00]: This can all help us identify congestion, even if we're not using the venous score to the T. And curious about common mistakes or blind spots people have when they're trying to learn how to measure venous congestion or interpret it.
[SPEAKER_02]: a great question, and to be entirely honest, there's a lot.
[SPEAKER_02]: The first thing I see is that understandably, people rely a lot on the Vexus score.
[SPEAKER_02]: And, for example, if the IVC is left in two centimeters on the Vexus score, you actually don't proceed with any of the dolphin markers.
[SPEAKER_01]: I don't think so.
[SPEAKER_02]: I'm just slightly a little bit challenging because we have a lot of data showing that patients with IVC smaller than two centimeters can have severe vids congestion.
[SPEAKER_02]: So unfortunately, stopping there is probably not a great idea.
[SPEAKER_02]: The next thing is trying to figure out the IBC and long access, which is what is traditionally done in the vexist school.
[SPEAKER_02]: I'm what we're traditionally taught internal medicine and ICU-pocus.
[SPEAKER_02]: Well, it turns out that like any vein, IBC's not actually round.
[SPEAKER_02]: And so, for example, if you go into the naked, you're putting in a central line as the internet.
[SPEAKER_02]: And if you see a very round structure that you're about to put a line into, stop, because there's a good chance that that's not the vein.
[SPEAKER_02]: We all know that the internal drive dealers kind of this ellipsoid is partially white.
[SPEAKER_02]: Well, the ABC is no different.
[SPEAKER_02]: It's a vein.
[SPEAKER_02]: It's a lipsoid.
[SPEAKER_02]: And so actually image it in long access, you're assuming that the access of this ellipsoid aligns perfectly with the long access.
[SPEAKER_02]: But when you actually look at it in short access, sometimes you see these bizarre IVCs that are like four centimeters on one diameter and like two millimeters in the other diameter.
[SPEAKER_02]: And if you can't just write a long answer, you can mostly make it look really, really, really, bigger, really, really small.
[SPEAKER_02]: And so we, for example, advocate for assessing IVC in short access, because you can actually kind of look at the scarcity or how round it is, because we know that as VNs get more extended, they get more round.
[SPEAKER_02]: So for how to talk to better metric to assess the IVC, for example, than long access.
[SPEAKER_02]: That's something that we're currently studying.
[SPEAKER_02]: It's similarly, when we go to the hepatic vein, or it'll vein it into a renal vein, it can be hard to figure out what you're looking at.
[SPEAKER_02]: I just believe the hepatic vein.
[SPEAKER_02]: And so what I advocate for for this is just kind of thinking a little bit more simplicity about it.
[SPEAKER_02]: Blood should flow forward.
[SPEAKER_02]: On the hepatic vein doctor, that's flow below the baseline.
[SPEAKER_02]: The more and more flow you have above the baseline, regardless of whether it's a SVD, you're kidding me to the care, the more congested you are.
[SPEAKER_02]: And so we're interested in thinking about how to gain Doppler, a little bit more, kind of simplicity, just saying, how much is backwards, how much is forward?
[SPEAKER_02]: Don't worry about which way Parmesan is which, because the more that you have retrograde.
[SPEAKER_02]: The worst thing to do is copy that I would say the portal vein is probably much Theevers.
[SPEAKER_02]: I mean, I was going to pick favorites.
[SPEAKER_02]: You shouldn't pick favorites among your children, but I will have a favorite here with the ultrasound.
[SPEAKER_02]: It would definitely be the portal vein.
[SPEAKER_02]: If you go from the right upper quadrant, the main portal vein or the right portal vein comes right out towards you on the screen.
[SPEAKER_02]: You put off Doppler on, and you look at the possibility, which is just the maximum velocity minus the minimum velocity divided by the maximum velocity is repeatable.
[SPEAKER_02]: And interestingly, it seems to be the least effected by things like tricuspid regurgitation and other potential kind of conchounders.
[SPEAKER_02]: And one of the reasons for that is when you actually think about the blood flow.
[SPEAKER_02]: It has to go from the right atrium into the IVC, into the hepatic vein, into the hepatic sinusoid, like through the liver prancoma to make it into the portal vein.
[SPEAKER_02]: So if you're seeing possibility and reversal there, that can be a pretty good indicator of true kind of congestion.
[SPEAKER_02]: And then the last one is the intra-renal venous Doppler, and I really like the intra-renal venous Doppler.
[SPEAKER_02]: And the reason why it is
[SPEAKER_02]: When you can get it, which is the biggest limitation, is that it's only a kind of attainable in about 90% of patients based on the literature, but if you get it, it measures directly kind of renal congestion.
[SPEAKER_02]: And often when we're talking about congestion, we're talking about it in the setting of renal dysfunction, either a patient with AKI, that we're trying to figure out, or a patient that we're done, or a re-sing, and their crattons going up.
[SPEAKER_02]: And if you're a measuring congestion at the kidney level and they're severe congestion, that's a pretty good indicator that renal congestion is probably at play with whatever process is going on.
[SPEAKER_02]: And it's also able to be tracked over time very nicely, because there's this concept of renal venous thesis index.
[SPEAKER_02]: And this might be getting a little bit into the weeds, but I think it's interesting.
[SPEAKER_02]: And so the idea is that normally, beans should drain in a hundred percent of the cardiovascular cycle time.
[SPEAKER_02]: There should just be continuously in a drainage.
[SPEAKER_02]: In water, in settings of significant congestion, you start getting periods of interruption.
[SPEAKER_02]: And as those periods of interruption of Venus flow get longer and longer and longer, your Reno Venus thesis index goes from zero, which is normal, up to 10% interruptions to 20%, it's already percent all the way up to like 60% or 70%.
[SPEAKER_02]: What most of your cardiac cycle there's no Venus drainage.
[SPEAKER_02]: That's what we've got, and going back to the compartment syndrome analogy, that lack of Venus drainage leads to worsening congestion of actual brantama, which swells within the capsule containing the kidney, causing worse Venus drainage, and it's this kind of really negative fetish type of, or actually a really bad positive feedback site, but I should send it.
[SPEAKER_02]: So normal is zero.
[SPEAKER_02]: You and I should say, but some patients, they're a normal might not be zero.
[SPEAKER_02]: And so I always think of this with like EF's, for example, like a normal EF is a above 65% that you can have a patient with and EF is 30% and that's just their baseline.
[SPEAKER_02]: So you have some patients that have baseline congestion and no matter how hard you die a resum or how aggressively you kind of manage their heart failure, they just will always have congestion.
[SPEAKER_02]: That's not to say that it's normal, but it's their baseline.
[SPEAKER_02]: And ideally, in an ideal world, it would be nice to fix that, but we can't always.
[SPEAKER_02]: And actually, this brings into a really interesting use case.
[SPEAKER_02]: For example, if you try to diaries people aggressively with severe TR, a severe primary tracuspid recurge, you can remade it to these, for example.
[SPEAKER_02]: And then you can never improve.
[SPEAKER_02]: their inter-renoviness Doppler.
[SPEAKER_02]: Unless, by diagnosing them, you've actually unmasked that this was not primary TR and this was secondary.
[SPEAKER_02]: They'd have severe renal congestion forever.
[SPEAKER_02]: They're ordled in, will normalize, or partially normalize, and you can use that to trap kind of de-congestion, but never their inter-renoviness Doppler.
[SPEAKER_02]: But when you send them for like, try Cuspid Clip or Tracuspid Repair, and you fix the Tracuspid Regers, they're trying to normalize it so just because we couldn't fix their congestive renal injury with DiResis didn't mean that it wasn't having an impact on organ function.
[SPEAKER_00]: Yeah, that's great.
[SPEAKER_00]: I think for me, this just really hammers home that every patient is different and different conditions will affect each of these for differently.
[SPEAKER_00]: So it is good to have a little bit more nuanced understanding of what affects what's so thank you for going through each and laying down with the high level nuances for what we should be thinking could be at play.
[SPEAKER_00]: Okay, let's bring this all together.
[SPEAKER_00]: Tell me about a case or cases you've had where Venus Doppler assessments really helped.
[SPEAKER_00]: Kind of male is this person fluid-tarrant or, you know, shaped your approach differently.
[SPEAKER_02]: Definitely.
[SPEAKER_02]: I think fluid tolerance is one of the really important emerging concepts in a future medicine.
[SPEAKER_02]: And the idea is that every treatment we do has a brisk in a benefit.
[SPEAKER_02]: The benefit of giving somebody ID sluts for example is that we can increase their credit output, and by increasing their credit output in their strobe volume, we increase the fusion.
[SPEAKER_02]: Things get better.
[SPEAKER_02]: But like any treatment, there's a potato rift, and the risk of ID sluts is really multifactorial.
[SPEAKER_02]: You can cost just to work an injury, you can cost.
[SPEAKER_02]: omega dma, we call it tissue edema, which can lead to a kind of a microcirculatory dysfunction, you can call it the endothelial dysfunction from over-aggressive fluid recestation actually like shredding like bicicletes in the vessels, there's a lot of potential ions, and we just need a concept to describe those potential, so nox fluid tolerance.
[SPEAKER_02]: How I think about fluid tolerance is there's kind of a few different domains.
[SPEAKER_02]: The first is the acute illness that some of these facing right now might make them more or less flu-tolerant.
[SPEAKER_02]: So for example, with the other patient that comes in with a acute decompacated heart failure, they're not flu-tolerant.
[SPEAKER_02]: We would never even think about giving those patients flu to try to improve their organism function because they're in pulmonary demand acute overloaded heart to it.
[SPEAKER_02]: There's other more subtle conditions, however, like paint creativates, for example.
[SPEAKER_02]: People with a cute paint creativates, they might respond well to fluid in the short term, but in the long term are actually not very fluid tolerant, because they third space a lot of that fluid in that third space fluid lead state, or yes, they can lead to double-cardman syndrome and other complications.
[SPEAKER_02]: In these situations, I think both, giving fluids kind of late tapping a credit card.
[SPEAKER_02]: You rise over friends, and you order around your drinks for some friends, and then you tap your credit card that night.
[SPEAKER_02]: Everything's all good because you're in the pit, also the morning.
[SPEAKER_02]: But the next thing you go out again, and then you go out again, and before you realize you have a drinking problem, you keep throwing out time and time and time and time and time and time and time and time and time and time.
[SPEAKER_02]: And you keep tapping your credit card.
[SPEAKER_02]: Eventually, that bill is going to have to heed.
[SPEAKER_02]: In other words, because it's going to make you really interest.
[SPEAKER_02]: Giving ID fluid bullises are a little bit like tapping your credit card.
[SPEAKER_02]: They definitely work in the short term to restore kind of forward flow, but you have to pay the price by mobilizing that fluid down the road.
[SPEAKER_02]: And you don't want to essentially have your credit card debt or your fluid debt build up so much
[SPEAKER_00]: That's great, excellent.
[SPEAKER_02]: So even with flu tolerance, a huge illness is kind of the first thing I think about, then I think about chronic comorbidities.
[SPEAKER_02]: So we intuitively know that patients that have DFs of 5 to 10% or severe pulmonary hypertension, we're gonna be much more cautious with the IV flu is because they're more likely to be harmed by it.
[SPEAKER_02]: And then finally, I consider things like congestion.
[SPEAKER_02]: And that could be left side of congestion or right side of congestion.
[SPEAKER_02]: So a patient with culinary edema is going to be less likely to be a fluid talk.
[SPEAKER_02]: A patient with severe venous congestion in our redist function is going to be less likely to be fluid talk.
[SPEAKER_02]: Because as we give them fluids, there's a chance that this worse is their congestive organ injury.
[SPEAKER_02]: And so integrating those three components is kind of how I approach fluid tolerance for patients.
[SPEAKER_02]: When I'm trying to weigh the risks of pregnancy
[SPEAKER_00]: Yeah.
[SPEAKER_00]: And then you also mentioned like the left, you have somebody with a low stroke of all you and you kind of weighing to get fluids versus vasopressors and how can better understanding docklers help you with that?
[SPEAKER_02]: Yeah.
[SPEAKER_02]: And I mean, I have to say this is one of the hardest questions that still remains in acute care resuscitation.
[SPEAKER_02]: When do you switch over from giving some of the fluid resuscitation into vasopressors?
[SPEAKER_02]: I think it's pretty clear in 2025 that purica bounds, like it gives 30 mills per kilo to everyone, make no sense.
[SPEAKER_02]: Nothing in medicine is a fixed dose, right?
[SPEAKER_02]: It was a particular to your patient and a friend of mine.
[SPEAKER_02]: But the question then, and a very important question is, well, how do you decide what would those do you get?
[SPEAKER_02]: And so my assessment of whether or not I should go into fluid fluids or vasopresistence with the microcirculation.
[SPEAKER_02]: Do they have surrogates of hypoprefusion?
[SPEAKER_02]: Refill, um, elevated lactate, allacuria, some term marker that this patient's profusion is, because often actually we get, we get call for these patients after four leaders, but then you look at them, you're like, you're lactate.
[SPEAKER_02]: It's clear, you're peeing.
[SPEAKER_02]: But it's not going to be fluids or vasopresists right now.
[SPEAKER_02]: Like you're just doing okay.
[SPEAKER_02]: But let me think the patient is hypoprefused.
[SPEAKER_02]: The purpose of giving a fluid force is to increase something called the mean systemic sling.
[SPEAKER_02]: And that pressure is represented by two things, the tone of vessels, the kind of oasters, but also how much fluid is in there.
[SPEAKER_02]: Think about a water balloon, for example, the pressure inside the water balloon is not zero, and the pressure inside the water balloon depends by what material the water balloon is made out of, is it really like a wine, water balloon?
[SPEAKER_02]: And how much water do you put in?
[SPEAKER_02]: And the more water you put in, the high pressure is.
[SPEAKER_02]: So the immune systemic filling pressure is actually the main driver of venus return, and cardiovascular output in our body.
[SPEAKER_02]: And it's the difference between the immune system
[SPEAKER_02]: And so what you give somebody a fluid bolus, we give it with the hope of increasing our immune system, it's feeling pressure to drive more being less return.
[SPEAKER_02]: And it works for that.
[SPEAKER_02]: Because when you give somebody a fluid bolus, it increases the volume inside the vessels, that causes pressure and increases the immune return.
[SPEAKER_02]: But it turns out that that's not the only way to increase your main system of gilling pressure, because there's the other component that compliance with the alastins of the vessel.
[SPEAKER_02]: And if you give some of the vasyl pressures, you can also squeeze the venous system and increase that immune system and make feeling pressure and drive more venous return.
[SPEAKER_02]: And so, whenever I think about giving it a slurred bowl, I always ask myself, and I have a bit of a luxury being in the ICU where I don't have to factor about resource utilization and transfer to kind of higher level beds.
[SPEAKER_02]: But I always ask myself, if this patient's hyper-prefused, they have low stroke volume, they're acting hyper-vealiment.
[SPEAKER_02]: In the treatment for this patient fluid, where is it actually vasopressors?
[SPEAKER_02]: Because maybe in this case, I could actually recruit someone at Venus volume by just giving vasopressors.
[SPEAKER_02]: And so how does this relate to the Venus congestion assessments?
[SPEAKER_02]: When I have a patient with severe Venus congestion, who I'm worried that are less fluid tolerant, that may push me to trial these oppressors earlier with the hope that I can recruit the mean systemic feeling pressure and kind of recruit that Venus volume increase forward flow without giving fluids.
[SPEAKER_02]: Because again, fluids are that credit card that I'm going to have to pay off down the road.
[SPEAKER_02]: And that patient already has signed that there there in too much debt so to speak.
[SPEAKER_00]: Oh, it's so great.
[SPEAKER_00]: Thank you for kind of walking, walking through all of that.
[SPEAKER_00]: I think, okay, the closest up to inspire the person who is, wow, the sound so cool, how will I ever learn this or what do you have to say in terms of, this is like the meta in us, like how often should one practice, how should one practice, to get somewhat competent in an evolving area.
[SPEAKER_02]: Yeah, that's a great question.
[SPEAKER_02]: I think the first thing I have to say is that, like, to put a side-oldre sound, I think the first thing is just recognizing that congestive organ injuries probably more prevalent than realized we're finding, oh my gosh, early in septic shock, a lot of patients have severe venous congestion.
[SPEAKER_02]: Wow, 70% of acute heart failure exacerbations have severe venous congestion on the present patient.
[SPEAKER_02]: And the patient's side, you prove their congestion is going to do way better than patients that don't have congestion.
[SPEAKER_02]: So I would say that hopefully this kind of excites us to say that we have this kind of very prevalent phenotype of patients that have severe congestion and organ injury as a result of it.
[SPEAKER_02]: For example, we're studying right now in the intensive care unit, the implications of being this congestion on delirium.
[SPEAKER_02]: And in terms of that venous congestion is associated with cerebral desaturations and we're delirium-free in the study of surgery.
[SPEAKER_02]: And so maybe some of these patients that we have on medicine or in intensive care unit are severely delirious and they're not too sure why, because they've been on any meds or menopause, so it will give me the treat.
[SPEAKER_02]: Yeah, those patients exactly die of recess.
[SPEAKER_02]: And I think it's basically going to encourage people to think about this kind of domain of organ injury, congestive organ injury, as something we're increasingly recognizing is probably more pathogenic in many of our populations than we previously realized.
[SPEAKER_02]: My second point is that if you're wanting to learn how to quantify being a congestion, if you're learning wanting to learn how to kind of really assess patient physiology on an individual basis, you need a tool that's repeatable, that's available, and that has some versatility.
[SPEAKER_02]: And I think if I was starting kind of really trying to get into this, I wouldn't start with Bexist.
[SPEAKER_02]: Rexist is like, level two, level three.
[SPEAKER_02]: Start with just kind of core acquisition of Poccus images.
[SPEAKER_02]: It's a heart, the lungs.
[SPEAKER_02]: There's so
[SPEAKER_02]: imported findings that can really change your clinical management and internal medicine and ICU based on all of a sudden and I would start there and then as that still set develops then we can start looking at being as congestion and learning how to do the do the doccler patterns and they're really not that hard.
[SPEAKER_02]: As part of one of our studies, we've actually taught 20 centers worldwide how to do access all remotely on webinars, and we do quality shirts on all the scans as part of the study, and there's excellent quality for these research scans, and so definitely is feasible even with just focus training, but all of these clinicians already knew how to use 20 characters down.
[SPEAKER_02]: And so I think that, to me, point of camera ultrasound, focusing on basic cardiac use, lung views, TVT assessments, introbdominal assessments, time for free fluid, those are kind of core applications, and then you can easily build on that by assessing working up a doctor.
[SPEAKER_00]: And then back to Dexis, or just some of the four core measures of it, how often are you getting these measurements?
[SPEAKER_00]: It's like a daily thing.
[SPEAKER_00]: Is it every other day?
[SPEAKER_00]: What in your practice, you find utility, or would you recommend?
[SPEAKER_02]: Yeah, a great question.
[SPEAKER_02]: I would say that it really depends on the clinical scenario.
[SPEAKER_02]: And so I really like to anchor any human dynamic assessment to be that Vaxis or cardiac assessments in starting with the microcirculation.
[SPEAKER_02]: Is there an organ dysfunction?
[SPEAKER_02]: Because if, yeah, it's, we need to move on to figure out why.
[SPEAKER_02]: And it's, you know,
[SPEAKER_02]: So I would start by saying, whenever I have a patient in shock with organ dysfunction, I'm considering congestion as one of those mechanisms of organ dysfunction.
[SPEAKER_02]: Because we know that some of those patients have good forehead flow, they have good map, but they have hypo-perfusion due to congestion.
[SPEAKER_02]: So we need to sort of, they're both the forward flow and the retrograde when assessing those patients.
[SPEAKER_02]: question then becomes, well, what do you reassess?
[SPEAKER_02]: Well, it depends.
[SPEAKER_02]: If a patient after we kind of initiate appropriate therapy and broad eggs, pressures on them with subsist, for example, their organ dysfunction is getting better, it might not assess them again, because if they don't have, if they have normal organ precision at this point, they're either paying up a storm, their pressures are coming down, their lactate's not realizing, what am I going to do differently if I find that they're still congested?
[SPEAKER_02]: Just going to keep doing what's work?
[SPEAKER_01]: Okay, then.
[SPEAKER_02]: And so I often use it when patients are stalling, when patients, whether it's uncertainty about which direction to go, or when there's ongoing high-volt perfusion that hasn't been resolved.
[SPEAKER_02]: Because, for example, say we see a patient with sexist with severe congestion and they're totally volume overloaded.
[SPEAKER_02]: We might start basal pressures and start gyereasing them, but if 12, 24 hours later, there's still high-volt perfused, it's all working.
[SPEAKER_02]: The question is, well, why are they still congested?
[SPEAKER_02]: Maybe they have a cold RV dysfunction that we didn't recognize of.
[SPEAKER_02]: Maybe they have commoner hypertension as a driver of this kind of right-sided compensation that we need to treat with inhaled nitric oxide, for example.
[SPEAKER_02]: So those would be the time that I'd start recessing, but I don't routinely reassess on a prescribed schedule unless there's kind of a clinical picture for it.
[SPEAKER_00]: Yeah, that's great.
[SPEAKER_02]: It was one more example that I'd be even more contextually relevant to confer internal medicine listeners with the patient with heart failure who is overloaded to start diaries seem for cardiorenal syndrome and volume.
[SPEAKER_02]: You put them on lay six, peeing up a storm their weights coming down.
[SPEAKER_02]: I'm not going to kind of see really follow their follow their Venus congestion Doppler.
[SPEAKER_02]: If their weights coming down, their credits come down, the good year now, they're coming down and watching and they're feeling better.
[SPEAKER_02]: You're going to see that, yes, it's kind of like who cares, but having a baseline at the beginning is really helpful when on day five, they're still overloaded, so the creatinine starts going up, and there you're now put starts going down, and you're starting to worry, gosh, could I have an over-diaries this patient or maybe their preload is actually too low?
[SPEAKER_02]: Having a repeat assessment at that time to say, no, this patient still has to be your renal congestion.
[SPEAKER_02]: Instead of having the dose of laziness you're holding and giving out
[SPEAKER_02]: the dose of lay six and add some mental zone and really double down on what we know and what we think should be working.
[SPEAKER_02]: And so that would be kind of when in a heart failure population I'd like.
[SPEAKER_00]: It says that that makes a lot of sense.
[SPEAKER_00]: And you take on points or things that you're like, I want people listening to get discs out of the episode of Subbiotic on points you have.
[SPEAKER_02]: Yeah, a few final take-homes here.
[SPEAKER_02]: The first is that genus congestion is not a new concept.
[SPEAKER_02]: We've known about this for close to a century, but really excitingly, we now have tools available at our disposal, actually detected, and to quantify it, but then monitor in response to treatment.
[SPEAKER_02]: And I think that this will really open up new areas of research.
[SPEAKER_02]: In diseases that we manage every date, it'll add a lens and potentially an explanation for some of the reason why these patients do well or do poorly.
[SPEAKER_02]: And it may be related for some of these conditions to whether or not you just should or not.
[SPEAKER_02]: The next thing is that congestion is separate from volume overload.
[SPEAKER_02]: Congestion reflects that interplay between cardiac function and the filling pressure.
[SPEAKER_02]: For some patients, they might be overloaded like an acute decobocated heart failure with a cardiorenal syndrome, and they might have severe B-discogestion.
[SPEAKER_02]: But for other patients, they acute RB failure itself.
[SPEAKER_02]: The paroperative fusion, the plural effusion, the intra-dominal process going on can cause direct congestion.
[SPEAKER_02]: Then I think the final thing is just, and this is kind of the distinction between B-discogestion and Vexus.
[SPEAKER_02]: Just because we have a new scoring system or a new tool to assess something that doesn't have a lot of evidence base doesn't mean that the concept and the theory behind it is new as well.
[SPEAKER_02]: And that's one criticism I've heard commonly of Vexices that well there's just not enough data.
[SPEAKER_02]: I totally agree.
[SPEAKER_02]: I don't use Vexices in my own practice because there's not enough data for the population that I'm using in there.
[SPEAKER_02]: But as a concept congestion has been well established and I think
[SPEAKER_02]: Having that in your mind, regardless of how you assess it with Doppler or JVP or CVP or any other method that you choose, is still really valuable.
[SPEAKER_00]: And that is a wrap for today.
[SPEAKER_00]: Our ask is that you send this to one colleague who might find learning about Venus congestion or Vexus helpful, some just someone who maybe on the fence without learning ultrasound or even loves it already.
[SPEAKER_00]: Thank you again and take care.