Thanks. So I'm going to be talking about bedside monitoring techniques that can be used to identify patients who are fluid intolerant and who may be ready for fluid removal. I have no financial disclosures. So we're going to be talking about what it means to be fluid intolerant, talk about some ways to identify this in your patients, and that's mainly going to surround ultrasound and VEXIS protocol. So firstly, what is fluid intolerance? So fluid intolerance is when you get volume overload that leads to organ congestion and organ dysfunction. While this typically occurs after the resuscitative phase, it's important to note that this can occur at any point during your patient's ICU stay. With the increasing evidence that volume overload leads to poor outcomes in patients with volume overload, it's critical to not only realize when fluids are no longer helping your patient, but also when they are harming them. Patients may also show signs of fluid intolerance while also simultaneously showing signs of fluid responsiveness. So it's important not only to continue giving fluids only after assessment of volume responsiveness, but to also look for intolerance. So firstly, the physical exam is something that everybody can perform as easy at the bedside with the patient. However, overall, it's largely unreliable. You can look for pulmonary edema, but studies have shown that over 40% of patients that have elevated JVD and wedge pressures will not have pulmonary edema on exam. Patients with atelectasis also may have RALs on exam. Peripheral edema is also not super helpful for your patients. A lot of our ICU patients are bedbound, and so most edema is going to accumulate in the sacral area, so it may not be often identified on exam. Edema also, studies have shown, may not be present in up to half of patients that have elevated JVD and wedge pressures, and it can also be present in patients that are hypovolemic or euvolemic. JVD is probably the best physical exam sign for volume overload, but it may not be easily identifiable in all of our patients with their anatomy between having obesity, short necks, lines in their neck, or trach ties, and so forth. So we also have CVP monitoring, which is a nice objective measure. We know CVP monitoring is not helpful for guiding fluid resuscitation, but it can be used to signify elevated filling pressures as a marker of volume intolerance and to help guide de-resuscitation. The main issue with this is needing the presence of an invasive central line, which may or may not always be present. So the majority of this talk, I'm going to be talking about ultrasound. There's a variety of ways that you can use ultrasound at the bedside to sort of identify fluid intolerance, depending on your level of comfort with each one. I will say that vascular ultrasound of the three is probably the best, because it can be used not only to signify the presence of venous congestion, but be able to also quantify the degree of congestion as well. So starting with lung ultrasound, which is the most straightforward, typically with lung ultrasound, you're depending on the reliance of interpretation of artifacts. So when you identify B lines, that's what looks like lights in the fog that we see here. The main caveat with looking at B lines is that it's not pathognomonic for pulmonary edema. You can see focal B lines with pneumonia, irregularly in ARDS or pulmonary fibrosis, and with atelectasis as well. So interpretation is important when you're looking at it. When you have symmetric B lines, with evenly spaced B lines, with a thin, plural line that's most consistent with pulmonary edema. And when you have B lines, studies have shown that these correlate with chest imaging as well, with three or more B lines per lung space, consistent with curly B lines on chest X-ray, and five or more with ground glass opacities on CT imaging. B lines have also been shown to identify sub-clinical pulmonary congestion, with findings appearing before those you can see on chest X-ray. They also correlate with filling pressures and the E to E prime ratio, which I'm going to talk about next. So E to E prime ratio of cardiac ultrasound is looking at the peak E wave transmitral velocity compared to the peak E prime tissue velocity that's measured at the septal or lateral annulus. This ratio is typically performed when evaluating diastolic dysfunction, but it can also be used in the ICU to evaluate filling pressures and as a marker of volume intolerance as well, where an E to E prime greater than 14 indicates higher filling pressures. If you're uncomfortable using this, or if your bedside ultrasound machines don't have tissue Doppler, the formal echo reports will often report this value as well, so you can look for it there. The E to E prime ratio is also not a perfect marker for organ congestion by itself. It relates to both volume status and cardiac filling pressures. So if somebody does not have diastolic dysfunction, filling pressures will be lower for that patient with the same overall circulating volume status as another patient that has elevated filling pressures, elevated or impaired relaxation. So vascular Doppler ultrasound can be used as another modality that will also use spectral Doppler, but it can demonstrate and quantify the presence of venous congestion directly from the venous vascular system. Specifically, I'm going to talk about IVC ultrasound as well as a spectral Doppler analysis of the hepatic portal and interlobar renal veins that's collectively known as something you may know as the vexus scoring system. So this is a schematic of your venous vascular system as changes occur with increasing venous congestion. Normally, you should have smooth, continuous flow with only mild undulating respiratory phasic variation. And as you get increasing venous hypertension, cardiac pulsations will be transmitted back to the venous site, and you'll get increased pulsatility to these vessels. Starting with the IVC, there's a difference in interpretation of this, whether you're talking about a patient breathing negative pressure spontaneous breaths versus somebody receiving positive pressure vents with mechanical ventilation. In somebody who is spontaneously breathing, the IVC represents a surrogate of your right atrial pressure or your CVP. When they are on the vent, you're looking at inspiratory distensibility, which can be used as a dynamic marker of fluid responsiveness that is irrespective of your CVP. So in a spontaneously breathing patient, IVC ultrasound is not helpful for fluid resuscitation, but a clethoric IVC may be helpful in identifying patients with volume intolerance, where a clethoric IVC can help you guide de-resuscitation. The remaining vascular views involve use of spectral Doppler. Once you apply your pulse wave gate to the hepatic vein, you should get a waveform as shown on the left, where you have an A wave that's above the baseline, followed by an S and a D wave below the baseline. Normally, your S wave velocity should be greater than your D wave. With increasing congestion, you get reversal of flow. So now your S wave will be less than your D wave velocity. And at the severe end of the spectrum, that flow will actually become biphasic and sinusoidal. The interlobar and renal veins are probably the most difficult of these to obtain because the flows are the lowest, but they can also demonstrate evolving congestive patterns as well. The interlobar, renal vein, and artery are close together. So when you apply your pulse wave Doppler gate, you'll often get both the arterial flow that is above the baseline, as well as venous flow that is below the baseline. Normally, your venous flow should be continuous and occurring throughout the cardiac cycle. And as you get increasing venous congestion, it'll take on more of a pulsatility pattern. And then on the severe end of the spectrum, you may get flow only in diastole. The portal vein is not difficult to obtain, especially as you become more comfortable obtaining the views. Similar to the other patterns, it should be a smooth, continuous flow. You can actually measure the pulsatility index, which is the degree of pulsatility, with the Vmax minus Vmin over the Vmax. So the normal PI should be less than 0.3. When you get a PI between 0.3 to 0.5, that indicates mild to moderate venous congestion. And then a PI greater than 0.5 indicates more severe congestion. On the very severe end of the spectrum, you may get a sinusoidal biphasic pattern, again, indicating very high Philly pressures, or very high pressures. So the VEXUS scoring system was created that utilizes these waveforms as a conglomerate. So it makes an overall scoring system of venous congestion. It's hard to have this memorized, so it's important for bedside use just to remember that the more evidence of pulsatility you see on more waveforms indicates increasing venous congestion. And so when you start to see congestion in multiple waveforms on the severe end of the spectrum, that's a sign that you should not only stop your IV fluids, but maybe as a sign to start de-resuscitation. This is, again, just for review, another basic schematic of how these waves will change with increasing right atrial pressure. So in review, we're increasingly aware of this association between fluid overload and worsening ICU outcomes. It's important for us to recognize and correct venous hypertension, to not only stop further IV fluids, but also to manage de-resuscitation. Bedside ultrasound is probably going to be your easiest and best tool to help identify and grade degrees of venous congestion, and it's just important to note that one thing by itself is not the best, but to use these as a conglomerate, as an overall view of your marker of volume status. And that's the end of mine. Okay. Thank you.

bedside monitoring techniques

fluid intolerant patients

fluid removal

ultrasound

venous congestion