Hello everyone, it's a pleasure being here. Topic that's very near and dear to my heart. My pathway here is a little different from most of you because I am by training an intensivist, but then I made the decision to join the dark side and I did a cardiology fellowship. So I'm a critical care cardiologist, but it's very humbling because throughout the years I've realized that if you want to understand more about the heart, you have to examine other organs. And I will tell you an adage that I tell all my trainees is that physiology is always, always correct. The problem is a lack of understanding. That's what leads us astray. So with that, I'll start. And what I'm going to really focus on is, obviously I have no disclosures here. We're going to talk about venous congestion. And for most of you probably have not seen this or have incorporated this in your practice. So I'm going to give you a primer to understanding this. So these are my hand drawn organs. If the brain looks like a broccoli, that's my fault, but I tried my best. And so when it comes to physiology, we've really forgotten Guytonian physiology. We've forgotten the basics and now we try to implement simple reflexive algorithms. And it's very important in these complex patients that we actually take a step back, understand what we're looking at and understand what our diagnostic and therapeutic modalities are doing. So as far as the right side of this here, we know a lot about cardiac output. We understand that the mean arterial pressure is a good guide when it comes to resuscitating patients. We've all been inundated and flooded with this equation about MAP and cardiac output and vascular resistance. And we're in the business of delivering oxygen to the tissues. And we know for the most part when we've maintained hemoglobin and your SATs look okay, the principal determinant when it comes to delivering oxygen to the tissues is actually cardiac output. Now we've always maintained MAPs over 65, which is a good target, but we know vascular beds sometimes require different targets depending on your patient's physiology. Now let's talk about the dark side of the moon, which is the venous return side. This is a side that we often forget. Now as far as pressure or perfusion to tissues or flow, we always know that when we have an upstream pressure and a downstream pressure, we can create a gradient. And you can see here in a patient who's got a MAP of 75 with a near normal right atrial pressure about zero to five, you will always have that forward flow. But how about on the venous return side? When you look at the post capillary venules that drain into the capacitance vessels, that go into the resistance vessels, and finally into the right atrium, what is that gradient there? And we've actually measured this experimentally by inducing cardiac standstill, and you can actually measure this, and it's known as mean systemic filling pressure and mean capillary wedge pressure. And we found that that mean systemic filling pressure is around eight to 10 in a completely normal patient. Can you notice that the upstream pressure here where the mean systemic filling pressure is only eight to 10 and your downstream pressure is zero to five? What does that tell you? That's a very delicate balance. If we just blindly follow algorithms and bombard our patients with volume in hopes of increasing the central venous pressure, you will definitely increase the central venous pressure. You'll increase your mean systemic filling pressure by a little bit. But what happens is that once your right atrial pressure is higher than your mean systemic filling pressure, what will you see? You'll start to see back pressure. So flow will start to go backwards. And what does that manifest clinically as? It manifests clinically as organ dysfunction, especially your organs that have capsules like the kidneys and the livers. You'll see your AST, ALT start to go up. You'll start to see renal dysfunction. You'll start to have sphinctic congestion as well. And all of this leads to multi-organ dysfunction. Even though you've maintained your maps above the targets that you've wanted, the problem, the physiology or the pathophysiology going on here is now venous congestion. And this is oftentimes forgotten. All right, so let's talk briefly, we had a great summary of volume status and how we nowadays look at volume status, but where have we really failed? And again, I'll say this again, the physiology is there, the problem is our lack of understanding physiology. Here's an example of a patient completely normal with a collapsible IVC as all of our IVCs are here today. And you can clearly see that the patient after you're adding positive pressure, what happens to the IVC? It gets large. There is no change in this patient's volume status whatsoever. You brought up the great example. If we suddenly develop obstructive shock from a PE, suddenly your right atrial pressure goes up. That is not a marker of volume status. That's mainly indicative of what? A congestion parameter. You have a point where there's an obstruction and everything proximal to that will increase in terms of its filling pressures. The wrong answer to the question would be to diuresis a patient who has obstructive PE. So we also talked about volume responsiveness, but again, what does volume responsiveness tell us in terms of physiology? We all hear our volume responsive. That is our natural physiological state. If we all got injected with an endotoxin and we suddenly vasodilated, we'd still be what? Volume responsive. The main issue is the vasodilation that's occurred. Yet we have this overwhelming desire to give patients volume until they reach that point where they're no longer volume responsive. And that can get you in a lot of trouble. When you reach that point where the patient's no longer volume responsive, you're actually contributing to what? Increasing filling pressures and leading to back pressure and venous congestion. So reaching that point where the patient's no longer volume responsive is not a good target or measure for us when we're resuscitating patients. All right, and these are the Frank-Starling curves that we know so well. Why would we want to go to that flat part of the ascending curve? Why? Because if we reach that, we may get into trouble in terms of developing more extra vascular lung water, more congestion in the organs. So we really want to keep our patients in the ascending part. All right, so if we can't rely on the IVC and we can't really rely on targets such as volume responsiveness, there's always been this discussion about using the old trusty Swann-Genz catheter. And we had a multitude of different studies that showed us that there was no benefit. Unfortunately, these studies was in a mixed population. And I always say this, garbage in is garbage out. If you don't know what you're doing with your numbers, then you're not going to actually be doing the right thing for your patient. And so there are a lot of inherent problems with these study designs. We've realized over the last five years or so, especially when it comes to patients with mechanical circulatory support or patients who have cardiogenic shock or have a mixed picture, the Swann-Genz catheter can be very, very useful. However, it's invasive. Some units may not use it. And if you don't use it all the time, you may not be comfortable using it for that odd patient who may need it. So we need to come up with a better way to assess our patient's volume status, whether or not they're fluid tolerant and to institute the appropriate therapeutic modalities. And this is where venous congestion comes into play. And it's so important because we're actually taking a step back and we're trying to understand physiological waveforms, flow patterns in different organs that can tell us about pathology. Now, if you've seen over the past five years, there's been this surgence on social media about the use of vexus scoring systems, et cetera, that actually incorporates some of these Doppler flow patterns. This is a great thing because it's opened the eyes to many intensivists to start using it. But just like where we were led astray with the IVC and volume responsiveness, we have to be careful about what these waveforms actually mean. And although this is a simplified version of what you can do, and I do suggest you guys use it, you have to understand the key components of each of these vascular parameters. So we'll start with number one, which is the portal vein. Now, the portal vein, we know drains the mesenteric. You have to understand the flow patterns that you normally see. It's very easy to obtain the portal vein with point of care ultrasound. You just place the probe trans hepatic view, and if you do an anterior tilt, you'll see the portal vein. Now, the portal vein, you know, look here, it drains. It's called hepatopedial flow. Why? Because it drains from the sphincter circulation towards the liver. So you would expect this color to be red. Now, the flow pattern is very unique. It's monophasic. It's completely flat. Think of it as a waterfall or a Venus hum. That's flow going from your sphincter towards your liver. Now, as you start to give this patient more fluid, so some overdue dishes fluid resuscitation, for example, a septic patient, what do you start to see? You start to see a little bit of pulsatility. You've lost that nice monophasic waveform. Now you're starting to see a little bit of phasicity here. And as this patient becomes much more congested, you'll start to see pulsatility. This is pathological. This means your patient has extreme sphincter congestion and you need to do something soon. In the most severe form, you'll actually see biphasic waveforms, biphasic because it actually crosses the baseline. So not only is it pulsatile, but it's pulsatile, and it reverses flow as well. This is the most severe form of congestion in the sphincter circulation. And usually these patients need IV diuresis or some form of volume removal as soon as possible. All right, here's another example where you can actually use it in the reverse way in terms of de-resuscitation. This is a patient who got about six liters of fluid on the left. You can see a little bit of pulsatility developing. And the patient was on some minimum vasopressors as well. We decided to diurese the patient. And as you diurese the patient, look at what happens. You actually reestablish that monophasic flow. So we're no longer looking at static or dynamic. We're actually looking at physiological waveforms and we're trying to turn these waveforms back into normal. And even though that patient was on pressors, as we diurese the patient, guess what? The pressors were weaned off as well. All right, number two is intrarenal venous Doppler. Remember we talked about the portal vein. Now we're looking at another organ as well that can be very susceptible to venous congestion. Now, if you look at the bottom, again, you're using the same view, which is that trans-hepatic view. You can find that kidney as well. And what you're going to do is you're going to throw color Doppler and you're going to see a smorgasbord of different colors. And what you want to do is closer to the medulla, you want to put your pulse wave Doppler there. Now you're going to see two different waveforms. Waveforms that are above the baseline and waveforms that are below the baseline. For the purposes of venous congestion, just look at everything that's below the baseline. On top is actually the renal arterial waveforms. So if you look at the bottom, what do you notice? Similar to the portal vein, you have continuous venous flow. Not sure if you see my arrow there, yeah. Continuous venous flow, monophasic flow. There may be a little bit of pulsatility during systole and diastole, but that's fine. As you start to develop more venous congestion in the kidneys, what do you see? You start to see what we call discontinuous flow. You can actually see the pulsatility of the S wave and the D wave. And in the most severe form of renal sarco, which is edema of the kidneys, what do you start to see? You start to see clearly discontinuous flow, but actually that S wave has actually had flow reversal. So now you have only monophasic waveforms. So this is actually the spectrum that you start to see in these patients. Again, another example, continuous flow in a patient who is probably euvolemic. As you give the patient more volume, they become discontinuous, but you see at least two waveforms, right, for each cardiac cycle. And in the most severe form, you only have monophasic flow, which means that your systolic waveform has reversed, and now it's somewhere within, hidden within this arterial waveform. So this is good, this is bad, this is getting worse. And again, this is the spectrum, and you can actually use the spectrum in reverse as well. So if you have someone who has significant congestion, you can start to diurese or use CRRT or some form of volume removal to try and reestablish normal flow. Okay, the last one is my favorite, which is a hepatic vein Doppler. And I say it's my favorite because it truly is a window to the right side of the heart. Unlike the portal vein or the intrarenal venous Doppler, this is affected by what I call the right heart apparatus. And the right heart apparatus is your tricuspid valve, is your RV, and is your pulmonary pressures as well, because there's a direct connection to the right side of the heart. So you have to be very careful when it comes to actually interpreting these waveforms as opposed to the portal and the intrarenal venous Doppler, which are a simple monophasic versus discontinuous. Okay, so you have to understand what the mechanical, what is the correlation between the mechanical events that occur and the electrical events. So with the P wave, we have atrial contraction. Remember, you're sitting at the level of the hepatic vein, so you're watching or observing what's happening in the right atrium. And so when there's contraction of the right atrium, there is retrograde flow towards the hepatic vein. That's why you have an A wave. And then the peak of the R wave is when systole occurs. And when systole occurs, the tricuspid annulus pulls downwards. And when it pulls downwards, what it does is it opens up your right atrium. Now, suddenly you have flow rushing into the right atrium. And that's where you have the S wave. And as flow continues into the right atrium, it's fills it up until the pressure increases. And then until the pressure of the atria overcomes that of the ventricle, then the ventricle opens and that's why you have diastolic flow. This is why it's called the S wave for systole and the D wave for diastole. All right, like I said, very easy to get these views, just like how you get your IVC. All you have to do is focus on the hepatic vein, put color Doppler on the hepatic vein, make sure you do pulse wave Doppler, and then you can actually see these waveforms. All right, it's very important to understand you can mix up what this actually means if you don't understand physiology. If a patient takes a deep breath in and increases flow into the right heart, you'll notice that during inspiration, you have an increase in the anti-grade flow, which is the S wave and the D wave. But the same patient can be taking a deep breath out and guess what happens? Your S wave and your D wave gets smaller and your retrograde waves become more prominent. And you can see it very clearly here in this example, always find your QRS complex that denotes the beginning of systole. So that waveform that occurs after that QRS complex is the S wave. This patient is taking a deep breath in, you can see that the anti-grade waves have become large. Now the patient is taking a deep breath out and now they've become small. I bring this up because when you use simple methods like the VEX's scoring system, you may be fooled into thinking that this is blunting of the S wave because of volume congestion. And it's not, it's just simple breathing in and out. And here's another example, a little big breath here, you can see the S and D waves progressively getting bigger and bigger. Here's an example of someone breathing out and look at how these reversal waves got much larger because of expiration. All right, here's a very important concept. When you have a good atrium, the atrium actually helps augment the function of the cardiovascular system. So for example, when you have atrial contraction, if you have good atrial relaxation, it brings down the pressure. Is there a way I can go back please? It brings down the pressure to this point right here, which is known as S1. Then your ventricular contraction takes place. Notice that because of that augmentation, because of that relaxation, because of that good atrium, you've actually led to what? Increased forward flow. This is why when you lose atrial kick in specific patient populations, it leads to hemodynamic compromise. So when for example, you don't have an atrial kick like atrial fibrillation, you may notice that your S wave has gotten much smaller. That's because it's no longer augmented. This is not because of volume overload, this is because of an atrial dysrhythmia. So now we start to understand as we break down each component of these waveforms, that we can actually start to build a differential diagnosis. So for example, that initial A wave, that first part of that hepatic vein waveform, it could either be completely absent, it could either be prominent all the time, or prominent only sometimes, or it can be completely biphasic. If you look at atrial fibrillation and flutter, because you don't have consistent atrial contraction, what's going to happen to your A wave? It's going to disappear. And so basically because you've lost that atrial kick, you're going to have very small S waves. That blunted S wave has nothing to do with volume congestion, it's due to an atrial dysrhythmia. And here's the example of someone who has atrial fibrillation, here's someone who has atrial flutter. How about prominent reversal waves? Remember I talked about the right heart apparatus? Anything that goes on with atrial dysrhythmias, or the tricuspid valve, or the RV and pulmonary pressures can lead to augmentation of those reversal waveforms. And so for example, here's someone who has a AVNRT, so AV nodal reentrant tachycardia. Because the P wave is so close to the QRS complex, the atria contracts at the same time as tricuspid valve closure. So what are you going to see? You're going to see prominent A waves every single cardiac cycle. Here's a patient, this clinical entity is very rare, but tricuspid stenosis, look at those giant A waves, right? Now, sometimes your A waves, these reversal A waves may be prominent, but just sometimes. Here's an example, if you have someone who has a PVC or has heart block, if that P wave lands at the same time as the QRS complex, boom, you get a big A wave. Again, here's another example, this happens to be, I think the PVC. Again, only when that PVC lands on that QRS complex. So sometimes that A wave is going to be large. Now, this is very interesting. Sometimes you can unmask a patient's RV compliance issues by asking them to breathe in. So for example, someone who takes a deep breath in, increases flow, only when you have increased flow to the right side of the heart, do you notice that the atrial reversal wave becomes larger. So you've actually unmasked RV dysfunction. So now you start to really understand that I can actually break down things happening to my patients that have nothing to do with volume overload but may contribute to this patient's demise. All right, so another hand drawn thing for me here, this is what you're going to be taught when it comes to venous congestion, that if the S wave normally is greater than the D wave, and as you increase volume, your S wave becomes smaller, that's called blunting of the S wave, it can disappear or it can actually reverse altogether. And remember, we talked about certain instances where it's just not volume, but other things that cause these flow reversal. And again, it's lack of atrial contraction, tricuspid regurgitation, volume overload, RV dysfunction, et cetera. Now it's very important to understand when you're looking at the S wave, in terms of tricuspid regurgitation, your septic patients don't know that they're just septic, they may also have other clinical issues, and one of them is valvular issues. So if you have someone who has tricuspid valve regurgitation, remember that the flow reversal occurs late in systole. So because the regurgitation volume increases as systole progresses, then you will notice that late systolic flow reversal. Conversely, with RV systolic dysfunction, because it's pump failure from the get-go, you will have early systolic flow reversal. And again, because it's pump failure, it's early systolic flow reversal. These always occur in combination. So if you have severe RV dysfunction with TR, what are you going to see? You're going to see pansystolic or hollow systolic flow reversal. So basically it looks like biphasic waveforms, and this is a big red flag right here when you have a patient that looks like this, okay? And so again, you start to see that S waves can be diminished, they can be normal, or they can show reversal for different reasons. All right, so now we start to understand that we actually have a spectrum, a continuum, and when we look at these vascular Doppler waveforms, we start to understand that as a patient gets congested, we can follow these waveforms, either during the process of resuscitation or de-resuscitation. So let's take some quick illustrative case examples. Okay, two minutes, great. Here's a patient who had a cabbage, was extubated, and has some respiratory failure. It's hypoxemic, and we don't know why. These are from the bedside. You can see the patient probably has preserved biventricular function. IVC here is collapsible. We were told that they thought that the patient was volume overloaded. I went ahead and we did a paddock vein Doppler. You can see here, you can have all blue flow that means blue is away. This is hepatofugal flow. This is completely normal. Hepatics drains into the IVC, and this is, you can see, that has predominant anti-grade flow. We looked at the portal vein. It's completely flat. So should we diuresis this patient, yay or nay? No, this was just someone who actually just aspirated shortly after. We actually saw B lines, and they were mainly in the right upper lobe. All right, next is a 57-year-old woman with COVID-19 pneumonia, very severe refractory hypoxemic respiratory failure, sedated, intubated, paralyzed, proned. You're called six days later. You're asked to see the patient because of worsening AKI and hypotension. Here's an image, a personal long axis view showing hyperdynamic LV and RV, and you can see here a representative example of the anterior lung fields that show B lines. It's really not helpful. Hyperdynamic LV and a bunch of B lines. So what did we do? We took a look at the hepatic veins. What do you see here? This is bad news. When you see biphasic waveforms, where are my triphasic, tetraphasic waveforms? They're not here. That means there is volume overload. And if you see the portal vein consistent, what? Portal vein pulsatility when it's supposed to be flat. So splenic circulation is now congested, and hepatic veins are also congested. So what did we do? We did CRT for volume removal. Mind you, this patient was on three pressors. As we removed volume, the hemodynamics improved. We shifted from these biphasic waveforms to more normal-looking hepatic waveforms. And as we did that, the patient's pressure requirements decreased. Lastly, I have the 28-year-old with tricuspid valve endocarditis with respiratory failure, worsening shock, and acute kidney injury. This is the B lines all over the chest, probably because of septic emboli. And if you take a look here at the tricuspid valve, the technical term for this is a goomba, all right? Really bad tricuspid regurgitation, and the patient has worsening AKI. We're told to diurese, diurese, diurese, because the CVP is high. But of course, the CVP is going to be high because the patient has tricuspid valve regurgitation. So we took a look here. Mind you, if you look here at the S wave, the S wave is blunted, and you have flow reversal that's late. That's indicative of a valvular issue. We combined this with our understanding of the portal vein that has just minimal pulsatility. So we actually gave this patient fluid. The AKA resolved. The patient was able to get surgery. Lastly, this patient was actually transferred from an outside hospital. We were told that the left ventricular end-diastolic pressure was 27 when they did a CAP. BMP is 1,000, the setting of AKI. This is actually taken out of the patient's chart. We actually record these images, and we put it inside a report, a POCUS report, and you can clearly see good anti-grade flow, and you can actually see flat wave form, but as the patient breathes in, it actually disappears, but this is monophasic form, monophasic waves in the portal vein. So this patient is practically what euvolemic. They didn't believe us. They wanted us to do a SWAN. We did the SWAN, and if you can clearly see, the wedge was in single digits. So you can actually use a non-invasive means of assessing venous congestion without having to actually use the SWAN. That being said, the method I use to assess patients is what I call the congestion cascade, and you start yourself from the aortic valve to the LVOT, LV to the lungs, RVOT, RV, IVC, and then the venous parameters that we talked about. If you do at least three or four of these, you will find a problem, and once you find the problem, start to look proximal or distal to it, and you usually find the answer, and I always say, in critical care, it's not the smartest people. It's the people who are most, what, systematic that always find the answer, and I'll leave you with this here. A lot of times, the trainees, for 40 minutes, I will be doing a scan, and then we'll ask the patient, how do you feel? He says, sir, I'm as dry as a bone. So use this carefully. This is a tool for your clinical acumen, and thank you very much. Thank you.

venous congestion

physiology

critical care

Doppler flow

organ function

hemodynamic issues