All right. Hi, my name's Tony. I'm a nurse practitioner at the Surgical Critical Care Unit at the VA Medical Center in Philadelphia. Been a nurse practitioner for at least probably almost 10 years now. Did most of my training at Penn and recently transitioned over to the VA. And in addition to that, the lovely ultrasound SCCM course is all here in the front row. And I get to be faculty with them, which is quite an honor. Let's see, how do we move forward? Just click, ah, perfect, okay. So I have no financial disclosures. I will disclose though that this is my first time presenting at SCCM and this is a very full room. So I'm a little bit nervous. And if my voice cracks, I promise I finished puberty. I'm just nervous. All right, so when we talk about fluid management by echocritical cardiography, really what we're talking about is just, you have your patient, your ICU clinician using bedside ultrasound to make a decision. In this case, what we're talking about is fluid guidance. The only reason I talk about this, this is a little different than your traditional cardiology echo where it's performed by a tech then sent over to a cardiologist to be read. That's usually a much more comprehensive exam. Whereas this, we're doing live bedside and we're trying to answer a specific question. In this case, we're talking about sepsis and fluid management. You can also, you'll hear this called POCUS, bedside intensive, bedside intensive cardiography, bedside echo, all the same thing. So why is POCUS essential? Well, you know, when I was in school, they told me that edema didn't really matter and we would just kind of give people fluid and see if it worked. Of course, they lied to me. We now know that edema not only leads to organ volume, but organ dysfunction, decreased wound healing, increased infections. And there's evidence that shows that those with sepsis that end up with higher CVPs or positive fluid balances will have higher mortalities. In addition, only 50% of your patients are gonna be volume responsive. And of those 50%, most will only be responsive in the first few hours of resuscitation. So we need to figure out who are these 50% that will benefit from volume. And so when we say fluid responsiveness, really what we're talking about is usually a 10% increase in cardiac output, usually delivered with a rapid fluid bolus infusion or passive leg raise. And the goal is to figure out where your patient is on this Frank-Starling curve and whether they're on the steep curve where increasing preload will increase your stroke volume. Of course, I was lied to again, because they showed me this very beautiful picture of a Frank-Starling curve. And then I went into practice and this is what I got. One patient with multiple curves. And these curves are dynamic depending on your patient's pathology, whether they're getting better or getting sicker, they can shift. And so our traditional static measures, such as CBP, left ventricular wedge pressures, they can be helpful in our extremes. Most patients with a CBP of zero will be volume responsive and someone with a CBP of say 30 would not be volume responsive. But of course, a lot of our patients are gonna sort of fall in this gray area. And this is where our dynamic measures may come into hand. Also to think about it, I like to think about this Rose approach to fluid management, where we can think of resuscitation in four distinct phases. We have our resuscitation phase. This is usually characterized by patients that have severe hypotension. They have evidence of tissue hypoperfusion and we're usually rapidly giving volume to. Then you have your optimization phase where you still have tissue hypoperfusion, but now you're sort of fine tuning, adding vasopressors, maybe slowing down the amount of volume you're giving. And we can move on to our stabilization phase where we've sort of captured the patient. There's no longer evidence of tissue hypoperfusion and we're trying to maintain our fluid balance or maybe even restrict. And finally, the last phase, which I think it's forgotten a lot of times, which is the evacuation phase, where the patient is better now and we need to actively diuresis, whether it be a diuresis or dialysis or however we're gonna get this volume off. And so while this talk is mostly focused on these two resuscitation and optimization phase, I think bedside POCUS can actually take you through this full continuum of stabilization, help you titrate your pressors and decide when you're gonna diuresis the patient. So from here, we're gonna talk about basically four parameters that we can use with bedside echo to determine volume responsiveness. The first one is gonna be your inferior vena cava, the IVC. This is probably the most studied and the most common parameter you're gonna see. Most people that do bedside echo will have at least looked at the IVC at one point or another. When we look at the IVC, we do need to think about it as mechanical ventilated patients versus our spontaneously breathing patients. And the benefit of the IVC is that it's actually pretty simple to interpret and to also acquire the image. Those with mechanical ventilation, we tend to talk about our IVC distensibility and that's due to the positive pressure effect of the ventilator. With our spontaneously breathing patients, we'll look at our IVC collapsibility. As far as mechanical ventilation goes, the evidence for it is all done on patients with no spontaneous effort and at least eight mils per kilo of tidal volume. The IVC assessment, we start with our patient usually in our supine position, subcostal four chamber is obtained. The probe is then rotated 180 degrees and we usually take our measurement just distal to the hepatic vein or about one to three centimeters in from the right atrium. And we'll see a live image of the IVC in a minute here. But before we do that, just so you guys have an idea of what we mean when we say collapsibility, these are the formulas that are actually used for collapsibility index where you're looking at our IVC max minus our IVC min divided by our max times 100. We'll do that for our spontaneously breathing patients. For our mechanically ventilated patients, there's actually two formulas you can use. Both have been validated in the literature. The first one would be our distensibility index, which is our max minus our min divided by our min times 100. And the other is our change in distensibility, which is our max minus our min divided by the average of the two, which you just take your max plus your min, divide that by two times 100. And so here we have a live image of the IVC. For those that aren't too ultrasound familiar, what you see here is ultrasound probe is up here. You have liver, liver, and this is the IVC running through the liver. Here is the hepatic vein, and this is your right atrium and right ventricle up here. All right, over here on the right, we have something called M-MODE. M-MODE stands for motion mode. What it does is put this little dotted line down the screen. And what it's gonna do is measure motion wherever you put that line. And so down here, you see the IVC represented here. And as the patient takes a sniff, here is his collapsibility right here. For measurement purposes, you would take one more measurement at its biggest, down here. Oops, let's see, can I go back? Thanks. All right, take one more measurement over here. And depending on if your patient is ventilated or spontaneously breathing, you just plug in your numbers. Again, even qualitatively looking at that though, you can see that's a big plethoric IVC with minimal variation. So the patient's unlikely to be volume responsive. I think the comment we get a lot of times is, does anyone actually do these measurements? And I think when it's really obvious like this, there's no need to really do the measurement, but if it's kind of questionable, it's worth knowing your formulas. As far as our evidence for this goes, you can see here are four spontaneously breathing researchers and all with fairly small sample sizes, but they looked at collapse of the index anywhere 40 to 50% with pretty high specificities for volume responsiveness. And LANSPA is actually in the audience right there. So this is one of your authors. As far as our mechanically ventilated patients here, you can see both the three studies. Over here, this one looked at the change in IVC diameter and the other two looked at your distensibility index. Thresholds were anywhere from 12 to 18% with pretty high positive predictive and negative predictive and sensitivity and specificities. The last study down there with 540 patients, which is much larger than all the others we've looked at, had a threshold of only 8% and a much lower sensitivity and specificity. The caveat to that was they did not control for tidal volume. They left their patients on lung protective ventilation of six mils per kilo. And they also had patients with open abdomens in that one where about a quarter of the patients they couldn't even get an IVC view. So moving on to our next parameter, that same study actually looked at the superior vena cava collapsibility index as well. And what they found with that is that the SVC is actually much more accurate than the IVC. With a 31% collapsibility index in the SVC, they had a 90% specificity for volume response for this. Of course, the challenge to this is that to get a good SVC window, you really need TEE. A lot of times this can be done intra-op with cardiac anesthesia, or if you're lucky enough, I know some facilities will have the opportunity to do bedside TEEs. So what SVC variability looks like is this. Over here, we have our ultrasound probe. It's shooting across the SVC. Over here is your SVC. You can see it collapsing throughout inspiration. And you would do the exact same thing as you do with your IVC, but this time you're measuring an area. You would just pause it, and with your echo machine, you could trace it at its biggest and at its smallest, and then just plug in those numbers for your collapsibility index. Again, 31% is what you're looking for. Moving on, our third thing we can look at is the left ventricular end diastolic area. So instead of looking at the right side and the filling from there, we can actually just look directly at the LV itself and see how well it's filling. You can obtain this view either through the transgastric if you're doing TEE or the parasternal short axis. This is about as easy as it gets. It's pretty straightforward. You just look at the left ventricular end diastolic area. You measure it. If it's small, which would be considered less than five centimeters squared per meter squared, and it's hyperdynamic, you're very likely to be volume responsive. The caveat I would say here is pay attention and make sure you do have a small LV cavity. I think a lot of times when I see people bedside echoing, they'll look at the hyperdynamic portion and they say, oh, I see the kissing papillaries. They must need volume. But any pathology where you lose SVR will lead to probably hyperdynamic kissing papillaries. So please look for the small LV in combination. And this is what it looks like here. We have our, this is a TEE probe coming down, shooting up through the LV. Over here, we have our RV. This is, this circle here is your LV. These are your papillary muscles. Whenever you're looking for a general idea of your LV, kind of LV, the papillary muscles represent sort of about mid chamber. So that's where we want to look. And you would just find where you think end diastole is, and you would just trace through that, and you would cut through these papillary muscles as if they weren't there, and get that area and figure out how small or big your LV is. Finally, the last thing we're gonna talk about is the velocity time integral variation. If I have one to pick, this is my favorite parameter to use for volume responsiveness. The concept behind this is that as blood is leaving your LV, it must first go through the left ventricular outflow tract. This tract is cylindrical in shape. So if we know the diameter and the height, we can essentially guess that volume. But we're gonna make it even easier. The diameter is actually fixed. So the only variable that will change my stroke volume is now the height, okay? There's no medication you can give that can constrict or dilate your LVOT tract. But to make it even easier than that, because I'm not actually concerned with the exact volume, what I'm really concerned is the change in volume with interthoracic pressure, I can just use my peak flow as a surrogate for my stroke volume change. And so it looks something like this. This requires you to get an apical five or an apical three chamber view. Up here is an apical five. It's a little difficult to see, but here's your echo probe up here. This is your LV apex. This is the aortic valve. And what you're gonna do is activate something called the pulse wave Doppler, which is gonna tell the machine, I want you to measure flow in this area wherever I put this little equal sign. You're gonna take that and put it right in the LVOT tract and activate it. Once you activate it, you're gonna get these waveforms. Again, flow is going away from your echo probe. So you're concerned with these waveforms that are going down from away from baseline. We'll slow our sweep speed so that we can get multiple cardiac cycles. And we're gonna look at the change in our peak. You can think of this as equivalent to sort of your A-line stroke volume variation, but instead of measuring it peripherally, now we're gonna look directly in the LVOT tract. What's been validated here is the change in peak velocity, which is your max minus your min divided by the average of the two, and greater than 12% would represent volume responsiveness. So you take one measurement at your peak, one at your lowest, and then you plug it in for the math. But to make it even easier, if I were just gonna qualitatively look at this, if I take my probe and I just follow these peaks, you can see there's a decent amount of variation. So even without plugging in all the math and taking that time, this patient likely could benefit from fluid if they were hypotensive. As far as our studies go, again, both of them looked at our change in peak pressures, our max minus our min divided by our average. One used a threshold of 12%, one used 18. In your practice, you can pick whichever one you wanna follow. I do 12 personally. Both have pretty high specificities and sensitivities. So to recap real quick, we talked about four things we can look at for volume responsiveness, which are IBC variation, SVC variation, left ventricular end diastolic area, and BTI variation. Of course, there's a ton of other options. You could also look at your hepatic vein flows. You could look at your left ventricular filling pressures. You could add junk things such as lungs, looking for B lines, and seeing if you have a lot of pulmonary edema. What you choose to do in your practice kind of sort of depends on how strong you are with echo and what you're able to interpret. So I would encourage, if you do find echo to be helpful, there's plenty of courses, and the more you learn, the better decision you can make. And really what the big picture is, for bedside echo and trying to determine volume status is you have your operator, the skills that you bring to it, the different parameters we can make, but then those parameters have to be in conjunction with your patient. So what does your patient bring to the table? What's their past medical history? And so I think one of the big issues with research is when we look at just single parameters. If I just look at IVC and say, oh, this is gonna determine my volume status, well, that's gonna work most of the time, but when you think of a physiology like PE or obstructive shock that we talked about, if I just look at my IVC, that's gonna look big and dilated. I'm gonna say he doesn't need volume. But if I go over and look at my left ventricular and diastolic area, that will be small, underfilled and hyperdynamic, which will say he needs volume. So what's the answer? Kind of depends. You gotta put the whole picture together. And so I think the future, anyways, is gonna be something in cardiovascular clustering data. In intensive care medicine in 2019, they did a post hoc analysis of a bunch of different cardiac parameters in septic shock. And what they found is that if you have a combination of a high SVC change, a low cardiac output, and low filling pressures, you're 99.3% likely to be volume responsive. And so with that, I'm actually done. I'm gonna leave you with references. And I don't know, I can stop sweating, I think. Thank you.

echocardiography

fluid management

point-of-care ultrasound

fluid responsiveness

resuscitation phases