Okay. Thank you very much. It's nice to see everyone here on a Monday. So we're going to have a nice discussion today, I hope, about monitoring and shock. And I'm going to take the pro side that multimodal monitoring is important. I have nothing to disclose other than that I'm a cardiologist, and so I may be a little biased towards certain monitoring devices, such as pulmonary artery catheters and echocardiography. And I look at these as the basics for monitoring and shock, and something that I'm well used to using and enjoy using. And as far as the PA catheter, I really look at it as the tried-and-true modality for monitoring and cardiogenic shock, because I believe it provides continuous feedback that helps us guide our vasoactive medications, identify the need for mechanical circulatory support, and then wean mechanical circulatory support. Now the story of PA catheters I think is well known to most of us in critical care, and that's a story of, well, really a lack of use over the last maybe 20 years due to some pretty large studies that were done. And this meta-analysis from JAMA in 2005 that was published at the same time as the ESCAPE trial really demonstrated that there is no difference in mortality or length of stay in patients in all comers with PA catheters. And so because of that, in general ICUs, PA catheters have fallen out of favor. Now that being said, I think the pendulum has swung a bit far here. And in my practice, I work with a lot of trainees, many of whom just are not familiar with what a PA catheter is and what it can do for us. And if we take a look at the ESCAPE trial, which I think within cardiology is something that has driven the use of PA catheters, we need to understand that that trial excluded the most critically ill patients. So this was not a trial that looked at the use of PA catheters in cardiogenic shock. And if we look at trends in utilization of PA catheters over the course of the last 18 to 20 years, over that period of time there's been a decreased use of PA catheters. However, what's really interesting and what this study showed was that when PA catheters have been used, they've been associated with a decrease in mortality. And if we look at PA catheters being used in patients with cardiogenic shock, so cardiogenic shock without a PA catheter here is the broken line, and cardiogenic shock with a PA catheter here is the solid line, we see that there is actually this crossover event around the time that the Intermax registry was started where there was a decrease in mortality in those patients with a PA catheter. And then if we look at patients with heart failure without cardiogenic shock, we see that there has been an absolute decrease of 57.7 percent in mortality in those patients that had the PA catheter. Now again, this is a registry database, this is not perfect data, but it does start to tell a story. And more recent data, and this comes from the cardiogenic shock working group, looking at about 1,500 patients with cardiogenic shock, 84 percent of them had mechanical circulatory support, and actually the vast majority of those were aortic balloon pumps, and the largest percentage of patients were those in stage D, sky shock stage. And what they found was those patients that had a complete hemodynamic set of parameters done by a PA catheter had the lowest mortality, whether or not you broke it up overall or by severity of shock. This data was actually also seen in this registry of patients, a registry of patients for Empella, one of the percutaneous VADs that's available, and it's found that in those patients in that registry who had a PA catheter, a PA catheter was associated with increased survival. It was actually only one of two things associated with an increased survival, which was the use of an Empella prior to PCI. And so then we're sort of painting a picture here for the importance of a PA catheter in patients with cardiogenic shock. And if we look at these newer care plans, models, protocols for the treatment of patients with cardiogenic shock, a lot of them are incorporating PA catheters and invasive hemodynamics. And this was a nice look at the use of a team-based approach for cardiogenic shock patients at Inova. And they had a nice protocol, which unfortunately you may not be able to see terribly well up on the screen, but for inclusion criteria and then monitoring. And monitoring included serial assessments with PA catheters, specifically the cardiac power output and the PAPI, as well as daily bedside echocardiograms. And involving this multidisciplinary group with these parameters for the protocol, they saw this almost 40% absolute increase in survival over the course of that implementation. And this, again, is mirrored in the shock team approach at the U of U or the University of Utah, where having a multidisciplinary group of physicians caring for patients with cardiogenic shock, and in that protocol, including a right heart catheter or a CCO, continuous output SWAN, they found that there was a decrease in in-hospital mortality, as well as a decrease in 30-day all-cause mortality. So more data here for the importance of invasive hemodynamics for monitoring these patients. And the Inova group, they came up with a risk scoring system for patients to identify those at low, moderate, and high risk for 30-day mortality. And the two key components that they used from that PA catheter to develop that risk score were cardiac power output, which was found to be the most important prognostic marker in the shock registry of cardiac power output equal or less than 0.5. And then they also used the PAPI, or pulmonary artery pulsatility index, as one of their risk markers. And why the PAPI? Well, the PAPI is an important metric. The PAPI tells us a lot about RV function and that pulsatility. And we can use that as we monitor patients, particularly those that we're using, for example, univentricular percutaneous mechanical circulatory support and understanding what's going on with the right side of the heart and whether or not that patient would need right-sided support. It also tells us something about mortality in these patients that have either had a large myocardial infarction or are presenting with acute decompensated heart failure. And so we can put this all together. Again, a nice illustration here of a protocol from the Inova group where we can look at patients in cardiogenic shock, and then we can phenotype them based on their invasive hemodynamics, for example, biventricular, left-dominant, or right-dominant, using these markers of cardiac power output and the PAPI, and then using our filling pressures to help guide us and ultimately lead us down a path for how we want to support these patients and whether or not we need to upgrade them to mechanical circulatory support, and if we do, whether or not they need right, left, or biventricular support. And this, I thought, was a really nice illustration from the guideline statement that was in circulation for how we can think about using continuous filling pressure assessment, continuous hemodynamic monitoring with a PA catheter to understand how we're caring for patients with mechanical circulatory support. And, for example, if we look at this patient, patient number three here, that's presenting with elevated pulmonary capillary wedge pressure consistent with cardiogenic shock, that we put a left-sided device in the patient, and we see with that, although we drop the wedge pressure, the central venous pressure increases. This person's right ventricle is not tolerating univentricular support, and this person needs a right-sided support. And with that, we can drop that filling pressure on the right side with diuresis, get the patient where we need them to be with normalized hemodynamics. The same thing here in a patient that we put on ECMO without, for example, a venting strategy. With a venting strategy, we see that with percutaneous ECMO, for example, and that high afterload, the wedge goes up, and this person needs an impella to help offload the ventricle. So we talked a bit about the classics for hemodynamic monitoring in shock, and the first one was pulmonary artery catheter, and now I'm going to talk about echocardiography, which is important to me as that's half of what I do in my practice. And the way I think about echo is it allows us to visualize a complete picture of hemodynamics and the pathology. It allows us to look behind the curtain and see really what's driving the shock picture for the patient. And hopefully people get the reference to the Wizard of Oz. I don't know. Maybe I'm so close to 50 now that that was just a sign of it right there. But echo, I couldn't think of anything even more contemporary than that. That's the most amazing thing. So when I talk about echo, I talk about echo revealing the complete picture. You get anatomy, you get hemodynamics, you get pathophysiology, and we can think about this patient with ovarian cancer post-op day two, intubated with increasing pressure requirements, has some GPCs in the blood. I'm not sure what that means. What is driving the hemodynamic decompensation here? How should we manage the worsening shock? She's hypotensive and hypoxic with the lactate. And so what we can do is do an echocardiogram just at the bedside. And we can see when we do that that we find interesting things. We find what's driving the picture of shock here. And this patient has acute RV failure and something bouncing around here in the right atrium. And so has thrombus that is actually in transit and has very high PA pressure. So we get the hemodynamics and we get the understanding of what's driving that worsening picture. And we can get a lot from echocardiography. As I think all of us in critical care are embracing bedside ultrasound and critical care ultrasound, which I think is really important, critically important, as you're able to get your own images, as you're able to look at the 2D images and interpret them, when you add Doppler hemodynamics to that, you really can do a lot. And this is a paper from ASE just talking about some of the monitoring you can do with echocardiography at the bedside, talking specifically about the hemodynamics that you can derive from echocardiography. And one of the ones that I teach a lot and I help with the pre-conference course here for ultrasound is I talk a lot about cardiac output and how you can get that with echo because I think it's really important and it helps us when we're monitoring patients understand whether or not our therapy is driving the patient in the right direction. Now, I want to bring up Jake Jensser. He's done some wonderful studies looking at echocardiography in shock and has come up with all these different metrics, again, that we have used classically invasively, but being able to derive those non-invasively with echocardiography, looking at cardiac power output and seeing that just around 0.6 as derived by echo, we see that inflection point with increased mortality just like the more classic studies with invasive hemodynamics. Other ones looking at LVOT-VTI, so that's our marker of forward flow, that's our stroke volume or our stroke distance with echocardiography, how important that is for prognostication in patients and mortality. And then even looking at more advanced things like right ventricular or pulmonary artery coupling with echocardiography and how metrics of that can be used to risk stratify patients. Now, echo-derived cardiac output correlates incredibly well with PA catheter-derived cardiac output. We see the R values there, not just for an individual number, but also for changes, right, changes in cardiac output. And for those of us that aren't as familiar with how to look at stroke volume or stroke distance with echo, essentially what we're doing is we're doing pulse-wave Doppler, the LVOT, and we're looking for and tracing the velocity-time integral there. That gives us a distance, that's the stroke distance, and we're able to multiply that by our cross-sectional surface area of the LVOT and calculate a stroke volume, which again correlates incredibly well with our invasive hemodynamics. And what's really nice here is that we can use that number, that LVOT VTI, one, to determine what the cardiac output is. So if normal is 18 to 23 and someone has a VTI of 14, they're going to have a low stroke volume. And then we can see what happens when we try to change that, when we add dobutamine, whether or not that LVOT VTI increases, in this patient it did, by 28%. And if the heart rate stays the same, then our cardiac output is going up by that amount. And the fidelity is incredibly good for this. So this was a patient that I was in the OR with, and I just had them, we were trying to determine whether or not the patient truly needed a balloon pump. And you can see with the balloon pump off, the VTI is 6.3. Again, normal is 18 to 23. So there is just a couple of drops of blood coming out of the LV, with each cardiac cycle. And then we can see when the balloon pump is turned on, that almost doubles. So it's a way for us to really think about what we're doing for patients and monitoring them. And then using that LVOT VTI has been well demonstrated in the literature to guide fluid responsiveness for the same reason. If you're giving someone increased preload, and that stroke volume goes up, then they like that preload, right? And that's a way for us to easily assess that at the bedside using ultrasound or echocardiography. And then for weaning of mechanical circulatory support, again, we can use that VTI, a very simple metric. And this is a patient, again, I was in the OR, and we were determining whether or not we could wean ECMO in this patient. And we can see that as the ECMO flow is really gone, is really dropped to 0.75, 0.5, and then off, the patient maintains that forward flow the whole time on fixed dose, low dose inotrope. And so we are happy that this patient is going to be able to tolerate being decannulated. So these are some of the metrics that have been used for successful weaning using echocardiography based on different papers. But again, that VTI being a really good one. And then when things aren't going well, we can apply ECHO. So this is a 40-year-old female in stage cardiomyopathy who presented with VT-STORM and was placed on VA ECMO. They were trying to avoid inotropic therapy and arriving arrhythmias. So the patient was on quite high dose vasopressors. There was a PA catheter and a balloon pump in, but there was difficulty getting a wedge pressure. And there was increased hypoxia. There was increased pulmonary vascular congestion on the X-ray. So what do you do? You get an ECHO. And what does the ECHO show us? Well, the ECHO shows us that the LV is not being unloaded well. And we see that not just because of the size of the LV, but the significant amount of mitral regurgitation that's present. And so we took the patient to the cath lab, and now we just switched our ECHO modalities, right? We went from a surface study to a transesophageal study. And with the transesophageal study, I'm able to see everything quite well and help guide the intraatrial cannulation here to put a vent here in the left atrium. And then when that vent's placed, what do we see? Well, we see there's really almost no ejection still with the balloon pump going and with the vent in. And we see actually stasis here in the ascending aorta. And why is that? Well, because the patient is really hypertensive. And so, again, we made that diagnosis with the ECHO, helping the team. We see that with the balloon pump going, there's significant AI in the setting of that high afterload. And then we just start clavitapine quickly in the cath lab. We drop the systolic blood pressure to 109 over 78, and we see the resolution of that aortic regurgitation with the balloon pump and the resolution of the spontaneous contrast, the stasis in the ascending aorta. So ECHO is really like what you need to use when there is that check engine light that comes on in the patient. You're driving your car and the check engine light comes on. Well, the car's still running, but what does this mean? I don't know what this means. And so ECHO kind of helps you make that diagnosis. And this was a 53-year-old on VV ECMO with COVID, ARDS, worsening vasopressure requirements, increasing lactate. And they were worried that the patient was going to have a cardiac arrest. So what do we do? We do a quick TE at the bedside, and what do we see? We see the patient has significant RV dysfunction, significant pulmonary hypertension. In fact, they're not filling the left ventricle. And in that setting, we can still even do our VTI, which is 9. There's really low cardiac output. In fact, the cardiac index calculates to 1.5. This is a patient that needs escalating hemodynamic support. And we can make that diagnosis right at the bedside. So I'll finish there, and I guess the points that I'm making are that, well, the PA catheter is not dead. Its use is associated with some mortality benefit, I believe, in cardiogenic shock. And it can help us guide our therapy, specifically thinking about patients with mechanical circulatory support. And then ECHO, what can I say about ECHO or critical care ultrasound? I think it's incredibly important. And I'll go back to my terrible analogy to the Wizard of Oz behind the curtain. But it really does, it allows you to pull the curtain back and see what's going on, see really what's driving the decompensation in front of you. And also, not only what's driving the decompensation, but allows you to visualize whether or not what you're doing is improving things, right? Whether or not the patient is going to benefit from fluids, whether or not the patient is benefiting from the dobutamine, whether or not the patient is benefiting from the balloon pump. So I will end there. Thank you very much.

cardiologist

multimodal monitoring

shock

pulmonary artery catheters

echocardiography

hemodynamic monitoring