Penn Medicine Critical Care Cardiologist Jessica Fleitman, MD, provides an overview of what’s new in the modern cardiac intensive care unit. She also discusses how to triage and prognosticate cardiac patients, updates in the stabilization of cardiogenic shock patients, and up-to-date literature on hemodynamic and vital sign monitoring.
The Living Valve: Repair and Replacement Options for Long Term Durability, Survival, and Quality of Li The Penn Aorta Center: A New Comprehensive Model for Patients with Aortic Disease Twitter @PennMDForum Dr. Fleitman’s physician profile Yeah, all right, we'll give. We'll give everyone a minute here. Thio log in. So, unfortunately, we're having some issues with the CMI office for today's talk. They were closed last week for the entire week, and we have not received the code yet for today's talk. Hopefully, we'll have it by the end of the talk, and in that case, I'll read it at the end. We also put it in the chat section. Linda is actually going toe. Also, keep track of all the attendees. So worst case scenario, Hopefully we'll be able to retro grant everybody CMI credit if you log in to zoom either by your phone or not by your full name. If you please just email either Linda or myself. And that way we can make sure that you get your CMI credit. Alright again for those logging in, unfortunately, do not have the CMI code yet. We're hoping that we'll get it during the talk and if not, worst case, we'll try to keep track of everyone that's logged on and make sure you receive credit after the fact. All right, we'll give everyone a couple seconds here and then we'll get started Okay. All right. Good morning, everybody. Welcome, Thio pen. Cardiology Grand rounds today. Very excited to announce one of our newest faculty members who joined us last year. Jessica Flight Mint. Um, Jessica has a very, very impressive CV. She did her undergraduate from Princeton University actually taught science after that before going to Colombia for her medical degree. She stayed there as an intern and then came to pen for her cardiology fellowship and really had the insight in the foresight to realize that critical care cardiology is something that's rapidly growing and evolving. Yeah, I think years ago the CCU or H B I C. U was really, ah unit designed for post m my patients. And over the last several years, we've really seen that the unit has evolved tremendously while they're still posted my patients. It now involves very complex, um, card, heart failure, patients, cardiac patients, and now a lot of patients with multi organ involvement. So we're very excited to have Jessica join us here last year and really lead the efforts in the CCU toe help help with more modern day management as well as sort of a more specialized approach. So Jessica actually did an additional training after her cardiology fellowship in critical care medicine. So for those of you, we'll probably see her name and speak to her on a lot of the patients that are being cared for at the H B I. C. You hear a pen Presbyterian? So with that introduction, I'm gonna let Jessica control the screen and get started. And once again, the CMI code. I don't have it, unfortunately available yet. I'm hoping that we'll have it by the end of the talk and worst case, um, afterwards, we will retro grant everybody credit that's logged in. So if you're please, either log in by your full name so we can keep track of it Or alternatively, send me or Linda Lafferty and email. And that way we could make sure that you get credit. All right? Jessica, do you wanna I'm taking the screen, if that's okay. Yup. To slide show. Hi. So I'm Jessica Flateman. I'm going to talk today about some of the updates and cardiac critical care And what's new in the modern seat cardiac intensive care unit. I have no disclosures. So Theobald actives I want to talk about is number one. How do we triage and prognosticate cardiac patients? I e who belongs and the modern CSC you? And what skills does the modern cardiologists need to manage them? Um, second, I want to talk about some of the updates and how we stabilize our cardiogenic shock patients, and we'll review some of the more recent studies in this area. And then finally, I wanna touch on the up to date literature on how we do chemo, dynamic monitoring and vital signs monitoring Onda. We'll discuss some of the current debate on the best way to monitor our patients. So triaging patients, Um, what does the modern see? I see you look like so as, uh, Samir briefly touched upon the modern cardiac intensive care unit developed from the coronary care units where patients could be monitored after they had an acute coronary syndrome. Um, this is prime developed in the age prior to revascularization when patients would come in with ventricular tachycardia in time to defibrillation would improve outcomes. However, the modern cardiac intensive care unit is not primarily a C S s o. This is basically a breakdown of the patients who admitted from 2013 to 2014 at the University of Virginia Health System, which shows that really only 25% of their patients were coming in with a CS, and of that, really the majority of them were non stem ease, not stem ease. There were a whole host of other diseases that was coming into that unit at that time. Brigham also looked at this, And, uh, this slide really shows their breakdown. And what you should note is first of all, about one in five patients in the cardiac intensive care unit these days, air coming in with non cardiac primary diagnoses, whether that's respiratory failure, generalized medical illness or they're just make you overflow. The other thing is, our patients are getting sicker. Noticed that a quarter of the patients really air coming into the unit in shock. Moreover, it's not just that we're having patients with diagnoses other than other than a C s that are coming into our unit, but secondary diagnoses air changing as well. So this study it, Duke showed that really, there's been a decrease in the patients in their units that are stem ease and increase in end stem ease. But other critical illnesses are significantly increasing in our cardiac issues. There's more sepsis, there's more liver failure. There's more renal failure, and the procedures that we're doing in our cardiac I. C. U s have been changing as well. So while there hadn't been a change in the 10 years prior to this and the number of interventions they were doing, P A catheters have decreased in frequency, and things like bronchoscopy and mechanical ventilation are becoming more prevalent in our I c. U um. Moreover, in a recent study at the Brigham, there's significantly more mechanical ventilation. About 45% of their patients are also getting supported with a new trump surveys oppressors. 8% of their patients were on renal replacement therapy, and over half had vascular access and you know they had about a third of patients were being managed by mechanical circulatory support. So in this setting, there really has been, ah question of should we have patients with intensive have physicians with intensive care skills being involved in the treatment of our patients? And how do we develop those skills? And so this has been looked at in a couple of studies, the first really big one was actually in South Korea, where one of the Quaternary care centers in the country decided to change from having a cardiac intensive care unit that was primarily staffed by general cardiologists to switch over to having everyone have dual training in both cardiology and critical care. And they did the outcomes of a year prior in the Year Post and noted that there was a significant drop in mortality from about 7.5% to 3.7% more close to home. Um Christiana, down in Delaware, actually looked at changing their staffing model from just a cardiologists rounding in their cardiac intensive care unit to having a cardiologists and a car handed intensive ist co rounding. And with that, they found a significant drop in mortality from about 6% to about 3.5%. Finally, University of Maryland came up with another model where they looked at cardiologists rounding on the patients and then had intensive ist consul to on all of their patients. Um, they did find that there was a significant decrease in length of stay both in the cardiac intensive care unit in the hospital. They did not find a significant decrease in mortality. But there was a decrease in mortality was non significant. Notably in that study, the patients in the year prior to their new staffing model in the year Post actually had significant changes in the signal the severity of illness, with the patients in the second year having higher Apache scores. And so when they controlled for Apache score, there was a significant drop in mortality. Given this data, really, the question has been, Should we have everyone in a cardiac intensive care unit be dual trained in cardiology and critical care? Um, however, in 2014, there was a survey of all the people in North America who had dual boarding. Um, there was about 350 people at that time in all of North America who had dual boarding, and the majority of those were people over 65 who had been cardiologists at the time that critical care boarding came around and were able to be grandfathered in. And there were about Onley 120 people in North America, United States and Canada at that time who were dual boarded, having dual trained It's more now, but that's probably not enough to staff every unit or even every coronary care unit with someone who has dual training. So at that point, there's been some questions should be used other models, Or do our patients really need to go to the cardiac intensive care unit? Um, and this was looked at by Jason Katz's group down it, Uh, U N C um, So they looked back at every patient who had been admitted from the E d to the i. C. U s with cardiogenic shock and the way that they did this as they looked at all the patients have been admitted from the to the I. C. When they're discharged, diagnosis is cardiogenic shock. And then they retroactively looked. Was that cardiogenic shock present on admission, they found about 144 patients. Who it waas 97 of those went to the cardiac intensive care unit and 47 of them went to the Mick. You are sick. You the patients who went to the mix, You are sick. You were more likely to have mixed shock, just not pure cardiogenic shock. Um, but they did find that there was significantly different utilization of resource is in the different units. So the patients who went to the cardiac intensive care unit were much more likely to have a pulmonary artery catheter 41% versus 6.4% the difference in the use of positive pressure, ventilation or vase oppressors. And I know Trump's was not different. Then they interestingly, looked at just the patients who had pure cardiogenic shock. That was 83% of patients in the cardiac intensive care unit in about 44% in the non cardiac intensive care units. And when they looked solely at those patients, there was still a significant difference in the support that they were given. So it was about a 10 time more frequent use of pulmonary artery catheterizations, 40% versus about 4% P. C. I was done in about 50% of patients who were admitted to the cardiac intensive care unit with cardiogenic shock and only about 10% of patients in the non cardiac intensive care unit. The time to get that PC I was one hour versus 125 hours. Patients who went to the cardiac intensive care unit were about about 40% of them got mechanical circulatory support and only about 10% who went to the sick. You're the Mikio and in hospital mortality was not significantly different. But you can see that there was a lower in hospital mortality in the cardiac intensive care unit patients than the non IT cardiac intensive care unit patients. And so this study to me suggests that comfort with cardiogenic shock that comes with working in a cardiac intensive care unit regularly leads to different treatment options in different platforms being used in this main, um, influence outcomes. Eso I think that this data demonstrates that cardiogenic shock patients really deserve to be treated in a modern, cardiac intensive care unit where we have some support for people who are well trained in intensive care. So now that we know that these patients probably should be going to a cardiac intensive care unit, how have we been prognosticating them? And how are we thinking about cardiogenic shock patients? So acute myocardial infarction with LV dysfunction remains the most frequent cause of cardiogenic shock. A lot of our evolution in the treatment of cardiogenic shock dates back to the shock trial in the early two thousands, which demonstrated that early revascularization in cardiogenic shock improves mortality. Um, prior to PC I in hospital, mortality of cardiogenic shock was about 81%. Further efforts in the modern era to reduce cardiogenic shock mortality have been directed towards improvement in mechanical circulatory support and mechanical circulatory support devices. And so, in terms of trying to figure out who needs to be on this and how to study, um, improvements in this the sky Consensus group last year came up with a better classification of cardiogenic shock that we all kind of need to be aware of eso. I've included it up here. Um, they classified patients in risk and risk Category A is being people who are at risk of cardiogenic shock. They don't have the hypertension and they don't have the signs and symptoms, but they have one of the risk factors. I e having an acute myocardial infarction having acute or chronic heart failure. People with the beginning of cardiogenic shock or people have relative hypertension, but they don't have evidence of HIPAA perfusion. Yet classic cardiogenic shock are patients who have hypo profusion with hypertension hypotension being a systolic of less than 90 for more than 30 minutes. Um, in signs of hypo profusion being altered mental status and Yuria elevated lactate. Um, and this is not responsive to just volume resuscitation. So they either require an in a trope, oppressor or mechanical circulatory support. And that's the majority of the patients that we see. However, we do see these people who are in Category D, which they called deteriorating or doom thes air patients who are getting worse on one support so they may require an in a trope plus mechanical circulatory support. Or they may require to in a tropes, or they may require, you know, increasing levels. And then e is our sickest patients. These are the patients who have circulatory collapse. They're requiring being crashed onto ECMO. There are multiple support systems without stability. So this triage system, in terms of the prognostication was actually, uh, looked at and verified. And so this is really a demonstration of applying this sky classification toe a patient population in the modern. See, I see you and we see that obviously are patients who are coming in an extremist have really a significant mortality in the hospital. More than 80% in our A. C s group and over 60% in our heart failure group. Stage D patients still have a significant mortality as well. And then once you get to people who are stable on one support system, whether it's, um, in a tropes or mechanical circulatory support, they have, like they have a decreased mortality compared to the others. There are other predictors that have been shown to be useful in cardiogenic shock. Most of this comes from the shock trial. So the best predictor human dynamic, predictor of mortality and cardiogenic shock is the cardiac power output. Um, this is calculated by taking the map times the cardiac output and dividing by 4 51 to get it in watts. Um, the discriminating value for that in the shock trial was 0.53 watts that predicted, uh ah, 58% more in Haas mortality. Um, whereas a probability of survival above that was 71%. This makes intuitive sense to us. We all think about our patients who come in with low cardiac indexes, and we usually want to treat them by trying to decrease thereafter, load or get them on a nine a trope, which is an I know dilator. But obviously those patients who already have a low math we don't have that opportunity to do these air patients with really weak hearts. Other predictors that have been useful, we all know is our cardiac output index. And then the Pappy was one of the other predictors that was seen in the shock trial and really in trials. I'm looking at RV function. Um, this was the best predictor of RV failure after l've odd on DSO. This is calculated as your pulmonary artery pulse pressure. So the p a systolic minus the p a diastolic divided by the right atrial pressure, happy less in the shock trial, less than 1.85 was predictive. And really, we think about Pappy's of less than two is showing that the patient has a poorly functioning RV. The other thing that has been shown in several trials to be predictive of mortality is lack. Tates, um, and clearance of lactate after coronary revascularization predicts good outcomes, whereas elevated lactate in heart failure in general and in D compensations predicts mortality. Finally, in a survey of interventional heart failure in general cardiologists, um, there's several scoring systems that people use to try to predict mortality. Thes air the scoring systems that are used most frequently in order of the in order of frequency. So Inter Max the Apache, which looks at the overall sickness, is also used in the medical I See you, the Grace score for a CS, and then SOFA scores for general. I see you patients, and so these are all great things to look at, but they require your data coming into the I c e o on DSO. The Mayo Group wanted to know, Can we prognosticate patients in the E. D. Or on arrival to know, Is this patient going to do well or do we really need to be upping our support? And this patient really needs to be in the i c E o. The high risk of death. The sofa an Apache scores need more than 24 hours of data, so they created this risk score based on all undifferentiated patients coming into their cardiac intensive care unit. Um, and there's several factors that they found to be associated with mortality at different ratios on DSO they created into your values to do this score. Cardiac arrest is worth two points. Cardiogenic shock or shock in general is worth two points. Respiratory failures worth one point the brain and skin score with I think I'm not a lot of people use but really is a risk score for your risk of skin breakdown, they found. To be independently associate ID, it's worth two points if your score is less than 13 and one point of your scores between 13 and 15. Elevated anti and Gap is associated with one point and increase in our d. W. Um, it's associated with bad outcomes and then elevated B u N. And they really found that patients. And then they check this in a separate cohort. And they really found that patients who had a score of over seven, you know, had mortalities of over 50%. Um oh, and just to finally comment this, um, risk or did have an area under the curve of 00.86 which was actually higher than both the Apache score and the sofa score at one day. So now that we kind of know how to get our patients to the cardiac intensive care unit and think about how we're managed. We need to start thinking about how we're managing our cardiogenic shock patients in the modern era. Yeah, So, as I mentioned earlier, one of the major moves you know, since the advent of revascularization is trying to get patients onto mechanical circulatory support who are not adequately supported on I know tropes. Um, s o all the earlier studies of the intra aortic balloon pump did not really show significant improvements in mortality. And so this idea of like creating the impel A and having kind of higher levels of impel a support with the CPI, it was thought maybe this would improve our outcomes. So the impress trial was performed in 2016. They looked at 48 patients, um, randomize them to get a balloon pump person and policy p. Um, the inclusion criteria, however, were patients who were post, um, acute myocardial infarction in cardiogenic shock and required mechanical ventilation. They shot showed no difference in mortality. And a lot of people have referred to this. Um, sorry. Ah, lot of people have referred to this as evidence that, uh, there's no benefit to the impel SCP or to mechanical circulatory support in supporting our patients. However, the inclusion criteria of mechanical ventilation ended up leading to a lot of the patients who were included in this tri ALS being post cardiac arrest and the major cause of death in these patients, um was actually, uh, anoxic brain injury. And so, if you've already had the insult in your dying from anoxic brain injury, it doesn't seem like you would see a benefit in supporting their cardiogenic shock after the fact. And this may have biased this small trial to being a negative trial. It's unclear, so this leads to the cardiogenic shock initiative. So this started as the Detroit Cardiogenic Shock Initiative, where they really wanted to create a best practices to see if that could improve outcomes. And so three hospitals in Detroit developed this practice serious, and then they kind of spread it out to 35. Hospitals between 2016 and 2019 looked at these patients. They instituted, um, protocols in patients who came in and cardiogenic shock with acute myocardial infarction. Three idea being If a patient comes in with acute myocardial infarction, they go to the cath lab and they get started on support prior to revascularization prior toe up tight trading. I know tropes. So the protocol waas you come in and cardiogenic shock with an acute myocardial infarction. You go to the cath lab, you get a p a catheter place, you get in Pella place and then you get revascularization. This was a single arm perspective. Try a while on dso these air. Really? The outcomes that are important from this. So just the time for support door to support time was 85 minutes. Door to balloon time was still under 90 minutes. Despite requiring going on to support first on Ben, there was really good adherence to the trial. So 74% of patients in this trial had mechanical circulatory support place prior to PC I and they had a 72% survival to discharge. And this is really what people point thio in terms of thinking about the benefit of having mechanical circulatory support platform and the benefit of having invasive chemo dynamics. So if you look over here on the right, you can really see that Historically, prior to PC I, the mortality for cardiogenic shock was over 80%. But in the modern era with PC, I over here. You really still with PC I Over here, You really still see that There's around a 50% mortality and these patients who are coming in and this trial really was able to get it down to 28%. And these patients were justice stick A. The patients in the other trials they had elevated lactate. So at the same level, they had low blood pressures at the same level, you know, they were on fewer in a tropes, but they were really put onto mechanical circulatory support early on. So the next thing I want to talk about a little bit is some of the ideas in the newer data behind positive pressure ventilation in cardiogenic shock patients. So there is this idea if you read about the basic physiologic parameters, that positive pressure, ventilation and indeed positive and pressure ventilation can be favorable in left ventricular cardiogenic shock. And that's really because of the effect of the positive pressure ventilation on the L V. So the first effect is when you have positive pressure ventilation, as a lot of us already know, you're having a decreased Venus return to the RV in a decreased pre load and that actually can result in a decrease pre load to the Elvia as well. And it's been shown that, um, you actually, with positive pressure, ventilation, decrease the pulmonary capillary wedge pressure. The trans mural pressure that we think about really is the LV pressure minus the pressure of the pleura that you see over here exerting and so in Patients who are on positive pressure ventilation with a pleural pressure of 10, you are actually decreasing the trans mural pressure on the L V. And you could decrease the after load and that can in term decrease the myocardial oxygen demand, um, and improve outcomes in these patients. Moreover, when you have positive pressure ventilation, do you case the work of breathing? This decreases the total body need for oxygen, and so you get an increase in cardiac index and increase in oxygenation with positive pressure. Ventilation. Um, there are many studies that have kind of looked at this over the years, um, a couple of studies in acute myocardial infarction where they looked and showed that by adding keep you actually have an increase in cardiac output in a decrease in filling pressures, um, in patients with them are going for mitral valve repair. Hire people is associated with a decrease in the mitral valve Manulis diameter and, um, noninvasive positive pressure ventilation would still gives you keep, um, was associated with a decrease in mitral regurgitation and increase in the ejection fraction. Um, and in this study, where they looked at patients post cabbage if you put someone on positive pressure, ventilation with and without peep patients on Peep had higher cardiac output, pulmonary capillary, wedge pressure and maps. This data really all lead thio. This small study, um, which is intriguing where they use the triumph data, set the triumph data. The Triumph Study was a study that randomized patients and cardiogenic shock to either get nitric oxide, Cynthia's inhibitors or placebo. And they use this because the timing of cardiogenic shock was time stamped. And so they looked at the time from onset of cardiogenic shock diagnosis to the initiation of mechanical ventilation and whether this was associated with mortality. And what they found was there was a significant improvement in mortality, um, with mechanical ventilation and for every one hour delay, mechanical ventilation, there was an increase in mortality. Now this is an extremely small odds ratio, but it's intriguing and provocative and is something that we should be thinking about. So if you're in doubt about whether or not use positive pressure ventilation on a patient for work of breathing for hypoxia mia, it might be beneficial to think about something that's positive pressure as opposed to, like a high flow nasal cannula. Maybe a bypass, maybe something with extra Keith. And if they're struggling to breathe, these air patients that maybe need to be intubated earlier. So now that we're thinking about stabilizing, we really think about how we should be monitoring these patients. And this gets into the whole debate about the P A catheter. So prior to the two thousands p A. Catheters were used pretty frequently in the generalized you, not even just the cardiac I C E o. In the early two thousands, however, several studies came out showing the pulmonary artery catheter had no benefit. The primary big study was in the general. I see you, however, the escape trial in 2000 and five randomized heart failure patients to getting a P a catheter versus not getting a P. A catheter on DSHEA showed no difference in outcomes. The notable things about this trialing, really we're number one. They discouraged in a trove use and really had goal directed diary assist number two on Lee. Patients who had clinical equipoise were included, so these were patients that heart failure. Doctors felt comfortable managing without a P a catheter, and it really excluded critically ill patients. Those who are being worked up for transplant. Those who are being worked up for L VOD and as such only about 0.5 percent of patients had cardiogenic shock in that trial. But these two trials really lead to a significant decrease in use of P A catheters and the search for less invasive chemo dynamics. So I'm just going to briefly go through, like all the different stuff that people have tried. So one of the types of monitoring that really has been recent, more recently attempted, is the flow track. The flow track works by using an arterial line and by using waveform analysis to predict what the stroke volume is and then calculating a cardiac output. It was validated in surgical patients on DSO subsequently was found in Visa dilatory states to be inaccurate. So you really can't use in patients with sepsis and patients with liver failure on then. Some more recent smaller studies have questioned whether this is really accurate in cardiogenic shock. It's such I don't think it's particularly useful in our cardiac intensive care unit patient. The PICO is also a big idea for how we can monitor patients with the invasive support that we already have without the need for a pulmonary artery catheter. It requires the use off a central line and a central arterial line like ephemeral or breaking our breaking well. Um, and combines Pulse Contour analysis similar to the arterial waveform analysis and thermo dilution. Thio calculate multiple things, including free long water but also cardiac output. However, in ah large study where it was compared, uh, Thio, a pulmonary artery catheter, it was found that patients who had PICO used had increased fluid balances and decrease invent free days. So really, it's underestimating the amount of volume that the patient has on board, and thes patients are not getting optimal treatment and heart failure. And so I think that this is not an optimal way Thio manage our patients in the cardiac intensive care unit So this is the more recent study that I wanted to talk about. Um, it's the study of the Nikon. So Nikon is a non invasive cardiac output monitor. Um, it uses measurement of bio reactant and the thoracic cavity, so it's totally external to the body. Um, it's been validated in several cohorts and a sepsis cohort in a cardio, my ah Tomy cohort in acute respiratory failure cohort. However, this study that I'm going to talk about right now is a study of 50 patients who had P a catheters that were being used for cardiogenic shock, and they basically measured at the same time the patient's NYT com. The patient's thicken. The patient's thermo dilution. Yeah, and this is really the graph of their data outputs, so you can see over here comparing the night calm to the thick. There are patients who had, you know, lower lower NYT, com's who still had normal cardiac outputs, and there are patients who had high fix who have lower ny com So it's not really well, um, they're not really concordant PR value is 0.132 and the same thing happened when you compared it to Thermo dilution. Thea our values 0.275 on DSO. This is really not a great tool to be used in our cardiogenic shock patients. Moreover, Correlation didn't really improve with normalization of cardiac index or with improving you've Olympic status. So even though the theory is that in cardiac patients, this is not a good use because of the extra vascular lung water improving their stat, their volume status didn't improve the outcomes of the Nikon. And so this makes me really question. Is this a valuable tool for us to be using in our patients to monitor their hemo dynamic status? This leads us back to the P A catheter. And so, in this setting, um, there have been a couple of more recent studies that have attempted to figure out is the p a catheter useful and cardiogenic shock patients? Thanks. So the card shock study was presented in 2020. Um, it's really a study of an observational cohort of patients between 2010 and 2012 who had cardiogenic shock. They looked at patients who have in this cohort who had p a catheters and did propensity score matching for patients who had Nope, a catheter, so they found 50 pairs of patients that they were able to compare notably in this cohort catheters were using about 37% of patients when they have their propensity, score matched patients. Um, there was no significant difference in cardiovascular risk factors, and co morbidity is after the score matching. But still the Apache two score of the P A catheter patients was higher p a catheter. Patients were managed more aggressively. They had more mechanical ventilation. They had more renal replacement therapy. They were more likely to get mechanical circulatory support. They found that there was no significant difference in 30 day mortality or in short term mentality. This study is pointed to as a reason we shouldn't be using Kiai catheters, although it is notable that you know the decision on whether or not to use the P. A catheter was made up front and there was a different Apache score, which is, ah, risk score for how sick patients were between the two groups. Two other studies have really looked at this, so the attend registry was an observational cohort of cardiogenic shock patients. Similarly, in this study, uh, 64% of patients had P A catheters used. This was a study in Spain. Um, and they did show instead of doing propensity score matching, they adjusted for co morbidity. Ease on day showed a lower mortality rate in the use of P A catheters that mortality rate and that benefit primarily came in the non coronary, um non a CS patients, non acute myocardial infarction, patient cohort. And they didn't find that there was any benefit in the acute myocardial infarction cohort. This leads to this really interesting study between multiple different centers by Rashad Goran Um, where they looked at this was a really interesting trial methodology. Basically, they looked at a cohort of patients similarly in cardiogenic shock and looked at, um, number one What class of shock they were in. And then number two, What did they have a p A catheter? And did they have complete assessment of their human dynamics? To show is the thoroughness of the amount of him Oh, dynamics that you have related to your outcomes. So just a reminder. This is how they kind of conceptualized which class of shock you were in so beginning shock, where patients who didn't need support if you were on either one in a trope or one device you were thought to be in classic cardiogenic shock patients who required more than one in a trope or more than one device were the patients who are deteriorating, and then patients who were on both more than one in a trope and more than one device were thought of as being in that extremist category. So they really classified patients in terms of patients who did not have any, he mo dynamics. So you didn't know their P A pressures. You didn't know their wedge pressures. You don't know their p a stats, and you didn't know there are a pressure if they had some but not all, of their hemo dynamics done so You knew their PPA pressures, but you didn't get a wedge or you didn't get a sad or you didn't have an R a pressure. Then they were thought to have incomplete assessment. And then, for patients who had everything done from a full set of him, oh dynamics to manage them were put into the complete assessment in three. Overall, there is an improvement immortality for people who had complete assessment versus people who had incomplete assessments. But this was not like a large value. But then you can really see in the sicker patients in the Class D patients and Class E patients that there's a stepwise impressed improvement in the amount of information you have. So patients who had some him, oh dynamics, but not complete chemo dynamics did better than patients had no chemo dynamics in patients who had complete hemo dynamics did better than patients who had incomplete chemo dynamics. And this is really suggestive, at least in our sicker patients, that the more data we have about their hemo dynamics, the better we are managing them and the better outcomes they have. Um, and this, along with the Cardiogenic Shock initiative, really leads me to think that they're This may be the best way that we have to manage are really sick patients at this point. Finally, I'd be remiss if I didn't talk about the recent New England Journal research letter that's been making a big stir in the critical care world. Ah, lot of us are managing our patients with pulse ox symmetry. You know, we really don't want to be doing frequent a BGs. It's painful having a lines, is it in his invasive And it was really a risk for infections and vascular injury. Um, but in the era of co vid, there's been a lot more hypoxia me in a lot more occult hypoxia mia on dso the University of Michigan really took advantage of this large patient population to do a study on the pulse oximeter remembering that, ah, lot of our studies and our device development is done in patient cohorts that may not be diverse and maybe more white than our general patient population. They wanted to look at the pulse oximeter in the black patient population compared to the white patient population. And so what they did is in every patient who had a paired pulse ox symmetry read with when they had an a B g drawn. They looked at all the patients who had sat in the 92 to 96% range in what percent of them had actually had a cult hypoxia mia, meaning there saturation on their A B J. Their true saturation was less than 88% and they found that in black patients this was over 10% of patients whereas in white patients it was only about 3%. And so it's really imperative that when when we're treating our patients, um, we're on the lookout for a cult hypoxia. Me in patients who appear to be struggling and peer toe have to keep Mia because the pulse oximeter maybe missing high poxy mia in our black patients. Um, and it's also like a good reminder to think about patient populations. One. We're developing new devices and studies and and so in this setting and just want to kind of talk about, um, in summary, these were the things that we kind of talked about. Today. Patients in our cardiac intensive care unit are sicker. They have more multi organ failure, and they may benefit from having specialists, um, involved in their care who have expertise in multi organ failure. Um, the triage of cardiogenic shock to the cardiac intensive care unit really improves care and offers additional interventions to our patients. Algorithms that include include early mechanical circulatory support and Huma. Dynamic monitoring may improve outcomes in our cardiogenic shock patients. We really should be considering positive pressure ventilation early in patients who seemed like they're struggling to breathe and have, ah LV dysfunction. Recognizing that it in patients with RV dysfunction, it can have some deleterious effect on him. Oh, dynamics on Ben, the p a cat, you know, the old is still new. P a catheters may still have a role in the management of our cardiogenic shock patients. Thank you for your time. All right, Jessica, great job. Give me one moment. I'm gonna let me stop the share. Jessica. Thank you. It's Harvard here. I was a great talk, you know, I just did some background. We all Presbyterian, actually one of the first ccs in the country in the sixties. And the evolution that you sort of outlined here has just been over the last. What, You know, 60 years going from a unit was there to treat arrhythmias purely with the advent of cardioversion, then moving on to watching people that might have complications and deal with complications, then moving on to PC I and treating patients after stem ease. Now, this whole new generation off managing the critically ill patients with new vitality has been fascinating. So thanks for going through that. What an exciting evolution. Um, while we're waiting for a couple questions. I'll just ask if you don't mind a question that two questions. What? Some questions that you pointed out that putting on a cattle addresses this Amira's well, putting patients on mechanical circulatory support with shock Prior to PC, I you know we're here. Our interventions, I say, How about this? And they look at me and say, What do you mean? We gotta get this artery open? It's all about opening the artery, but the data would point maybe to putting them on support first. Can you guys comment about that? Um, so what? I'll say having listened to Nuveen a bit toughs, a lot is like, This is definitely something that there's certain people who strongly believe in. And there's definitely data to support it. This idea of mechanical unloading prior toe, um, PC I. But I know that there are a fair number of interventional ists who think it's more important to get the or artery open first. And so I think that I will defer that conversation a little more severe. Harvey, I think it's a great question. Um, you know, we looked at this several years ago, and what we found is Oftentimes patients get sicker before they get better as they're going through the intervention. And I think that's really where this idea of the mechanical support coming first. And I'm not sure if you're alluding to the idea of unloading routinely versus the patients in shock. But if we concentrate more on the patients that are sort of pre shock or early shock, um, those patients, I agree. I think the more aggressive we are upfront with mechanical support. Now sometimes it Zeina trope, sometimes a balloon pump. Sometimes it's in Pella. Sometimes it's Eckbo. Um, like Jessica showed it really does not delay significantly your door to balloon time. I do think there is great value in offering those patients some type of additional support before you undertake the intervention, because again they oftentimes get sicker before they get better as they're going through the procedure. Um, what we found was the group that you struggle through the acute coronary syndrome with China tropes and then go to the unit that they tend to without mechanical support, but are in shock, tend to get worse. So then you go from one presser to to pressers on. Then you know hours later. You're trying to go back to the cath lab for mechanical support. Those patients don't do well, so we tried Thio tryto wrap all that up while we're in the cath lab. I think Jessica was also alluding to this concept of unloading the ventricle routinely. So the idea here is that if you have a large if you're having an M, I that if you can unload the ventricle, you dramatically decrease um, kind of the myocardial oxygen demand of the heart, which may be equally or more important or less important. We're not sure than actually opening up the artery. So allowing the heart that period of time to rest, really dramatically dropping your auction demand of the heart and then proceeding with the revascularization may have some benefit. I think that's a big paradigm shift that we'll see what the data shows over the next few years. But I do think like a lot of the sky, people really talk about the importance of getting someone on a stable platform in the cath lab before transitioning to the cardiac intensive care unit. All right, thank you. I'll just look at some other questions here. The question about peep Jessica. How much people is found to be most beneficial? So there's a single number 10 or something that you haven't been studies where they do like radiations. Most of the studies looked at five or 10. I think 10 has been shown to be beneficial. I don't they haven't done. It's not like, um, in a R d s where they've done keep titrate in trials to show this is the most. This is the best peep for cardiogenic shock. The idea of being the more keep you get, the more positive pleural pressure you have. And so the less, um, trans mural, um, trans mural pressure you're gonna have and so that will decrease the after load that the LV is truly seeing and can decrease ischemia and Connecticut increased cardiac output. You know, the one thing that I didn't really get a lot into is the effect of Keith on the RV and the effective people on the pulmonary artery pressures. You know, people also will it will decrease right ventricular preload, and so for patients were pre load dependent with RV failure it can cause are decrease RV output. Um, in terms of what it does. The RV after load. It's kind of a mixed picture, and someone who does not have high poxy mia and has elevated P a pressures, Um, putting people on will increase the pulmonary artery resistance that the are VCs and can't decrease cardiac output. And somebody who has high poxy mia, whether it's from Holman area Dema or from from a R. D. S. Uh, what people do is it will increase oxygenation, which leads to increase pulmonary vezo dilation, which can decrease after load. But that's counteracted by the positive pressure in the pleura adding to the after load. And so in those patients, it's unclear in each individual patient, and you may actually have to sit there and titrate Keith to say one of them. I like at this level. Am I having, um, I having improvements in my cardiac output, or am I having more hype, hype attention? And then, if you're having more hype attention, you have to bring it back down. Great. Thank you. So, another question here, how do you select aina tropes? Um, that's a great question. I So I think, um, I'll say a couple of things about that which is on that A lot of this is really cultural. So at the different places I've trained the approach to the choice of in a trope between Deputy Meena Miller and own eyes very uh, very location specific. I think the way that I tend to look at it is can the patient handle I know dilation, and if I can handle it, I know dilation. Then I either start to beauty me normal reknown. Um, if they have renal failure and I'm worried about, you know, getting them out of shock quickly. Then I'll put onto beauty me because it's something I can titrate quickly. And I'm not worried about over vase a dilating them because I can titrate it back down. But if it's somebody who I'm really, I have some more time with and I'm trying to get them home on something, Then I'll start Miller, known because Miller known something that has a longer half life in a more comfortable on them going home with, and, um, and I have some time to do that. Um, you know, there's a lot of people who, like, talk about Oh, this one's more Veysel dilatory or that one's more visa dilatory. I think the data is that they're pretty equivalent. And I think the data is probably that they're pretty equivalent in terms of risk of arrhythmia as well. Um, if they can't really handle the visa dilation, then you're really thinking about epinephrine versus leave A fed to support them? Um, there was a recent study that actually had to hit compared them in cardiogenic shock in patients who had acute myocardial infarction, which showed decrease in duration of I see you stay and leave a fed compared toa epinephrine. Um, there's some people who questioned some of that data. I really think about epinephrine is something like, That's my big gun. When I can't stabilize someone, I just want to throw them on it. But it really has a lot more arrhythmias. And the other thing is, epinephrine will cause a small increase in lactate independent of cardiogenic shock. And so you should expect that small bump, not a huge bump, but like, you know, 1 to 2 s o. Um, so I think it's also reasonable if you're not sure what's going on and you don't need, like, some big gun, you're not just trying to stabilize someone who's going down the tubes fast to reach for leave a fad. Thank you. Someone asks, Um, what are the attributes of the disparity and sat Oh, to set pulse ox versus arterial sat in African Americans. There any any thought? Why that might be? I think we're entirely sure, but I think part of it is that, like the way that the 02 SAT monitors developed, you know, you standardize it to levels and say, This is what the saturation is based off of this level of infrared that we're seeing come back and that was standardizing white patients. And so if you have people with darker skin tones, that may not be as accurate and it turns out it's less accurate. And so I think we have the data. I think that's the thought about why, what, like the higher degree mechanics and that I don't know. Interesting. I see a question here with the idea of patients on two devices being sicker. If we put someone on peripheral va ECMO, we almost always routinely put in impel a in would you consider them in the same category is absolutely requiring two devices um, I don't know. You know, I think I think once you're putting someone on ECMO, they're kind of almost in that extremist category anyways, Like what they define that category is is people who you're crashing onto ECMO requiring CPR for cardiogenic shock. So I think if you're putting someone on ECMO to stabilize them, they're probably in that category unless you put them on prophylactically for, like, a VT ablation or ah, high risk PC and you're able to kind of win them off. Great. Thank you, Samir. You see any other questions here that we want to bring up? I'm looking. There's a few more in the chat section. Um, why don't you go ahead and take it? One of those has to do. Jessica. People often described the Triple. Lumen is the poor man Swan. And from the Triple Lumen, you could at least measure a CVP, and you could measure a, you know, sort of at SBC saturation. How useful are those compared to an actual wedge and p a sat, and is that adequate? Um, I think that's a great question. I think there's no head to head data, right. So I can't say that it's not or is. I think, that the SBC sat sometimes. Does I use it when I have it? E think the SBC sat does sometimes make us more confident that we should be that a patient's doing well, and I think some are less confident, depending on how the patient's doing. You know, if they're in cardiogenic shock, maybe that coronary Sinus that is a lot lower on beacon tributes more to this being a lower mixed Venus than we thought. And so I think while it's useful, if that's what you have have, and I would use that, I do think that there's still a role for the Swan. And as we've seen more Huma, dynamic data does improve outcomes. So it's not just the are a pressure in the set, but you really do need to think like what's going on? How much of this is RV failure? How much of this is LV failure? How do I support those, Um, adequately. And the last question I see here from in the chat section has to do with by pap and CPAP, and it looks like both for equity compensation and is there any role in patients with chronic heart failure, uh, to you see, paper by pap, even potentially at home. So it is a great question. There was this sleep study, which I am trying to remember all the data for it. So first of all, in I talked about this years ago. Now I'm forgetting it. So there is a study that looked at patients with OS A in heart failure. Um, they tried to see Could they improve outcomes by having them where cpap onda study was negative. That being said, the adherence to CPAP was extremely low. Less than four hours a night. Um, that being said in terms of just heart failure without without osd, I don't think it's ever then studied or looked at first thing. Okay, great. Mm. Just It's one of a question from me. Um, as you look forward and nicely outlined the different models for staffing on H B I. C U. Given our current what we have in manpower in this country now, as you outlined also the limited number of people trained with your level of expertise what do you think? A reasonable model? That hospital gonna move to over the next number of years toe get the kind of care we need for these critical patients with different illnesses that we had in the past in the unit. So I think there's been a lot of conversation about this, and I think that there's a couple of different models that have really been discussed and suggested. I think one of them is kind of designating hospitals at CCU as kind of different levels. And so having like a level one CCU being, ah, coronary care center, where people are getting referred toe and having that be staffed by either cardiac intensive us and people who do have this training ultimately or by staff by people who have, you know, heart failure, training or interventional training who spend at least six weeks or more in the i. C. U A year. So they really are experts in dealing with these patients, even if they haven't gone through additional training, Um, and then having you know, in secondary level tier hospitals that have C I C. Use, but they're not quite merry care referral centers having either intensive care, um consults on their patients, um or involving kind of intensive it intensive this in their care. Um, they think that one of the big things that's been discussed is, even if you don't have people who have dual training is making sure that people are spending enough time in the C I. C u a year. And so it's not the old model of you. Spend two weeks a year and, um, your that's the amount of time you're spending. And that's the amount of comfort you have in managing renal replacement therapy and managing a ventilator. Because, you know, these are really our patients. You know, we have patients who get trapped in the sea. I see you and we have patients who obstruct their airway in the sea. I see you and you can't rely on a respiratory therapist to be the only person who's watching the ventilator. And you can't, you know, rely on, you know, the nef ProLogis to know what your goal is for your CRT. You really have toe be thinking about those things. Hey, Terrific. Samir thoughts. Last words. Oh, that was great, Jessica. Thank you very much. You know, I think, uh, congratulations being very forward thinking, because I think this is a field that is going thio continue to grow and prove very important. Patients are much more complicated than just straightforward acute coronary syndromes. Arrhythmias now and being able to tying him. Oh dynamics with image ing with management of other organ systems beyond just the heart eyes really going to be crucial. And, you know, I hope that yourself and the others leading this field will continue to gather data and and hopefully be able to show that by having a dedicated person, a dedicated system on DSO certain pathways in place that you can really impact length of stay mortality and outcomes. Because I think if you guys in the early stages contract that and hopefully you are already and show that I think that's going to be very, very important for the field. And that's a great shout out for the cardiac Critical Care Trials network. Thank you. Great. Thanks, Jessica, for a great grand rounds and Samir for leading us. And thanks for all the attendees. We will get back to you on the CMI code. Assumes we have that available against Samir mentioned earlier. Please, if you're not logged on with your name so we can't track you, please send an email to Samir or Linda, and we'll make sure you get credit for grand rounds again. Thanks all and have a great day appreciating. Thanks, Jessica. It's a mere.