Time Stamps

• 00:00 Volume overload vs. Venous Congestion
• 05:49 Venous Congestion and AKI, mortality, possible delirium
• 10:10 Measuring Venous Congestion and the Role of VEXUS
• 15:05 Common Mistakes and Best Practices of VEXUS score
• 23:13 Assessing Fluid Tolerance and Risks with Venous Doppler in Acute Care
• 25:29 Fluid vs. Vasopressor Strategy Guided by Venous Assessment

Show Notes

1. “Volume status” is a nonspecific term.

• • Pitfalls:
    • Lacks precision
    • Oversimplifies discussion to debate over administering IV fluids vs diuretics
    • Overestimates the benefits of IV fluids
  • A more rigorous framework for approaching hemodynamics is better!
    • Microcirculatory Dysfunction:
      • Does the patient show signs of end-organ hypoperfusion? Is lactate rising?
    • Volume Overload:
      • Are there clinical features of excess extracellular volume, such as peripheral edema or pleural effusions?
    • Venous Congestion:
      • Is there evidence of high retrograde flow? And is that causing organ injury, as in cardiorenal syndrome?
    • Fluid Tolerance:
      • Would administering IV fluids likely cause harm due to the patient’s acute illness, chronic comorbidities, or existing level of congestion?
    • Fluid Responsiveness:
      • Does the patient have a low stroke volume that is likely to increase with fluids or vasopressors?

2. Understanding Venous Congestion

• • Venous congestion: high back pressure leading to reversal of blood flow from the right atrium into the end-organs (e.g., kidneys, liver, brain, and bowel), which can cause injury.
    • Organ injury correlates more with flow reversal than increased venous pressure
    • Can occur without volume overload
      • Examples: pericardial effusions or RV dysfunction
  • Venous congestion results from the interplay between cardiac function + fluid delivery to the right heart
    • • Example: Poor RV dysfunction + Fluid bolus → severe venous congestion
  • How does congestive organ injury happen?
  • Pressure mechanism:
  • Perfusion pressure = Arterial inflow pressure – Venous outflow pressure
    • • • All organs maintain a perfusion pressure
      • Example: Kidney perfusion pressure = mean arterial pressure (MAP) – CVP
        • CVP increases → kidney perfusion pressure decreases → ischemic injury!
    • Flow mechanism:
      • Venous backflow → stasis and distension within the end organ
      • Example:
        • kidney injury: Retrograde flow → venous stasis & distension → increases intra-organ pressure → impedes venous outflow → worsening congestion
  • Current surrogate markers: Central Venous Pressure (CVP) or Jugular Venous Pressure (JVP)
    • Elevated CVP → Associated with worse outcomes
    • Poor predictive accuracy and inter-rater reliability
      • RA pressure does NOT reflect distal organ pressures
  • Direct markers: Doppler can show retrograde flow
    • Can be more pathogenic than pressure alone
    • More strongly correlated with worse outcomes than surrogates

3. What pathologies are common causes of congestive organ injury?

• • Cardiac Function:
    • RV systolic or diastolic dysfunction
    • Elevated pulmonary artery pressures
    • Severe tricuspid regurgitation
    • Pericardial disease
  • Thoracic Pressure:
    • High PEEP settings on a ventilator
      • Can compress venous structures and impede return to the heart.
    • Large pleural effusions
      • Draining a large pleural effusion can immediately improve renal congestion and function.
  • Abdominal Pressure:
    • Intra-abdominal hypertension
      • Can compress the renal veins and IVC, causing renal dysfunction.
  • Vascular Obstruction:
    • Proximal occlusions, such as an IVC stenosis or thrombus (e.g., post-liver transplant),
      • Can cause severe distal congestion unrelated to cardiac function.

4. Clinical Significance and High-Risk Populations

• • How does venous congestion impact patients in various clinical scenarios?
    • Sepsis:
      • Venous congestion → suspected to increase hazard for requiring renal replacement therapy or death.
        • At a single center, it was noted that 20% of patients in septic shock have severe venous congestion upon ICU admission
          • Suggests possible harm by standard fluid resuscitation protocols.
    • Heart Failure:
      • Venous congestion → linked to acute kidney injury, heart failure hospitalizations, and cardiac death.
        • Approximately 70% of patients with acute heart failure exacerbations present with severe venous congestion, and
          • Improvement in congestion correlates with better outcomes.
    • Acute Kidney Injury (AKI):
      • venous congestion → highly associated with mortality.
    • Post-Cardiac Surgery:
      • venous congestions →
        • predictor of AKI
        • associated with cerebral desaturations and worse delirium.

5. Modern Assessment: Doppler Ultrasound and the VEXUS Score

• • The VEXUS (Venous Excess Ultrasound) Protocol: grading system (0-3) developed in 2020 that combines assessments of (1) IVC with (2) Doppler waveforms from the hepatic vein, (3) portal vein, and (4) intrarenal veins.
    • Derived and validated in a post-cardiac surgery population,
      • showed improved predictive accuracy for AKI compared to CVP or any single Doppler marker alone!
  • Critique VEXUS:
    • Not generalizable
      • It was derived in a specific cohort of post-cardiac surgery population.
    • IVC limitations
      • The protocol’s instruction to stop if the IVC is <2 cm is problematic
      • Patients with smaller IVCs can still have severe congestion.
    • Note: Dr Prager states that the core value lies in the concept of multi-organ Doppler assessment, not necessarily the rigid application of one scoring system.
  • Component-Specific Insights for Doppler Assessment:
    • IVC:
      • Assess in short-axis to evaluate true size and sphericity.
        • Long-axis views can be misleading due to the vein’s ellipsoid shape.
      • As veins become more distended, they become rounder.
        • A distended, non-compliant IVC suggests high right atrial pressure.
    • Hepatic Vein
      • Look for retrograde flow (flow above the baseline).
        • Greater proportion of retrograde flow → more severe congestion.
      • Reflects the transmission of high RA pressure directly back into hepatic circulation.
    • Portal Vein
      • Measure pulsatility
        • High pulsatility or flow reversal indicates severe congestion.
      • Considered a very robust and repeatable marker.
        • If pulsatility is present here, it implies congestion has propagated through the entire liver sinusoids.
        • Least confounded by tricuspid regurgitation.
    • Intrarenal vein
      • Look for discontinuous flow (interrupted, biphasic, or monophasic patterns).
        • The Renal Venous Stasis Index quantifies the percentage of the cardiac cycle with no venous drainage.
          • A high index indicates severe impairment of renal venous outflow, often seen in AKI.

6. Clinical Applications and Decision-Making Frameworks

• • When is Doppler most useful clinically?
    • Differentiating AKI:
      • Distinguishing between hypovolemic vs congested causes of AKI.
    • Guiding De-congestion:
      • In cardiorenal syndrome, doppler can confirm ongoing renal congestion when creatinine is rising during diuresis.
        • Can guide the decision to intensify diuretic therapy vs stopping
    • Phenotyping Septic Shock:
      • Identifying the % of septic shock patients with congestion allows for a more tailored, fluid-restrictive resuscitation strategy, potentially involving early use of vasopressors and inotropes.
    • Investigating Delirium:
      • Congestion may be a treatable (via diuresis) contributor to delirium in some patients.
• Which patients have low fluid tolerance?
  • An acute illness predisposing to fluid extravasation (e.g., pancreatitis).
  • Chronic comorbidities that limit fluid handling (e.g., severe HFrEF, pulmonary hypertension).
  • Existing congestion, either pulmonary (edema) or systemic venous.
• Fluids vs. Vasopressor Dilemma in shock: The goal of both fluids and vasopressors in shock is to increase mean systemic filling pressure (MSFP).
  • • Fluids increase MSFP by increasing volume.
    • Vasopressors increase MSFP by increasing venous tone, mobilizing existing fluid.
  • Example:
    • A hypotensive patient with severe venous congestion (i.e., low fluid tolerance)
    • May benefit from a trial of vasopressors
      • Recruit existing volume and improve flow without adding to the “fluid debt.”

7. Recommendations for Practice and Additional Learning

• The most important step is to recognize venous congestion as a prevalent and pathogenic process that is distinct from volume overload.
• Skills to Master:
  • First: point-of-care ultrasound (POCUS),
    • cardiac, lung, and abdominal assessments.
• Advanced Doppler assessments are most valuable when:
  • There is unresolved organ dysfunction or hypoperfusion.
  • The patient’s clinical course is stalling or deteriorating.
  • There is significant uncertainty about the next therapeutic step (e.g., more fluids vs. more diuretics).
    • A baseline scan at admission is invaluable for comparison.

8. Final Take-Home Points

• Venous congestion is a century-old concept, but modern tools now allow clinicians to detect, quantify, and monitor it, opening new avenues for research and clinical application.
• Congestion is fundamentally separate from volume overload.
  • Congestion = interplay between cardiac function and filling pressures.
    • A patient can be congested without being overloaded, and vice versa.
• Concepts is more important than the tools
  • While more data is needed to validate specific scoring systems like VEXUS in diverse populations, the underlying principle of identifying and managing congestive organ injury remains a valuable and evidence-supported clinical goal.

Transcript

Dr. Ross Prager: We spend a disproportionate amount of time in medicine agonizing over decisions to give or remove fluids with either fluids or diuretics. Every low urine output prompts kiind of this discussion about, should we be giving this patient fluids? And if we actually think about it at kind of the most simple level, IV fluids are just salt and water. Salt water hasn’t and never will beat the treatment for so many diseases. So I guess I just hope that in 2025 and beyond, we can stop kind of overestimating the perceived benefit of fluids. And, and maybe just kind of focus more on the core things like have we addressed the underlying cause of sepsis?​

Dr. Shreya Trivedi: That’s Dr. Ross Prager, an intensivist and scientist who taught me a ton in this interview about the new advancements in assessing a patient’s fluid status, something I know plagues a lot of us, and I was actually surprised to understand just how relevant venous congestion can be for anyone who takes care of patients in any setting, not just the ICU. And of course, definitely motivated me to up my ultrasound skills. So let’s start with what is venous congestion? What does that actually mean?

What do we mean by venous congestion?

Dr. Ross Prager: At the most core level, venous congestion is when high high actually reversal of flow from the right atrium goes to the end organ; for example, the kidneys, the liver, brain, the bowel even, and causes congestive organ injury. 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, pleural effusions, and just kind of general puffiness.

Dr. Ross Prager: The reason why this distinction is important is that patients can have severe venous congestion without volume overload. And in fact, some conditions like pericardial effusions, RV dysfunction, can manifest primarily as congestion without concurrent volume overload. I think it’s probably also just worth mentioning the other term that gets thrown around volume status, which to, to be quite honest, means a lot of different things to a lot of different people.

Dr. Ross Prager: I think for the most part people use it as, “Do I need to diurese 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. And so I prefer more specific questions contained within that. For example, to start off, does this patient have micro circulatory organ dysfunction?

Dr. Ross Prager: Do they have signs of end organ dysfunction and hypoperfusion? Mm-hmm. Does this patient have clinical features of volume overload? Does this patient have venous congestion and and is that congestion on the left or the right side? Are they fluid tolerant? And fluid tolerance is the concept, would fluids in giving fluids to that patient actually harm them

Dr. Ross Prager: due to their acute illness, their chronic comorbidities? And then do they have low stroke volume? And is that low stroke volume going to be responsive to fluids or potentially even vasopressors? And so when you break down a generic turn like volume status into these subcomponents, you can start having more precise conversations and weighing the risks and benefits of fluids or lasix or any other hemodynamic intervention you might use.

Dr. Shreya Trivedi: These are all good Qs to ask yourself when someone throws around, follow up on volume status. And we will get into these more later but for now, what we really need to cement is that venous congestion is different from volume overload. Venous congestion is retrograde or reversal of flow from the R atrium to end-organs. And that is different from overt volume overload that you might see like peripheral edema. The distinction is important because you can have venous congestion without volume overload. For ex. a patient with RV dysfunction can have venous congestion but without signs of overt volume overloaded. Or as we will learn later, a patient who is in septic shock can have venous congestion without being overtly overloaded. And so that brings us to why do we care about venous congestion at the organ level?

Dr. Ross Prager: Well, it turns out that every organ actually has a profusion pressure. The kidney, for example, has a renal perfusion pressure, which can be approximated as kind of the in the inflow pressure, or your mean arterial pressure and the venous pressure, or central venous pressure. And it, and this is why actually when a patient’s central venous pressure goes up, that’s associated with adverse outcomes.

Dr. Ross Prager: But the problem is, elevated central venous pressure for an individual patient in front of us doesn’t have very strong predictive accuracy at predicting adverse outcomes. Mm-hmm. And there’s a few reasons for that. One might be that the pressure at the right atrium or that central venous pressure does not actually reflect the, the pressure that’s being felt by the organs, which are obviously distal to it, right?

Dr. Ross Prager: There’s other factors, intrathoracic pressure, intraabdominal pressure, compliance of the venous system. But perhaps more 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 this retrograde flow that people experience during venous congestion that might drive the organ dysfunction.

Dr. Shreya Trivedi: Yeah, that’s interesting. How do you, how do you distinguish like it’s not the pressure as much the flow.

Dr. Ross Prager: Yeah. I think the first thing is that there’s been a lot of studies that have associated elevated venous pressure, uh, with adverse outcomes like acute kidney injury.

How is venous congestion associated with adverse outcomes?

Dr. Ross Prager: Mm-hmm. Across critically, critically ill patients, patients with sepsis. But it turns out when, when in the same study, when you actually look at end organ doppler, markers of congestion that actually detect the flow abnormalities in the kidney or the liver, those are even more correlated with adverse outcomes.

Dr. Ross Prager: For patients with sepsis, for example, venous congestion is associated with an increased hazard for requiring renal replacement therapy or death for patients with heart failure, highly associated with acute kidney injury, but then also heart failure hospitalization and cardiac death.

Dr. Ross Prager: And then for patients with AKI that already have established acute kidney injury, venous congestions, highly associated with mortality. And so really the, the causal pathway for these patients is that venous congestion seems to cause multi-organ dysfunction that contributes to increased need for organ support and the intensive care unit, and then ultimately mortality.

Dr. Ross Prager: We’re studying right now in the intensive care unit, the implications of venous congestion on, uh, delirium.

Dr. Ross Prager: And it turns out that venous congestion is associated with cerebral desaturations and worse, like delirium, post cardiac surgery. And so maybe some of these patients that we have on medicine or in the intensive care unit that are severely delirious and we’re not too sure why, ’cause they, they’re not on any meds, their metabolic is okay, maybe the treatment of those patients is actually diuresis And I, that’s amazing. I just really wanna 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.

Clinical Scenarios to measure venous congestion

Dr. Shreya Trivedi: Yeah, absolutely. Can you ground us in like, what are the painful situations where you’re like, I am so glad we have Doppler VEXUS.

Dr. Ross Prager: I think that my favorite use case for venous congestion doppler and venous congestion assessments is acute kidney injury patients where you’re not sure whether or not this hemodynamic acute kidney injury is because they’re actually hypovolemic or they’re actually congested.

Dr. Ross Prager: And now I think in an ideal world on the textbook, it’s always easy to distinguish, but, but we know from real life it can actually be incredibly difficult to distinguish these patients and having a starting point that says that this patient’s congested and then following that over time, that is incredibly valuable.

Dr. Ross Prager: Also for patients with acute kidney injury, uh, with Cardiorenal syndrome, you think that they’re congested. You start diuresing them. At some point, somebody’s gonna inevitably ask, could they be intravascularly dry? Maybe the sodium’s climbing a little bit, the creatinine’s climbing a little bit and trying to determine when do you actually stop decongesting a patient? Having baseline and then trended markers of congestion is incredibly valuable.

Dr. Ross Prager: For patients with acute sepsis or even just acute shock in general, venous congestion can also be, um, quite helpful to assess.And so, for example, in our local data, in septic shock, 20% of patients when they’re admitted to the ICU have severe venous congestion with septic shock.

Dr. Ross Prager: Um, this is early on in their course. These patients actually arguably could be harmed by additional IV fluids. Many of them have RV dysfunction and, and biventricular failure. And perhaps the treatment for these patients is actually not more fluids, but a fluid restrictive strategy, potentially even Lasix decongestion with inotropes and vasopressors.

Dr. Ross Prager: And that’s what we’re really interested in, is how can we sub phenotype these patients with septic shock, for example.

Venous congestion in sepsis, why?

Dr. Shreya Trivedi: And look because I was so surprised to hear that this being invoked for, for patients, uh, who are septic. ’cause you know, you think of them as like, give them fluids, they have infection.But in these patients with septic shock who have severe congestion, is it they always have some type of RV dysfunction that’s causing that? Or is it something with a milieu ofinflammatory response?

Dr. Ross Prager: That’s such a good question. I think this is the most important take home point, probably from venous congestion.

Deeper dive into the pathophysiology of venous congestion and how to measure venous congestion

Dr. Ross Prager: Venous congestion is not just related to volume. Venous congestion is really the interplay between cardiac function and the loading conditions for the right side, and let’s just think about it from the left side of the heart, and we’re very familiar with this. We have patients in the community with EFs of 10% who are walking around, who have no pulmonary congestion at all. They’re dry. They have cardiac dysfunction, but because their preload condition is optimized through diuretics and heart failure therapy, they don’t have pulmonary congestion yet.

Dr. Ross Prager: When that patient comes to hospital with sepsis and gets three liters of fluid empirically, now suddenly they’re in florid pulmonary edema. They, they have the substrate for congestion, which is now manifested after receiving IV fluids. The same thing happens on the right side. You have a patient with a substrate for developing venous congestion. Maybe that’s RV systolic or diasystolic dysfunction, elevated PA pressures, pericardial diseases or pericardial effusions, tricuspid regurge, and then interplaying in with their acute illness and the volume and resuscitation they get for that, they now manifest organ dysfunction and venous congestion on the right side.

Dr. Ross Prager: And there’s a lot of different causes of venous congestion. It’s not just cardiac either. So for example, we know that patients that go on higher PEEP on the ventilator can develop uh, right-sided congestion if they’re over-distended. And in fact, titrating peep can, can actually help improve renal function for those patients.

Dr. Ross Prager: We know that patients with large pleural effusions can have severe venous congestion. And I think back to a case that we had where a patient was, had really, really bad renal failure and this massive right-sided pleural effusion, but they weren’t on much oxygen. We put a chest tube in, drain that pleural effusion and immediately saw improvement of the severe renal congestion and improvement of their acute kidney injury, just from draining that pleural effusion.

Dr. Ross Prager: We know that patients can have, can have elevated intraabdominal pressure and elevated intraabdominal pressure. Intraabdominal hypertension can also cause renal dysfunction and we’ve seen also patients that have IVC stenosis, for example, post liver transplant that have severe renal congestion and it’s not at all related to the heart at this point. It’s due to a proximal upstream occlusion from a thrombus and so we, we saw this thrombus on ultrasound actually, and the patient went back to the OR for kind of a thrombectomy for that and immediately had their renal function recovered.

Dr. Shreya Trivedi: Awesome. So thank you for clarifying. You know, the, the pain points where we’re. Maybe invoking some type of venous congestion

Dr. Shreya Trivedi: So how does one measure venous congestion and what in the world is VEXUS?

Dr. Ross Prager: Yeah. And I think it’s even helpful just to take a step back from that. So we are so familiar with left-sided physiology. We think about it all the time on medicine. So let’s start there. When you have a patient with elevated left atrial pressure that gets transmitted retrograde into the lungs, it causes pulmonary edema, and we can detect that on ultrasound with B lines, wrong chest x-ray, curly.

Dr. Ross Prager: Mm-hmm. Batwing, all the normal stuff. Turns out this is very similar to the right-sided, uh, physiology, elevated retrograde atrial pressure. Its transmitted retrograde causes organ level congestion, but the organs we’re talking about now are the brain, the bowel, the liver, and the kidney. For the most part, this can be detected by doppler at those organs.

Dr. Ross Prager: The traditional tools to quantify venous congestion, like central venous pressure measurement examination of the JVP are really, really limited because those are pressure estimates.

Dr. Ross Prager: And we’re, we’ve just talked about how flow is probably more important than pressure. And then also, even if you are looking at them as accurate metrics, there’s a lot of variability. Even for CVP, which is something that we assume is very repeatable, you just transduce it. There’s a lot of interrater reliability issues there. And similarly for JVP, and we know that there’s so, such significant issues with interrater reliability for JVP.

Dr. Shreya Trivedi: Do we have an understanding of like what type of patients might have a more compliant venous, um, system versus a more tight one?

Dr. Ross Prager: Yeah, so, so that’s a really good question. So that’s actually a little bit where the IVC measurement comes into play because if your IVC is super distended,

Dr. Ross Prager: you have, by definition, not a very compliant system anymore because it’s already full and stretched to kind of the maximum capacity. Versus if you have a totally collapsed, uh, IVC, that may be a patient that has some more compliance. And if you fill up more kind of, uh, fluid in there and, and if the pressure’s higher, it might not be transmitted retrograde, which is, which is a great segue into how do we actually measure it now on ultrasound here.

Dr. Ross Prager: And so, initially, venous congestion was quantified, uh, using individual doppler markers. So for example, after cardiac surgery, the group in Montreal, André Denault and William Beaubien-Souligny, they looked at patients with, uh, post cardiac surgery and examined their portal veins. And they found that portal vein ity was associated with adverse outcomes, particularly acute kidney injury, but also delirium and congestive encephalopathy following cardiac surgery.

Dr. Ross Prager: In the heart, in the heart failure population, a lot of the early work was done looking at intrarenal venous doppler. So actually looking at the kidney and looking at these tiny little interlobular vessels because the artery and the vein, they run right together, and you can pulse wave doppler, these vessels that run together and look at flow abnormalities there. And then in acute kidney injury, we’ve looked at it using multiple different metrics, uh, hepatic vein, portal vein, and um, and intrarenal venous doppler.

Dr. Ross Prager: But the problem is that each of these in isolation have some limitations. There’s certain conditions that over-exaggerate, some doppler markers. And actually there’s other conditions that dampen some of the, and so in 2020, Dr. Denault and Dr. Beaubien-Souligny, in Montreal, they said, how could we combine multiple measurements into one kind of scoring system. And they took the inferior vena cava, hepatic vein, portal vein, and intrarenal venous doppler, and they put it into something called the VExUS score that, uh, that’s become quite popular in the most recent years.

Dr. Ross Prager: And it’s a score that ranges from zero to three, with scores of two or three representing kind of moderate to severe congestion. And this was derived and validated post cardiac surgery. And what they found was that compared with central venous pressure and compared with any of the individual doppler markers, that by themselves there was improved predictive accuracy to predict acute kidney injury.

Dr. Ross Prager: Now, how did they, they choose the thresholds of portal vein, pulsatility in the abnormalities. You, you gotta start somewhere. So they just picked reasonable numbers and they looked at their data and picked reasonable numbers.

Dr. Ross Prager: And so actually in my practice, I don’t use the VExUS score at all, in our research, or in my assessment because it was derived in one population, we’re studying a different population. It was derived in the post cardiac surgery population,

Dr. Ross Prager: and so we’re interested in sepsis. Who’s to say that the thresholds of congestion in sepsis are the same as in cardiac surgery? Mm. And so for our large international prospective study that we’re, 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?

Dr. Ross Prager: And do we actually need all these different components? Or maybe the portal vein is, is, is one, one vein to rule them all, so to speak, and will actually have the same predictive accuracy as a more comprehensive score and is much easier to do, for example, than the intrarenal venous doppler. And these are some of the questions that we have here.

Dr. Shreya Trivedi: So it sounds like there are 4 main components which include the IVC, hepatic vein, portal vein, and intrarenal venous doppler which can help us identify congestion even if we don’t use the VExUS score to a T. Can you tell us about any common mistakes or blindspots people have when they are learning measuring venous congestion?

Dr. Ross Prager: Great question. And, and to be entirely honest, there’s a lot. The first thing I see is that understandably, people rely a lot on the VExUS score.

Dr. Ross Prager: And for example, if the IVC is less than two centimeters on the VExUS score, you actually don’t proceed with any of the doppler markers. Oh, interesting. Which is unfortunately a little bit challenging because we have a lot of data showing that patients with IVC is smaller than two centimeters can have severe venous congestion.

Dr. Ross Prager: So unfortunately, stopping there is probably not a great idea. The next thing is trying to figure out the IVC and long axis, which is what is traditionally done in the VExUS score and what we’re traditionally taught, uh, in internal medicine and ICU pocus. Well, it turns out that like any vein, the IVC is not actually round.

Dr. Ross Prager: For example, if you go into the neck and you’re putting in a central line as a, as a internist, and if you see a very round structure that you’re about to put a, put a line into, stop! ’cause there’s a good chance that that’s not the vein. We all know that the internal jugular is kind of this ellipsoid, partially collapsed structure,

Dr. Ross Prager: right? Well, the IVC is no different. It’s a vein, it’s it’s ellipsoid. Mm-hmm. And so when you actually image it in long axis, you’re assuming that the axis of this ellipsoid aligns perfectly with the long axis. But when you actually look at it in short axis, sometimes you see these bizarre IVCs that are like four centimeters in one diameter and like two millimeters in the other diameter.

Dr. Ross Prager: And if you catch that just right in long axis, you can falsely make it look really, really big or really, really small. And so we, for example, advocate for assessing IVC in short axis because in short axis you can actually kind of look at the sphericity or how round it is because we know that as veins get more distended, they get more round.

Dr. Ross Prager: Right. So perhaps that’s actually a better metric to assess the IVC for example, than long axis. And that’s something that we’re, we’re currently studying. Great. Similarly, when we go to the hepatic vein, portal vein, intrarenal vein, it can be hard to figure out what you’re looking at. Mm-hmm. Particularly the hepatic vein, and so what, what I advocate for, for this is, is just kind of thinking a little bit more simplistically about it, blood should flow forward. On hepatic vein doppler that’s flow below below the baseline, the more and more flow you have above the baseline, regardless of whether it’s A,S,V, or D, your kidney doesn’t care; the more congested you are.

Dr. Ross Prager: And so we’re interested in thinking about hepatic vein doppler a little bit more kind of simplicity, just saying how much is backwards, how much is forward? Don’t worry about which waveform is which, because the more that you have retrograde, the worse congestion you probably have. Right? I would say the portal vein is probably my favorite.

Dr. Ross Prager: I mean, if I, if I was gonna pick favorites here, you, you shouldn’t pick favorites among your children, but I wasn’t gonna pick a favorite here with the ultrasound, it would definitely be the portal vein. If you go from the right upper quadrant, the main portal vein or the right portal vein comes right out towards you

Dr. Ross Prager: on the, on the screen. You put doppler on and you look at the pulsatility, which is just the maximum velocity, minus the minimum velocity divided by the maximum velocity. It’s repeatable. And interestingly, it seems to be the least affected by things like tricuspid regurgitation and, and other potential kind of confounders.

Dr. Ross Prager: And one of the reasons for that is when you actually think about the blood flow, it has to go from the right atrium into the IVC into the hepatic vein, into the hepatic sinusoids, like through the liver parenchyma to make it into the portal vein. So if you’re seeing pulsatility and reversal there, that can be a pretty good indicator of, of true kind of congestion.

Dr. Ross Prager: And then the last one is the intrarenal venous doppler. And I really like the intrarenal venous doppler. And the reason why is. When you can get it, which is the biggest limitation is that it’s only kind of obtainable in about 90% of patients based on the literature. But if you can get it, it measures directly kind of renal congestion. 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 were diuresing and their creatinine’s going up,

Dr. Ross Prager: and if you’re measuring congestion at the kidney level and there’s severe congestion, that’s a pretty good indicator that renal congestion is probably at play with whatever process is going on. And it’s also able to be tracked over time very nicely because there’s this concept of renal venous stasis index.

Dr. Ross Prager: And this might be getting a little bit into the weeds, but I think it’s interesting. And so the idea is that normally veins should drain a hundred percent of the cardiac cycle time. There should just be continuous venous drainage. Mm-hmm. But in settings of significant congestion, you start getting periods of interruption.

Dr. Ross Prager: And as those periods of interruption of venous flow get longer and longer and longer, your renal venous stasis index goes from zero, which is normal up to 10% interruptions, 20%, 30%, all the way up to like 60 or 70%, where most of your cardiac cycle, there’s no venous drainage. That’s really bad. And going back to the compartment syndrome analogy, that lack of venous drainage leads to worsening congestion of the actual parenchyma, which swells within the capsule containing the kidney, causing worse venous drainage.

Dr. Ross Prager: And it’s this kind of really negative, uh, feedback cycle or actually really bad positive feedback cycle, I should say. So normal is zero. You and I should be normal. Right? But some patients, their normal might not be zero. And that’s why I always think of this with like EFs for example. Like a normal EF is say above 65%, yet you can have a patient with an EF of 30%, and that’s just their baseline.

Dr. Ross Prager: So you have some patients that have baseline congestion and no matter how hard you diurese them or how aggressively you kind of manage their heart failure, they just will always have congestion. That’s not to say that it’s normal, but it’s just un uh, it’s their baseline. And ideally, in an ideal world, it would be nice to fix that, but, but we can’t always, and actually this brings into a really interesting use case.

Dr. Ross Prager: For example, if you try to diurese people aggressively with severe TR, a severe primary tricuspid regurg, um, maybe from rheumatic disease, for example, mm-hmm.

Dr. Ross Prager: You can never improve their intrarenal venous doppler, unless by diuresing them, you’ve actually unmasked that this was not primary tr and this was secondary tr they have severe renal congestion forever. Their portal vein will normalize or partially normalize, and you can use that to track kind of decongestion, but never their intrarenal venous doppler.

Dr. Ross Prager: But when you send them for like tricuspid clip or tricuspid repair and you fix the tricuspid regurg, their creatinine normalizes. So just because we couldn’t fix their congestive renal injury with diuresis, didn’t mean that it wasn’t having an impact on organ function.

Dr. Shreya Trivedi: Yeah, that’s great. I think for me this just really hammers home that every patient’s is, is different and different conditions will affect each of these four differently. So it is good to have a little bit more nuance understanding of what affects what. 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

Is this patient fluid tolerant? What does fluid tolerance mean?

Dr. Shreya Trivedi: Now back to something you mentioned earlier was being more precise when people say volume overload and there is this idea of fluid tolerance, tell me more about that

Dr. Ross Prager: Definitely. I think fluid tolerance is one of the really important emerging concepts in acute care medicine. And the idea is that every treatment we do has a risk and a benefit.

Dr. Ross Prager: The benefit of giving someone IV fluids, for example, is that we can increase their cardiac output. And by increasing their cardiac output and their stroke volume, we increase their perfusion, and things get better. But like any treatment, there’s a potential risk. The risk of IV fluids is, is really multifactorial.

Dr. Ross Prager: You can cause congestive organ injury, you can cause pulmonary edema, you can cause tissue edema, which can lead to kind of this micro circulatory dysfunction. You can cause endothelial dysfunction from over aggressive fluid resuscitation, actually like shredding the glycocalyx in the vessels. There’s a lot of potential harms, and we just need a concept to describe those potential harms, and that’s fluid tolerance.

Dr. Ross Prager: How I think about fluid tolerance is there’s kind of a few different domains. The first is the acute illness that somebody’s facing right now might make them more or less fluid tolerant. So for example, if you have a patient that comes in with acute decompensated heart failure, they’re not fluid tolerant.

Dr. Ross Prager: We would never even think about giving those patients fluid to try to improve their organ dysfunction because they’re in pulmonary edema and acute overloaded heart failure. There’s other more subtle conditions, however, like pancreatitis, for example, people with acute pancreatitis. 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 and that third space fluid leads to ARDS.

Dr. Ross Prager: It can lead to abdominal compartment syndrome and other complications In these situations, I think about giving fluids, kind of like tapping a credit card. Mm-hmm. You’re out the bar with some friends and uh, you know what? You order a round of drinks for some friends and then

Dr. Ross Prager: You tap your credit card that night and everything’s all good ’cause you’re gonna pay it off in the morning, but the next night you go out again and then you go out again and before you realize you have a drinking problem, you keep going out time and time and time and time again and, and you keep tapping your credit card, eventually that bill is gonna have to be paid otherwise because they’re gonna accumulate interest. Giving IV fluid boluses

Dr. Ross Prager: are a little bit like tapping your credit card. 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. And you don’t want to essentially have your credit card debt or your fluid debt build up so much that you actually get organ dysfunction as a result.

Dr. Shreya Trivedi: That’s great. Excellent.

Dr. Ross Prager: So, with fluid, with fluid tolerance, acute illness is kinda the first thing I think about. Then I think about chronic comorbidities. So, we, we intuitively know that patients that have EFs of 5- 10%, uh, or severe pulmonary hypertension are gonna be much more, uh, we’re gonna be much more cautious with the IV fluids because they’re more likely to be harmed by it.

Dr. Ross Prager: And then finally, I consider things like congestion, and that can be left-sided congestion or right sided congestion. So a patient with pulmonary edema is gonna be less likely to be fluid tolerant. A patient with severe venous congestion and RV dysfunction is gonna be less likely to be fluid tolerant because as we give them fluids, there’s a chance that this worsens their congestive organ injury.

Dr. Ross Prager: And so integrating those three components is kind of how I, I approach, uh, fluid tolerance for patients when I’m trying to weigh the risks of potentially giving a a, a fluid bolus.

Dr. Shreya Trivedi: Yeah. And then you also mentioned like, you have somebody with a low, um, stroke volume and you’re kind of weighing to get fluids versus vasopressors, and kind of, how can better understanding dopplers help you with that?

Dr. Ross Prager: Yeah, and I mean, I have to say this is one of the hardest questions that still remains in acute care resuscitation.

Dr. Ross Prager: When do you switch over from giving somebody fluid resuscitation into vasopressors?

Dr. Ross Prager: My assessment of whether or not I should give fluid, uh, fluids or vasopressors starts with the microcirculation. Do they have surrogates of hypoperfusion – cap refill, um, elevated lactate, oliguria, some sort of marker that this patient’s perfusion isn’t adequate?

Dr. Ross Prager: Because often actually we get, we get called for these patients after four liters, but then you look at them, you’re like, actually, your lactate is cleared. You’re peeing. Let’s not give you fluids or vasopressors right now, like you’re just doing okay. But let’s say the patient is hypoperfused, they’re hypotensive.

Dr. Ross Prager: The purpose of giving a fluid bolus is to increase something called the mean systemic filling pressure.

Dr. Ross Prager: So the mean systemic filling pressure is actually the main driver of venous return and, and cardiac output in our body. And it’s the difference between the mean systemic filling pressure and your right atrial pressure. And so when you give somebody a fluid bolus, we give it with the hope of increasing our mean systemic filling pressure to drive more venous return.

Dr. Ross Prager: And it works for that because when you give somebody fluid bolus, it increases the volume inside the vessels that causes a higher pressure and increases venous return. But it turns out that that’s not the only way to increase your mean systemic filling pressure because there’s the other component, the compliance or the elastance of the vessel.

Dr. Ross Prager: And if you give somebody vasopressors, you can also squeeze the venous system and increase that mean systemic filling pressure and drive more venous return. And so whenever I think about giving a fluid bolus, I always ask myself. And you know, I have a bit of a luxury being in the ICU where I don’t have to kind of factor about resource utilization and transfer to kind of higher level beds.

Dr. Ross Prager: But I always ask myself if this patient’s hypoperfused, they have low stroke volume, they’re acting hypovolemic. Mm-hmm Is the treatment for this patient fluid or is it actually vasopressors? ’cause maybe in this case I can actually recruit some of that venous volume by just giving vasopressors. And so how, does this relate to the venous congestion assessments when I have a patient with severe venous congestion who I’m worried that are less fluid tolerant?

Dr. Ross Prager: That may push me to trial vasopressors earlier with the hope that I can recruit mean systemic filling pressure and kind of recruit that venous volume, increase forward flow without giving fluids, because again, fluids are that credit card that I’m gonna have to pay off down the road. And that patient already has signs that they’re, they’re in too much debt, so to speak.

Dr. Shreya Trivedi: Oh, that’s so great. Thank you for kinda walking, walking through all of that.

How often to repeat measures of venous congestions?

Dr. Shreya Trivedi: Awesome. Um, and then back to VExUS or just some of the four core measures of it. How often are you getting these measurements? Is it like a daily thing? Is it every other day? Um, what in your practice do you find utility or would you recommend?

Dr. Ross Prager: Yeah, great question. I would say that It really depends on the clinical scenario. And so I really like to anchor any hemodynamic assessment, be that xis or cardiac assessments in starting with a microcirculation.

Dr. Ross Prager: Mm-hmm. Is there organ dysfunction because if yes, we need to move on to figure out why and phenotype it.

Dr. Ross Prager: So I would start by saying, uh, whenever I have a patient in shock with organ dysfunction, I’m considering congestion as one of those mechanisms of organ dysfunction because we know that some of those patients have good forward flow, they have good map, but they have hypoperfusion due to congestion. So we need to kind of consider both the forward flow and the retrograde when assessing those patients.

Dr. Ross Prager: The question then becomes, well, when do you reassess? Well, it depends. If a patient, after we kind of initiate appropriate therapy, antibiotics, pressors on them with sepsis, for example. Their organ dysfunction’s getting better. I might not assess them again, because if they don’t have, if they have normal organ perfusion at this point, they’re, they’re peeing up a storm, their pressure are coming down, their lactates normalizing,

Dr. Ross Prager: what am I gonna do differently if I find that they’re still congested? I’m just gonna keep doing what’s working. Mm-hmm. For example. Mm-hmm. Yeah. And so I often use it when patients are stalling, when patients, when there’s uncertainty about which direction to go or when there’s ongoing hypoperfusion that hasn’t been resolved

Dr. Ross Prager: because, for example, say we see a patient with sepsis with severe congestion and they’re totally volume overloaded, we might start vasopressors and start diuresing them. But if 12, 24 hours later they’re still hypoperfused, it’s not working, the question is, well, why are they so congested? Maybe they have occult RV dysfunction that we didn’t recognize up front.

Dr. Ross Prager: Maybe they have pulmonary hypertension as a driver of this kind of right-sided decompensation that we need to treat with inhaled nitric oxide, for example. Mm-hmm. And so those would be the times that I would start reassessing, but I don’t routinely reassess on a prescribed schedule unless there’s kind of a clinical picture for it.

Dr. Ross Prager: I appreciate that.

Dr. Shreya Trivedi: That’s great.

Dr. Ross Prager: I just, one more example that might be even more contextually relevant, uh, kind of for internal medicine listeners, it would be a patient with heart failure who is overloaded, who you start diuresing for cardiorenal syndrome and volume overload.

Dr. Ross Prager: But having a baseline at the beginning is really helpful. When on day five, they’re still overloaded, but their creatinine starts going up and their urine output starts going down, and you’re starting to worry, gosh, could I have over overdiuresis patient?

Dr. Ross Prager: Or maybe their preload is actually too low. Having a, a repeat assessment at that time to say, no, this patient still has severe renal congestion. Instead of having the, uh, the dose of Lasix, you’re holding and giving albumin, let’s double the, the dose of Lasix and add some metolazone and really kind of, uh, kind of double down on what we know and what we think should be working here.

How should learn or practice these skills this evolving area?

Dr. Shreya Trivedi: Okay to close this out. To inspire the person who is, wow, this sounds so cool. How will I ever learn this? Or could, what do you have to say in terms of this is like the Med-Ed in us, like how often should one practice, how should one practice to, um, get somewhat competent in an evolving area?

Dr. Ross Prager: Yeah, that’s a great question. I. I think the first thing I would say is that, like to put put aside ultrasound, I think the first thing is just recognizing that congestive organ injury is probably more prevalent than we realize.

Dr. Ross Prager: So I would say that hopefully this, this kind of excites us and to say that we have this kind of very prevalent phenotype of. That have severe congestion and organ injury as a result of it. For example, we’re studying right now in the intensive care unit, the implications of venous congestion on, uh, delirium.

Dr. Ross Prager: And it turns out that venous congestion is associated with cerebral desaturations and worse, like delirium, post cardiac surgery. And so maybe some of these patients that we have on medicine or in the intensive care unit that are severely delirious and we’re not too sure why, ’cause they, they’re not on any meds.

Dr. Ross Prager: They’re metabolic or coa, maybe the treatment of those patients is actually diuresis And I, that’s amazing. I just really wanna 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.

Dr. Ross Prager: And I think if I was starting, kind of really trying to get into this, I wouldn’t start with VExUS.

Dr. Ross Prager: VExUS is like level two, level three, start with just kind of core acquisition of POCUS images, the heart, the lungs. There’s so many, really important, um, findings that can really change your clinical management and internal medicine and ICU based on ultrasound. And I would start there. And then as that skillset develops then we can start looking at venous congestion and, and learning how to do the Doppler patterns.

Dr. Ross Prager: And they’re really not that hard.

Take home message

Dr. Shreya Trivedi: That makes a lot of sense. Any take home points or things that you were like. I want people listening to get this out of the episode. Some final take of points you have?

Dr. Ross Prager: Yeah. A few final take-homes here. The first is that venous congestion is not a new concept.

Dr. Ross Prager: We’ve known about this for close to a century, but really excitingly, we now have tools available at our disposal to actually detect it and to, to, to quantify it, but then monitor in response to treatment. And I think that this will really open up new areas of research in diseases that we, we manage every day.

Dr. Ross Prager: It’ll add a, a lens and potentially an explanation for some of the reason why these patients do well or do poorly, and it may be related for some of these conditions to, to whether or not they’re congested or not. The next thing is that congestion is separate from volume overload.

Dr. Ross Prager: Congestion reflects that interplay between cardiac function and the filling pressure. For some patients, they might be overloaded like an acute decompensated heart failure with cardiorenal syndrome, and they might have severe venous congestion. But for other patients, the acute RV failure itself, the pericardial effusion, the pleural effusion, the intraabdominal process going on can cause direct congestion.

Dr. Ross Prager: And then I think the final thing is just, uh, and, and this is kind of, um, the, the distinction between venous congestion and VExUS. 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, is new as well.

Dr. Ross Prager: And that’s one criticism I’ve heard commonly of VExUS is that, well, there’s just not enough data. I totally agree. I don’t use VExUS in my own practice because there’s not enough data for the populations that I’m using it in. But as a concept, congestion has been well established. And I think 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.

Dr. Shreya Trivedi: And that is a wrap for today! Our ask is you send this to one colleague who may find learning about venous congestion or VExUS may be helpful. Send it to someone who may be on the fence about learning ultrasound or loves it already. Thank you again and take care!

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