Transcript
Speaker: Welcome to Critical Matters, a sound podcast covering a broad range of topics related to the practice of intensive care medicine.
Speaker: Sound provides comprehensive critical care programs to hospitals across the country.
Speaker: To learn more about our programs and career opportunities, visit www.soundphysicians.com.
Speaker: And now, your host, Dr. Sergio Zanotti.
Speaker: Cardiogenic shock represents a final pathway for many patients with cardiovascular disease.
Speaker: It is an important reason for admission to the intensive care unit, and although its mortality has improved over time, it still remains high.
Speaker: In this episode of the podcast, we will discuss advances in the management of cardiogenic shock.
Speaker: Our guest is Dr. Jacob Jenser.
Speaker: Dr. Jenser is a cardiac intensivist trained in both cardiology and critical care medicine who practices full-time in the cardiac intensive care unit at Mayo Clinic in Rochester, Minnesota.
Speaker: He's the director of cardiac intensive care unit research at Mayo Clinic.
Speaker: He is active in cardiac intensive care unit and looking at outcomes of patients with cardiogenic shock and cardiac arrest.
Speaker: Dr. Jenser has numerous publications, including a recent concise definitive review in critical care medicine entitled Advances in the Management of Cardiogenic Shock.
Speaker: Jake, welcome to Critical Matters.
Speaker: Thank you.
Speaker: It's terrific to be here.
Speaker: Well, like I said at the beginning, we were talking ahead of time.
Speaker: This is obviously a topic you're very passionate of.
Speaker: You work exclusively in a cardiac unit.
Speaker: You dedicate a lot of your time to studying cardiogenic shock and treating patients with cardiogenic shock and advanced patients.
Speaker: support for cardiogenic shock.
Speaker: But it's also, it's a common problem in ICUs all over the country.
Speaker: And it's not uncommon for intensivists who are in the medical ICUs or mixed surgical, medical surgical ICUs to deal with patients with cardiogenic shock.
Speaker: And I think with the increase of all sorts of percutaneous procedures being done in more and more hospitals, I suspect that a lot of our listeners will
Speaker: face more and more of these patients.
Speaker: So I think it's a perfect topic for us to cover today in the podcast.
Speaker: I would like to start as a more of introduction, maybe with some definitions, and obviously these are evolving, but if you can just give us from your perspective as a cardiac intensivist, how did you define and think of cardiogenic shock?
Speaker: Absolutely.
Speaker: You know, the way that you define cardiogenic shock to some extent depends on what the whole purpose is.
Speaker: And most of the definitions you see in the literature are based on research and randomized trial enrollment.
Speaker: And so the definitions historically have been very complicated involving invasive hemodynamics, patients who are hypotensive and have low cardiac output with high filling pressures documented, for example, on a pulmonary artery catheter.
Speaker: But we've been using pulmonary artery catheters less and less and less.
Speaker: And so as the result, the definitions clinically have evolved.
Speaker: And this is not just a research thing.
Speaker: This is a clinical thing.
Speaker: So the most common presentation of cardiogenic shock is a patient who presents with blood pressure.
Speaker: clinical evidence of hypoperfusion and low cardiac output and is in pulmonary edema.
Speaker: And that's what most of us see in practice.
Speaker: So for example, a patient with acute myocardial infarction who has exam evidence of hypoperfusion, maybe hypotensive and is in pulmonary edema would be a classic example.
Speaker: I think that the most important evolution in the way that we define cardiogenic shock is a focus less on the hemodynamics and whether or not the patient is hypotensive and what their cardiac output might be, and more on the end organ effects.
Speaker: And so really, the newer definitions emphasize the presence of hypoperfusion, and that can be defined in lots of different ways.
Speaker: And some
Speaker: Some definitions are a little bit more restrictive and require multiple different things.
Speaker: Others are a little bit more liberal.
Speaker: But the kinds of things that we see clinically at the bedside would be cold and model extremities with delayed capillary refill.
Speaker: We often an elevated lactate level.
Speaker: Also other biomarkers, evidence of acute kidney injury, acute liver injury.
Speaker: And there's a lot of other things that experienced intensivists will recognize as evidence of hypoperfusion.
Speaker: And so once you identify a patient who has hypoperfusion, if you see objective evidence that they have acute cardiac disease and adequate filling pressures, then that's generally enough to say that it's cardiogenic shock.
Speaker: One of the key differences between contemporary definitions of cardiogenic shock and some of the older definitions is that patients don't have to be hypotensive to meet criteria for cardiogenic shock, in my opinion.
Speaker: And there's this evolving concept of normotensive cardiogenic shock, which based on older invasive hemodynamic data and some newer non-invasive echo data that I've looked at,
Speaker: is really the patients who are early in the disease state who still are able to preserve their peripheral vascular tone.
Speaker: And so they might have a systolic blood pressure of say 100, despite the fact that they have a low cardiac output and otherwise meet all the other hemodynamic and clinical features of cardiogenic shock.
Speaker: And these are patients who over time typically lose that ability to preserve their blood pressure and become hypotensive.
Speaker: And so I think that's the real evolution is a focus on hypoperfusion
Speaker: really more so than the actual exact hemodynamic numbers, particularly the blood pressure.
Speaker: And I think that it's no different than maybe other states of shock, right?
Speaker: We're moving away from absolute numbers and really thinking about what's the impact on end organ perfusion and organ function.
Speaker: And I think it's important because, as we'll talk a little bit later, early identification might help us take care of patients in a time-sensitive way that might improve outcomes.
Speaker: Absolutely.
Speaker: The other aspect of cardiogenic shock that I find interesting is not only we have an evolving definition, but also an evolving and changing epidemiology.
Speaker: I'm a little bit older, have some white hair.
Speaker: And when I was in training, the reasons why patients came to a cardiac unit in shock were
Speaker: where almost exclusively or more commonly due to cardiac ischemia.
Speaker: How is that changing today in your practice?
Speaker: So this is really important.
Speaker: I think that there are two trends that are superimposed on each other.
Speaker: The first is we are recognizing and diagnosing cardiogenic shock more often.
Speaker: So the prevalence in epidemiologic studies and the incidents are going up.
Speaker: Now, whether that's actually a change in what we're seeing in reality or whether that has to do with the way that documentation occurs in the administrative databases we use for these big data projects, I don't really know.
Speaker: I think it's both.
Speaker: So that's the first thing is we're seeing more and more and more.
Speaker: But the excess that we're seeing is increasingly due to other causes of cardiogenic shock besides acute myocardial infarction.
Speaker: The whether or not the actual incidence and prevalence of cardiogenic shock in patients with acute myocardial infarction is changing is a matter of debate.
Speaker: There's enough reason to think that it should be going down because we're doing more early revascularization, PCI, and that should decrease the prevalence and incidence of cardiogenic shock.
Speaker: But we haven't really seen that in practice.
Speaker: but the proportion of cardiogenic shock cases that are due to acute MI has dropped fairly dramatically.
Speaker: And this is something that I think to some extent differs by centers.
Speaker: So if you're practicing in a community hospital intensive care unit, it may be that acute myocardial infarction remains the most common cause, but particularly in tertiary referral centers that are having very large heart transplant and LVAD programs, more and more and more
Speaker: of the overall population of cardiogenic shock cases is due to end stage cardiomyopathy.
Speaker: And so we're seeing more and more of these patients who have chronic cardiomyopathy with advanced heart failure at baseline that then has become tipped over into an overt shock state.
Speaker: And we're seeing more and more of these patients.
Speaker: They numerically outnumber acute MI cases in most tertiary ICUs.
Speaker: That's been shown both at Mayo Clinic and in the larger critical care cardiology trials network, which is a multicenter CCU database.
Speaker: And I think that that's something that is really important because the vast majority of randomized trials in cardiogenic shock have only focused on patients with acute MI.
Speaker: And those patients really differ in a lot of ways from patients without acute MI who are now more numerous.
Speaker: And I think it also speaks, Jake, to the evolution of CCUs, right?
Speaker: Back when I was a resident, it was mostly acute MIs.
Speaker: And now a lot of the tertiary care and high-powered CCUs have a lot of devices.
Speaker: There's a lot of cardiogenic shock.
Speaker: There's a lot of complex disease.
Speaker: And I would say higher acuity overall.
Speaker: Yeah, that's absolutely true.
Speaker: You know, at Mayo Clinic, we have a quality improvement protocol that we've implemented over the past several years where patients with ST elevation MI,
Speaker: who are otherwise stable and meet low risk criteria, which are objectively documented using something called the Zwolle risk score, they go to the floor.
Speaker: They never come to the intensive care unit at all.
Speaker: So the patients that do come to the intensive care unit predominantly have circulatory failure, either chronic or acute.
Speaker: And that spectrum of cardiogenic shock is most of our patients nowadays.
Speaker: Some are on the milder spectrum where they don't really have cardiogenic shock and then all the way up to full on
Speaker: shock, which is another topic I think we'll discuss later.
Speaker: But it really does parallel cardiac ICU care in general.
Speaker: And, you know, we really are seeing that most patients with acute MI can be safely cared for at, you know, in non-ICU settings once they've been revascularized.
Speaker: Perfect.
Speaker: And you did mention spectrum.
Speaker: So I think that's a good lead way to our next topic, which is classification and prognostication of cardiogenic shock.
Speaker: So I understand that over the last couple of years, there's really a new severity staging classification for cardiogenic shock.
Speaker: that in society for cardiac angiography and intervention sky has proposed and that a lot of intensivist in the cardiac arena are adopting and trying to to bring to the bedside could you tell us a little bit more about that
Speaker: Absolutely.
Speaker: So this has been a particular area of interest in research for me for the past several years.
Speaker: This, what we call it, SKY, short for the Society of Cardiovascular Angiography Intervention, shock classification.
Speaker: And this was introduced back in 2019.
Speaker: And essentially, it was a bunch of experts sitting down and thinking about the fact that what we call cardiogenic shock means something very different to different providers.
Speaker: And even
Speaker: patients meeting a very clear, very narrow research definition of cardiogenic shock will present with a fairly wide spectrum of illness.
Speaker: And in many cases, there's not a clear cut point between who absolutely is in shock and who absolutely isn't in shock.
Speaker: And there's these intermediate or pre-shock states that exist.
Speaker: And so what they did, based on expert consensus, is they sat down and they said, look,
Speaker: Patients who have acute cardiovascular disease, for example, acute myocardial infarction or decompensated heart failure, they're all at risk of developing cardiac shock.
Speaker: And some of them will and some of them won't.
Speaker: And many of those who will, will proceed through first a pre-shock state of impending hemodynamic decompensation or early hemodynamic decompensation.
Speaker: And then we'll go to a standard classical form of shock, which
Speaker: But then some of those patients with the classical form of shock will get better, and some will get worse, and some will deteriorate.
Speaker: And those patients who deteriorate are in many ways very, very different.
Speaker: And some of them will deteriorate but then be stabilized, and some will deteriorate to the point of circulatory collapse.
Speaker: And within the patients who have over unquestioned cardiogenic shock, there's this whole severity of illness.
Speaker: And so they defined a five-stage grading system for patients, and it's patients with or at risk for cardiogenic shock, and that's the sky shock classification.
Speaker: And, you know, this is a little bit easier to define graphically, and so there's some very nice figures that exist in the literature that can explain this.
Speaker: But essentially, the grading system goes from A to E,
Speaker: A are patients who are at risk and they have some acute cardiovascular disease that could cause hemodynamic decompensation, but up to now has not.
Speaker: And so they're hemodynamically stable.
Speaker: They have normal perfusion, normal hemodynamics, normal blood pressure.
Speaker: And most of those patients, of course, are going to be fine.
Speaker: But some of them are going to deteriorate and develop worsening hemodynamic state.
Speaker: And so the first hemodynamic compromise state is called stage B or beginning cardiogenic shock.
Speaker: But these patients, they don't yet have cardiogenic shock.
Speaker: I classify them as pre-shock.
Speaker: And so they have some form of hemodynamic compromise, which could be hypotension.
Speaker: It could be compensatory tachycardia.
Speaker: It could be low cardiac output or other things.
Speaker: hemodynamic abnormalities, but despite that, the patient is still compensated enough to have adequate end-organ perfusion.
Speaker: And so they haven't developed shock because in this construct, shock means end-organ hypoperfusion due to circulatory failure.
Speaker: So again, a lot of patients in stage B will stay there and will improve, but some do deteriorate and go to overt shock.
Speaker: And so shock or classic shock is defined as stage C,
Speaker: And patients in stage C have end-organ hypoperfusion due to circulatory failure.
Speaker: And importantly, it needs some sort of a higher level intervention, which doesn't mean just a little bit of fluids.
Speaker: This means even after fluid resuscitation, the patient still has hypoperfusion and they require inotropes, vasopressors, or MCS.
Speaker: And again,
Speaker: Most of these patients will stabilize with that initial intervention, but not all of them do.
Speaker: Some of them deteriorate to what we call stage D for, of course, deterioration.
Speaker: And these are patients who are worsening despite that initial therapy.
Speaker: The most common thing would be somebody who has a rising lactate or rising vasopressor and inutrope requirements.
Speaker: And so these patients, again, are, you know, sicker.
Speaker: And some of them do get stabilized with that escalating therapy.
Speaker: hemodynamic support, but in some cases, you know, the worst cases, they progress to what we call extremis or stage E. And there's a lot of different definitions of this, but you know it when you see it.
Speaker: So these are typically patients with actual or impending circulatory collapse.
Speaker: These patients may be pericode.
Speaker: They may be on very massive doses of vasopressors.
Speaker: They may have a code card at bedside.
Speaker: You know, these patients do not, you know, they don't stay in stage E for very long.
Speaker: Either you stabilize them or they, you know, crash and burn.
Speaker: And so the idea with the sky shock stages classification is although gradations exist either, you know, both within each of these stages and between these stages and the edges are a little bit blurry.
Speaker: When you say to someone who is talking the same language as you, this person's in stage C, you each know what the other one means.
Speaker: This means I have a patient who is clearly in cardiogenic shock.
Speaker: they have manifest hypoperfusion, and fluid resuscitation either is not the answer or hasn't worked, and now they're on some sort of a vasoactive drug or a device to stabilize them.
Speaker: The implication is that either you're very early and you haven't seen if they're going to deteriorate or they have been stabilized.
Speaker: And so when I tell you
Speaker: you know, this is a stage C patient, I'm transferring them to you, you have a general idea of what you're looking at.
Speaker: You're not looking at somebody on six vasopressors.
Speaker: You're not looking at someone who's, you know, got a lactate at 20.
Speaker: You're not looking at someone who's, you know, crashing and burning right in front of your eyes.
Speaker: On the other hand, if I tell you, man, I have this guy coming in hot, he's a stage E shock.
Speaker: You know, we've been bolusing him with small doses of vasopressors.
Speaker: He's on three drips.
Speaker: I'm thinking about what's the next step because we better do something now.
Speaker: And those are two very different looking patients who both have cardiogenic shock.
Speaker: And so the whole point of the SkyShaw classification wasn't just for research, although that's what it's been mostly used for.
Speaker: It's actually for communication.
Speaker: So if I'm in the intensive care unit and you're in the emergency department, or you're in the cath lab and I'm in the intensive care unit, or you're at one hospital in the intensive care unit and I'm at a different hospital, we can talk in the same language.
Speaker: And when I say that a patient is in a certain stage, you're going to understand and visualize what that patient might look like.
Speaker: And if we're using the same criteria to classify our patients, then they'll look even more similar to what our expectations are.
Speaker: And so with so, yeah, we use this for research and there's all these very complicated and somewhat sophisticated definitions of if this and this, but not that, then it's this stage.
Speaker: But that's not what it's about.
Speaker: You can take a look at the patient and you can define this based on what you're seeing at the bedside or their chart, either in the real time or retrospectively, and you can figure this out very accurately.
Speaker: And as long as you and I have a shared understanding of what this means,
Speaker: You and I will be on the same page.
Speaker: And so it's supposed to be a better and more consistent language for communicating about these patients so that within this wide spectrum of severity of cardiogenic shock, we can pin down where the patient is when we talk about a care plan or a transfer plan or a triage plan.
Speaker: Excellent.
Speaker: And I believe that I would imagine that it also has tremendous value for the individual clinician at the bedside to have a framework that helps them understand their patient and think about their patient in a more holistic way.
Speaker: So I could see, for example, that somebody just got admitted to my ICU and I walk into the bedside.
Speaker: and they don't look as sick as many of my other patients.
Speaker: However, if you really think about it, that an hour or two ago when they got to the hospital, they were at stage A, and now all of a sudden they're at stage B, maybe you could say, okay, well, what about what I need to do to prevent
Speaker: And from moving to a stage C, D, E, or is that even something that could be potentially happening in the next couple of hours?
Speaker: So I believe that it also helps us maybe think about these patients earlier and to pay more attention.
Speaker: Absolutely.
Speaker: And I think that, you know, translating this from the research arena, right?
Speaker: to the clinical arena has been a little bit difficult because a lot of the research definitions are just too complicated.
Speaker: You just can't do them at the bedside.
Speaker: But one of the things that some of my colleagues have done at Mayo Clinic is we've leveraged the electronic health record.
Speaker: And so I can't remember all the criteria for all of these things, but the computer can.
Speaker: And the computer can automatically import the data into an algorithm, and it can say, based on the rules that we defined,
Speaker: This person meets this stage.
Speaker: And so we're using that in practice as an early warning system.
Speaker: And, you know, honestly, the results are a little bit mixed because some of the patients, the computer is telling you what you already know.
Speaker: This person is sick.
Speaker: And the reason that the computer recognizes that the patient is sick is because you're doing things to the patient that are reflections of how sick they are.
Speaker: Oh, they're on three pressers now.
Speaker: Oh, you know, all these things.
Speaker: But we very frequently are finding patients on our cardiology wards, not in the intensive care unit, who have had subtle forms of early deterioration, particularly those normotensive shock patients where their blood pressure isn't dramatically low.
Speaker: Maybe it's a little bit low or maybe sometimes it's low and sometimes it's not.
Speaker: So it's kind of borderline.
Speaker: But then, you know, you realize, gosh, their lactate's five.
Speaker: Something is going on here that is not manifested in their blood pressure.
Speaker: And we are using the health record to help us identify those patients early, send out kind of rescue alerts, and sort of activate something that's analogous to a rapid response team where one of my
Speaker: Either my fellow or my advanced practice provider from the CICU will go to assess the patient at bedside.
Speaker: Then they'll talk to the team.
Speaker: They'll say, gosh, you know, what's going on here?
Speaker: Is this a patient who actually doesn't have cardiogenic shock?
Speaker: They actually have sepsis.
Speaker: Is this a patient who actually has impending or developing cardiogenic shock who now they're better off in the ICU?
Speaker: And I think that that is one of the first ways we've been able to leverage this directly.
Speaker: Ideally, the goal would be that you could come up with treatment algorithms by sky stage.
Speaker: Unfortunately, I don't think we have enough evidence yet to definitely do that.
Speaker: But I think that's what we hope for in the future.
Speaker: The idea being if you have worse shock, you need a more intensive intervention.
Speaker: This is, you know, sort of has face validity, but hasn't yet been studied.
Speaker: And I also, like you mentioned earlier, could find as an intensivist that by utilizing this classification, I can convey very clearly to a CT surgeon or an interventional cardiologist
Speaker: how sick the patient is, right?
Speaker: So if I call them, I think they have cardiogenic shock.
Speaker: Like you said, a lot of times that can mean many things for many people.
Speaker: But if I were to tell an interventional cardiologist or a CT surgeon who's involved with these type of patients, look, I mean, he was a stage C, he's moving to stage D. I think they understand, okay, we need to come to the bedside and try to figure out what we're going to do for this patient.
Speaker: Absolutely.
Speaker: You know, and some of this actually reminds me back when I was either an intern or a resident at Duke, and I had a patient who I thought had belly sepsis.
Speaker: And
Speaker: and, you know, I had looked at the SERS criteria because we, you know, did that back then.
Speaker: And, you know, the patient met SERS criteria and had suspected infection.
Speaker: And I said, this patient meets criteria for sepsis.
Speaker: They were on the ward.
Speaker: They didn't have septic shock.
Speaker: So I talked to the surgery resident and I said, look, you know, this person has, and I forget what it was.
Speaker: Maybe it was a gallbladder for the sake of discussion.
Speaker: Let's say that what it was.
Speaker: And I said, this person is septic
Speaker: You know, they have evidence of cholecystitis.
Speaker: I think that they need to go to the OR.
Speaker: And then the surgeon came by and because the patient wasn't on pressers and hypotensive and had a lactate of, you know, it didn't have a super high lactate.
Speaker: They said the patient's not septic.
Speaker: And I said, yes, they are.
Speaker: And like we, you know, we didn't get in too much of an argument, you know, but that was kind of a difference of opinion where, you know, the patient met.
Speaker: the contemporary definition of sepsis at the time, but I wasn't talking the same language as the surgeon because the surgeon didn't care about SERS criteria and other things that at the time were, you know, the things that all the residents and interns are learning.
Speaker: You know, they only viewed sepsis as septic shock and critical illness.
Speaker: And this is the same kind of an idea that if we had been talking the same language,
Speaker: it would have been easier to communicate.
Speaker: If I said, this person has sepsis without septic shock, this is why, this is what it means.
Speaker: And they said, oh, SERS criteria, of course, I understand that.
Speaker: Now we know that there's better ways to define sepsis, of course, but...
Speaker: In the context of cardiogenic shock, it's really the same type of a discussion.
Speaker: If you call up a surgeon to talk about more circulatory support in a patient who has relatively mild cardiogenic shock in the stage C spectrum who's been stabilized maybe with inotropes and vasopressors, they might see that differently.
Speaker: And they might say, oh, a person's not really in cardiogenic shock because you stabilized them.
Speaker: But if you're talking the same language and you say, I have stage C, this is what it is.
Speaker: You know, we stabilize them at stage C. They're on these therapies to keep them in stage C. You know, then they'll be expecting that when they see the patient.
Speaker: If you tell them this person's in stage E, you know, we're barely keeping them alive with aggressive therapy, you know, and I really need your help right now, then they'll know how to pace their evaluation and they'll be thinking about different
Speaker: levels of aggressiveness.
Speaker: So I think you're absolutely right.
Speaker: It's all about communication.
Speaker: Perfect.
Speaker: So could you tell us a little bit about how phenotypes play into how we think of cartogenic shock today and a little bit about prognostication, and then we can move to management?
Speaker: Absolutely.
Speaker: So phenotypes of cardiogenic shock is a complex topic that I'm really interested in.
Speaker: I got to work with kind of an all-star team to write a, you know, two paper kind of treatise on this recently that I think is an, I think it's, hopefully it's free online at Jack advances, one of the new journals, but what it comes down to is there are many different patterns that come up in large cardiogenic shock populations.
Speaker: And some of these are basic things like the cause.
Speaker: We talked about acute MI versus non, you know, versus all the other things.
Speaker: And what a phenotype means is that although the patients can be defined as having the same disease process, they look very different at the bedside.
Speaker: And that's, and that example of acute MI versus non-acute MI, those patients look and act very differently.
Speaker: They need different treatment pathways.
Speaker: Their ability to compensate and how that looks is very, very different.
Speaker: And so,
Speaker: That's one way to think about it, but there's a lot of other ways.
Speaker: And some of this, and in essence, what your purpose of defining phenotypes is will sort of help you figure out what they look like.
Speaker: So one way would be looking at the pattern of ventricular dysfunction.
Speaker: A patient with isolated left ventricular dysfunction will look and act and need treatment totally different from a person with isolated right ventricular dysfunction.
Speaker: And so you can think about it in terms of the etiology.
Speaker: You can think about it in terms of the ventricular dysfunction.
Speaker: You can also look at it in terms of hemodynamics, which may reflect, you know, is the patient vasodilated?
Speaker: Do they have right-sided or left-sided congestion?
Speaker: And that's something that's been described for many years as well.
Speaker: The really exciting aspect of phenotypes, though, is where you start getting into biomarkers and patterns of
Speaker: actual underlying pathophysiologic processes that might potentially define different treatment strategies.
Speaker: And we're at the very, very early phases of this.
Speaker: But one really exciting paper that came out a few years ago used machine learning and the admission laboratory values.
Speaker: And they said, look,
Speaker: What we do, what we're finding is patterns of laboratory values that are kind of different in three separate groups.
Speaker: And you have one group that really doesn't have a lot of laboratory abnormalities.
Speaker: And it turns out that those same patients are younger, healthier at baseline and less sick.
Speaker: Their shock is less severe and they look quite a bit different on paper than the other two groups.
Speaker: The second group is
Speaker: again, has a different pattern of laboratory values.
Speaker: In particular, they have really bad kidney function.
Speaker: And most of their other labs are not particularly abnormal, except that maybe they're more anemic and things like, you know, basic stuff.
Speaker: But they're
Speaker: population demographics in that group is quite a bit different.
Speaker: They're older, they have more comorbidities, and their hemodynamics aren't dramatically worse, but they have a lot of pulmonary congestion by comparison.
Speaker: And so they have, you know, they're congested and they have renal dysfunction and you could call them a cardiorenal phenotype.
Speaker: But then the sickest group and the most complex group have lots of extensive laboratory abnormalities.
Speaker: Their lactate's really high.
Speaker: Their kidneys are doing poorly.
Speaker: Their liver's doing poorly.
Speaker: And they have a lot of other abnormalities that go along with that.
Speaker: Their hemodynamics are terrible.
Speaker: They have a lot of right-sided congestion, which may contribute to the other organ dysfunctions.
Speaker: And then their hemodynamic compromise is worse.
Speaker: And so they were labeled the hemometabolic group.
Speaker: And so these different patterns of lab abnormalities identify groups that have other characteristics that are quite a lot different.
Speaker: And their prognosis was quite a lot different, even when you had looked at their shock severity.
Speaker: And so this is something that is really in its infancy, but it emphasizes that these different groups look different and act different.
Speaker: And it's possible that applying a treatment to one group or the other might yield a different result.
Speaker: And so the ultimate hope is that we can identify underlying disease processes in these groups or in some other way of defining the groups that allows us to select patients who are more or less likely to respond to a specific treatment.
Speaker: And so now that we're getting into some of these targeted biologics, the hope is that if you can identify a phenotype,
Speaker: that has higher low levels of a certain biomarker that then translates into a treatment either by giving back, you know, whatever that thing is, if it's too low or, you know, bringing it down, if it's too high, that that could translate into better outcomes.
Speaker: And so this is something that is extremely crude, but it mirrors what we're trying to figure out in sepsis and ARDS.
Speaker: And so we're trying to mimic the research programs that have been developed, particularly in ARDS, where they've really, I think, looked at this quite a bit and identified, for example, the
Speaker: groups within the ARDS population that are more or less likely to respond to steroids or anti-inflammatory therapies or things like that.
Speaker: And so this is a research field right now.
Speaker: It is not ready for prime time.
Speaker: It is not ready for clinical practice.
Speaker: But the hope is that in the future, if we can get this right and we can figure it out, we can then do tailored therapies, individualized, personalized medicine by defining
Speaker: a phenotype of cardiogenic shock for each patient, probably with different parameters, and then eventually link that to different treatment strategies.
Speaker: And like you mentioned, this is also being investigated in other disease processes relevant to critical care like sepsis and ARDS.
Speaker: And I think it is in its infancy, but definitely a very exciting development that hopefully will bring better therapies to the bedside.
Speaker: So with that, let's talk about therapy.
Speaker: Let's talk about management of cardiogenic shock and kind of where are we today and what's updated in this respect.
Speaker: And maybe, Jake, we can start with just early identification, which we talked already about, but how do you approach it as a clinician and your initial evaluation of these patients?
Speaker: Absolutely.
Speaker: You know, I think that the early identification is always a challenge in critical illness because most critical illness syndromes,
Speaker: although they might have a defined starting point, that occurs an unknown amount of time before you see the patient.
Speaker: So when you're dealing with acute myocardial infarction,
Speaker: It's often a lot easier to define the onset, although not always.
Speaker: You know, some people, they were fine yesterday.
Speaker: This morning, they had chest pain, clearly have an acute infarct, and you can define the time of onset.
Speaker: But, you know, unfortunately, we see a lot of people who have these subtle chest pains or they ignore it or they sit at home with it for a while.
Speaker: And you're not really sure when it actually started.
Speaker: All you know is that it's been going on for 12, 24 hours.
Speaker: And unfortunately, those are some of the folks we get who, because they didn't get treatment, end up in cardiogenic shock.
Speaker: But with some of these other things like heart failure, it is really hard to define the time of onset.
Speaker: And the harder we look at these patients, the more we realize that the time of onset is like two weeks before because they start getting a little bit congested.
Speaker: And that congestion really starts to compromise their end organs and their cardiac function.
Speaker: And then they sort of fall down this spiral of worsening hemodynamics until at some point they actually present and they're in shock.
Speaker: So early identification is tough.
Speaker: I think the key things are to recognize things that are in retrospect obvious, but recognizing at the time of.
Speaker: Patient has an elevated anion gap and, you know, check a lactate in that situation.
Speaker: Patient has, you know, for example, a heart rate that's higher than their systolic blood pressure, you know, that classic shock index.
Speaker: Even if they're not overtly hypotensive, the fact that they're having that tachycardia as compensation, think about that.
Speaker: Look at patients who are at risk, identify those stage A's and figure out among them who they're
Speaker: is actually in stage B, but you didn't realize it.
Speaker: And among those stage B's who might actually be in stage C and you didn't realize it.
Speaker: So a lot of this comes down to the bedside assessment, you know, because the truth is that the difference between a stage A, B and C sometimes is that the provider has identified that the patient is cool and modeled and has delayed capillary refill.
Speaker: You're not going to find that in a medical chart.
Speaker: You have to see the patient.
Speaker: you know, thinking, you know, checking that lactate in the, in a situation where you're have reason to be suspicious.
Speaker: You know, once you're in a position where you at least have some, you know, some idea, the kinds of things that I like to think about for the initial evaluation, because I'm a cardiologist, I obviously bring a lot of, you know, bedside cardiac ultrasound to bear.
Speaker: And the,
Speaker: There are so many things that you can look at with the bedside ultrasound that it can be hard sometimes to, you can get overwhelmed.
Speaker: And so you have to sort of do it in a focused manner.
Speaker: You know, what's the LV function?
Speaker: What's the RV function?
Speaker: Is there evidence of major valve disease that could be the cause?
Speaker: Is there evidence of a pericardial effusion that could be causing tamponade?
Speaker: And then...
Speaker: If you're facile with it, at least some assessment of the hemodynamics.
Speaker: The most important thing usually is to look at the volume status.
Speaker: Volume status by echo continues to be a bit of a controversial area.
Speaker: Simply looking at the inferior vena cava in a sort of gross way, a 2D isn't always all there is to it.
Speaker: But again, it can give you a general idea.
Speaker: Other, of course, urgent diagnostic tests you're going to think about, the 12-lead EKG, right?
Speaker: You obviously want to identify patients who have acute ischemia that might be a treatable and reversible cause of your cardiogenic shock.
Speaker: Your chest X-ray, remember the tension pneumothorax is going to mirror and mimic cardiogenic shock shock.
Speaker: very closely and can be very hard to differentiate just simply at the bedside without looking at that.
Speaker: Some patients, of course, are going to need more advanced imaging, particularly if they have RV dysfunction and thinking about pulmonary embolism or other causes of core pulmonale.
Speaker: Comprehensive laboratory workup, specifically focusing on your cardiac biomarkers and other evidence of hypoperfusion and end organ injury.
Speaker: I think with a lot of critical illness syndromes,
Speaker: you know, we, we oversimplify it, but we, you know, but it's still good to think about it in terms of ABCs and then we add deity, right?
Speaker: So airway breathing circulation, right?
Speaker: That's a, always a good way to think about your critically ill patient.
Speaker: Um, uh, and then I always think about D for damage control, which is essentially your end organ dysfunction.
Speaker: How do you reverse it?
Speaker: And then E for etiology.
Speaker: And so, you know, I, I,
Speaker: You don't always go through that in a, you know, in a stepwise sequential manner.
Speaker: You're often doing it simultaneously, thinking about, you know, multiple aspects, but you want to cover all the key management aspects there.
Speaker: Perfect.
Speaker: And obviously you mentioned you wear both hats.
Speaker: You're an intensivist and you're also a cardiologist.
Speaker: But for most non-cardiologists like myself, it is often that we get involved with these cases or we get called to the catholic because they need respiratory support.
Speaker: Could you just tell us how you think about initial respiratory support in these patients?
Speaker: Absolutely.
Speaker: You know, so as I sort of mentioned a while ago, one of the biggest things that you're going to see in patients with cardiogenic shock is pulmonary edema.
Speaker: And
Speaker: You know, that obviously can cause very severe respiratory failure.
Speaker: And of course, if you're hypoxic and having respiratory distress, then
Speaker: that added workload on your respiratory system actually can use a very sizable proportion of your cardiac output.
Speaker: And of course, if your cardiac output is low and that's the whole problem, now you're looking at giving too much, you know, uh, flow of your, you know, too much of your cardiac output to your lungs and your respiratory muscles and not to your other organs.
Speaker: So, uh, that's, you know, so respiratory support is really part and parcel of care for these patients.
Speaker: Um,
Speaker: As with any other patient, you have to use your judgment, right?
Speaker: Some of these patients, a lot of them actually are comatose after cardiac arrest, and those patients need a definitive airway.
Speaker: You know, you can't, you know, if the patient's comatose, can't protect their airway, that's kind of a no-brainer.
Speaker: But a lot of patients are in such respiratory distress that they're probably too sick for non-invasive support and they have to be intubated.
Speaker: Of course, intubating any patient who's hemodynamically compromised is, you know, risky proposition.
Speaker: These patients often will...
Speaker: have worsening hypotension after getting sedation, as many other critically ill patients with circulatory failure will.
Speaker: There haven't been any good studies, to my knowledge, about what's the optimal approach to induction of anesthesia for intubation of these patients.
Speaker: We often talk about using a hemodynamically stable agent like etomidate or ketamine, but all of the drugs that can be used
Speaker: can cause major hemodynamic compromise.
Speaker: And it hasn't been studied enough for me to say that I'm convinced that any one thing is any better than any other.
Speaker: I think the key aspect is to use the least that's possible to safely achieve whatever the plane of sedation is, to do it in a controlled manner whenever possible,
Speaker: and to be patient.
Speaker: When you give the drug, if the person has a low cardiac output, it will take longer for it to circulate and longer to get to the brain.
Speaker: And so often I'll get, you know, I've, you know, I've been in situations where the patient is clearly in distress.
Speaker: They clearly need sedation analgesia for their safety and comfort.
Speaker: And you give some, but it just doesn't work.
Speaker: And the reason is that it, that you're
Speaker: onset of drug effect is much slower than you think and then you give more and then you give more and then finally it stacks up it hits them and then you can deal with hypotension on the back end so that's something to to avoid um and i think that giving a lot of any one thing is almost certainly the wrong answer and i think that as long as you are familiar with the drugs and you're using them at the lowest effective dose
Speaker: You could probably use anything, but if you think you're going to give someone two milligrams per kilogram of propofol to intubate them and not have hemodynamic compromise, I think that's, that, that is, you know, not going to happen.
Speaker: Lower doses carefully given can be just fine, but there's those standard induction doses that you'd give to a person who's in the operating room, for example, cause usually a lot of havoc.
Speaker: But what you hope is that you don't have to intubate the patient, right?
Speaker: You hope that you can get away with non-invasive support.
Speaker: And so if a patient is, um,
Speaker: you know, as a candidate for non-invasive support, sometimes that can be really effective.
Speaker: We know that administering positive pressure can be really, really good for the left ventricle and for patients with pulmonary edema.
Speaker: Remember that positive pressure, you know, positive intrathoracic pressure, increasing that pleural pressure with CPAP or BiPAP or obviously invasive ventilation, it reduces the wall tension.
Speaker: And so it functionally reduces the preload pressure and the afterload pressure on the left ventricle.
Speaker: And so sometimes that's enough to really help the patient's ventricle.
Speaker: And there's evidence that it can actually increase cardiac output.
Speaker: So if you have a person who's not an extremist, who can protect their airway, who, you know, then who at least has some hope of oxygenating with non-invasive positive pressure ventilation, that can be really beneficial.
Speaker: beneficial in the setting of LV failure.
Speaker: The issue, of course, is that patients who have isolated RV failure, which again, usually is due to some sort of a core pulmonale situation, PE, or, you know, occasionally right ventricular infarct, those, the opposite is true.
Speaker: We know that putting a lot of positive pressure in the chest can actually, in some of those patients, compromise RV filling and increase RV afterload.
Speaker: And so when I have a patient who has, you know, critical pulmonary hypertension,
Speaker: I try at all costs to avoid intubating them.
Speaker: And indeed, I'll usually try to do Optiflow or, you know, excuse me, high flow nasal cannula.
Speaker: as an alternative to positive pressure.
Speaker: And so some of these folks, you know, they may need, you know, a non-rebreather on top of their high flow nasal cannula just to get enough oxygen.
Speaker: But if you can avoid intubation in those patients, it often is hemodynamically beneficial.
Speaker: If you're stuck and the person is failing, they're profoundly hypoxic.
Speaker: And you know, of course, that profound hypoxemia can worsen the pH state and cause them to spiral and you have no choice but to intubate them properly.
Speaker: This is one of those all hands on deck situations.
Speaker: And I always make sure that I have an airway expert with me, because even though I'm an intensivist and even though I do airways, I know that I'm not as good as some people in my hospital and I and I have to respect my limitations.
Speaker: And so I try to find the best airway person and I try to do it in the most controlled manner possible.
Speaker: If you're able to do and you have time to do.
Speaker: you know, an awake fiber optic intubation with, you know, minimal sedation and, you know, local anesthetic, that's ideal.
Speaker: Can't always do that.
Speaker: And so really doing it with the, whatever's the gentlest way possible and avoiding high pressures, avoiding, you know, hypercarbia and hypoxia and, you know, over, over pressuring during bagging are, are, are key factors.
Speaker: Perfect.
Speaker: Let's talk a little bit about hemodynamic support and obviously the three areas I would like to hear your thoughts on are invasive monitoring, vasopressors, and inotropes.
Speaker: Absolutely.
Speaker: One thing that I actually wanted to mention that's actually more important than any of this that goes sort of in your evaluation is the need for coronary angiography.
Speaker: So the only clinical trial that we have in the field of cardiogenic shock is
Speaker: that appeared to show an improvement with the treatment arm versus the standard of care arm is from 1999, the original shock study, which looked at early revascularization.
Speaker: And so one of the core tenets of cardiogenic shock care is to identify and treat acute myocardial infarction.
Speaker: And so any patient, in my opinion, who there's a chance that they have acute myocardial infarction as the driver of their cardiogenic shock,
Speaker: is a person who probably needs a coronary angiogram.
Speaker: And if they clearly have acute MI, it's an urgent coronary angiogram, you know, get it done as soon as possible, try and open up the vessel as soon as possible, you know, door to balloon, time is muscle, all those acute MI treatment mantras.
Speaker: But even patients who it's not clear whether they truly are having an acute MI
Speaker: it's still likely to be important information to know because even if they clearly have a chronic cardiomyopathy, if you don't know their coronary status, it can be harder to treat them.
Speaker: So I'm a big advocate for early coronary angiography.
Speaker: So I'm going to just put in a plug for that and we'll kind of move on.
Speaker: The key thing there is that if you do find an occluded artery, a culprit artery,
Speaker: That's what you treat.
Speaker: You don't go around looking for other things to treat.
Speaker: You don't try to fix the chronically, you know, chronically occluded or chronically stenosed other artery that's not part of the problem.
Speaker: Because we know that one of the only other randomized trials that's shown a difference in survival is looking at that multivessel PCI versus culprit PCI.
Speaker: And culprit PCI is associated with better outcomes, which is different than what we expected.
Speaker: So if you bring the person to the cath lab, find the problem and treat the problem and then move on, get them to the ICU to keep stabilizing them.
Speaker: So as we think about treatment, you have to, you know, it's all a spectrum.
Speaker: And so some of this, of course, is going to be started in the cath lab.
Speaker: In terms of invasive hemodynamic monitoring, having accurate measurement of the blood pressure is probably the most important thing.
Speaker: And so I'm a big advocate for placing an arterial line.
Speaker: I know that that hasn't been well demonstrated to improve survival outcomes in other critically ill populations.
Speaker: But in particular, patients with low cardiac output, I find that the non-invasive outcomes
Speaker: assessment of blood pressure tends to be fairly inaccurate.
Speaker: You end up with these frequent blood pressure checks that lead to these numbers that are kind of nonsensical.
Speaker: And so I think measuring it invasively is a pretty easy and straightforward thing that I think is important to do early on in the process.
Speaker: The more complex question is whether these patients all need a pulmonary artery catheter.
Speaker: So as a cardiologist, as a critical care cardiologist, I am very familiar and comfortable with the pulmonary catheter.
Speaker: I do it a lot.
Speaker: You know, it's, you know, generally a quick and easy procedure in experienced hands.
Speaker: But we do know that it's been it's been unproven to to improve survival outcomes, you know, in any trial that has previously been done.
Speaker: Part of that, of course, is that they never looked at cardiogenic shock patients because everyone assumed that they weren't safe to randomize.
Speaker: And there is a randomized trial going on now that's actually trying to answer this question, so that'll be helpful.
Speaker: I think that the time when you need a pulmonary artery catheter is when things aren't going according to plan or you don't know exactly what's going on.
Speaker: So if you have an accurate evaluation of the patient's blood pressure,
Speaker: You have some way to evaluate the patient's cardiac output and its effect on the end organs.
Speaker: And you have a general idea of what is the hemodynamic phenotype you're dealing with, meaning is it a right ventricular problem, a left ventricular problem, or both?
Speaker: Does the patient have abnormal vasodilation?
Speaker: If you can figure all those things out with less invasive means, I'm not convinced that a pulmonary artery catheter adds much.
Speaker: However, it can be very difficult to figure things out with less invasive means, and so
Speaker: The reason that the pulmonary catheter is the gold standard is because it is the way to directly measure these things and figure them out.
Speaker: So I tend to place a PA catheter early.
Speaker: I have a bias towards that.
Speaker: When this randomized trial, the PACCS trial comes out, if it shows that that's not a necessary strategy, I'll probably have to change my practice.
Speaker: But until then, I am more likely to do a PA catheter than not.
Speaker: And
Speaker: I feel strongly that a PA catheter should be placed when things aren't going well.
Speaker: So if I have a patient, I start them on appropriate therapies and their lactate gets better, their urine output gets better, you know, their creatinine is starting to come down, everything looks good, then I actually, you know, might choose not to place a pulmonary artery catheter.
Speaker: I might say, you know what, this is treatment success.
Speaker: Let's let the dust settle and, you know, see if we can avoid an extra invasive procedure.
Speaker: But if I put the patient on inotropes and vasopressors, which I'll obviously get to in a second, and the doses are going up and the lactate's not getting better, and I'm not really sure what's going on, particularly whether I'm thinking about mechanical circulatory support, gosh, that's a time where I really need to know what I'm working with.
Speaker: And I will pretty much always want to place a pulmonary artery catheter in a patient like that as I'm looking forward to mechanical circulatory support, which I'll get to later.
Speaker: So, so thinking about the medical therapy of cardiogenic shock, which quite frankly, we haven't proven yet that anything's better than that.
Speaker: Um, and so therefore currently standard of care is medical therapy.
Speaker: And so I personally start with vasopressors because I believe that critical hypotension is the primary problem.
Speaker: If your blood pressure is too low, your organs cannot auto regulate.
Speaker: They're going to get hypoperfused regardless of your cardiac output.
Speaker: And even worse, your heart may become hypoperfused and may get stunning from global ischemia just driven by hypotension.
Speaker: So getting the patient's blood pressure up is the key priority.
Speaker: And so the question is, how do you do this most effectively and most safely?
Speaker: And now let's be clear.
Speaker: No one knows what the proper blood pressure goals are for patients with cardiogenic shock.
Speaker: I typically would say a map of 65 is probably...
Speaker: reasonable like we would for most patients.
Speaker: Some patients, you might be a little bit more liberal and go sort of 60 to 65.
Speaker: But the key is to do it safely, which means using the minimum dose of whatever vasopressor you're using and to try and use vasopressors with a better safety profile.
Speaker: So for many years, we assumed that because cartaginous shock is a low output state that we had to use drugs as vasopressors that had inotropic properties.
Speaker: And so we always so the guidelines for many years said you use dopamine.
Speaker: which has very powerful beta agonist activity at adrenergic beta receptors that increases heart rate, cardiac output, stroke volume, all those things.
Speaker: And so we thought that you had to do that because you had to raise the cardiac output.
Speaker: But it turns out that at the doses that are required for vasopressor effects –
Speaker: Dopamine causes horrendous toxicity, particularly in patients with cardiogenic shock.
Speaker: And the real issue is arrhythmias.
Speaker: And so a sick heart with cardiogenic shock is going to be extremely prone to arrhythmias.
Speaker: If the patient develops an arrhythmia, it can be fatal or can really compromise their cardiovascular function.
Speaker: And so the SOAP2 trial, which Daniel DeBacker did, showed that dopamine is more toxic and potentially harmful compared to norepinephrine, which was kind of your standard approach.
Speaker: So then they said, well, maybe dopamine is an outlier.
Speaker: Maybe it's maybe it's, you know, maybe epinephrine, which is a little bit more direct.
Speaker: And maybe that's better.
Speaker: Turns out, no, it's not.
Speaker: The data looking at epinephrine and cartagenet shock are not as don't have the same numbers, but the signal is exactly the same.
Speaker: That.
Speaker: It turns out if you give someone with cardiogenic shock lots of epinephrine versus norepinephrine, what you mostly see is a dramatic increase in their heart rate.
Speaker: But their cardiac output doesn't change all that much because the stroke volume doesn't really go up because the stroke volume is as high as it can be and you just see tachycardia.
Speaker: And importantly, you see more arrhythmias, more toxicity and more bad outcomes.
Speaker: So epinephrine is not a great option either.
Speaker: So based on those studies, I would say that norepinephrine is the safest option.
Speaker: first line drug as a vasopressor for cardiogenet shock, and that's where I start.
Speaker: I start norepinephrine.
Speaker: I figure out what's the lowest dose that will get me to an adequate mean arterial pressure to support the organs.
Speaker: I try to avoid overtreatment, and that's kind of my first line approach.
Speaker: The other vasopressors that we'll use in sepsis that are primarily vasoconstrictors and don't have any inotropic properties, drugs like vasopressin and phenylephrine, I generally don't use because they're well known to lower the cardiac output.
Speaker: And so those aren't drugs that I tend to use as a first line.
Speaker: That being said, if you're in an emergency situation, you have to use what you've got.
Speaker: And so if you have no choice but to use, for example, boluses of phenylephrine for a patient who's in carotid G shock and their blood pressure is crashing, you can try it.
Speaker: But I typically don't find that it's particularly effective because it raises the systemic vascular resistance, which presumably is already high in that setting.
Speaker: So once I have started norepinephrine and I have it at an adequate dose to get a reasonable blood pressure,
Speaker: Then I'll usually add an inotrope to try and increase the cardiac output with the primary goal of reversing end-organ hypoperfusion.
Speaker: So although it's logical to titrate whatever your inotrope is to normalize the cardiac output, the fact is there's no such thing as a normal cardiac output.
Speaker: There's only a cardiac output that's either adequate to meet the metabolic demands of the body or one that's inadequate.
Speaker: And of course, if you h ave a patient who's septic, that'll be different than a patient with cardiogenic shock versus a patient who's, you know, totally intubated, intubated and totally relaxed with neuromuscular blockade.
Speaker: So really, I try to focus on the end organ perfusion to lactate, urine output, clinical exam.
Speaker: So if I start a patient on an inotrope and those things get better and get back to normal,
Speaker: and then I measure the cardiac output and realize that it's still low, I actually might not worry about it.
Speaker: I might say, you know what, that's fine.
Speaker: On the other hand, if all those variables aren't better, then I measure the cardiac output, realize that it's low, then I might go up on that inotrope to try and get those end organ markers better.
Speaker: Tricky situation, of course, is if the cardiac output looks normal and the end organ perfusion looks bad.
Speaker: And then you have to decide, is raising the blood pressure going to help?
Speaker: Is raising the cardiac output further going to help?
Speaker: And there's a little bit of trial and error involved.
Speaker: The question is, what inotropes should you use?
Speaker: Well, the best quality data that we have comes from the DoReMi study, where they compared dibutamine and milrinone and basically found them to be completely equivalent.
Speaker: Now, my personal bias is towards Dubutamine because it has better pharmacokinetics.
Speaker: It kicks in faster.
Speaker: It has a faster onset and allows you to titrate it more rapidly to get the perfusion and cardiac output back towards where they need to be sooner.
Speaker: So that's my bias, as I prefer that.
Speaker: But Milrinone is a perfectly good drug, particularly if you're in a situation where the degree of end-organ hypoperfusion is a little bit less critical and you have a few hours to let the drug build up and take effect.
Speaker: Now, an interesting thing that people don't talk about enough, but is an unknown answer is what about low doses of dopamine or low doses of epinephrine?
Speaker: You know, if I'm using high doses of dopamine, I know it's toxic, I know it's harmful.
Speaker: But what about those low doses, like two to five mics per kilo per minute?
Speaker: I will use that sometimes if, for example, dobutamine causes the patient to vasodilate too much.
Speaker: I might switch over to dopamine and see if it can get me that inotropic effect without the vasodilation.
Speaker: But it doesn't work quite as well as dobutamine, so I don't use it as first line.
Speaker: And epinephrine, again, same logic.
Speaker: Again, 0.0 something, 0.02, 0.05 of epinephrine sometimes can give you that inotropic effect without causing a ton of toxicity.
Speaker: So those are alternative agents that haven't really been well studied, but I will use them sometimes if I'm dealing with a mixed cardiogenic vasodilatory problem.
Speaker: Perfect.
Speaker: Interestingly, one last thing I would mention is there is a randomized trial trying to decide if
Speaker: inotropes added to vasopressors even have any advantage.
Speaker: And so we'll see that's the do re mi to study.
Speaker: And we'll see if that actually see what that happened, what that result turns out to be.
Speaker: So I think it's going to be thought provoking either way.
Speaker: But I think, like you mentioned, a couple of important points to reemphasize.
Speaker: First is that as we go to the next stage of therapy, which is mechanical circulatory support, the truth is that with the evidence that's available right now, focusing on our medical therapy is probably the most important thing that we should all be doing, right?
Speaker: I mean, regardless of what's next,
Speaker: We got to get that as good as we can for each individual patient.
Speaker: And like you mentioned, Jake, I think it's understanding what is safest, understanding what likely is going to help, but not being living and dying by the numbers, but really assessing the whole patient and the impact of our therapy on every marker that we have to our disposal to try to figure out are we making an impact on that patient or not.
Speaker: Absolutely.
Speaker: And, you know, I actually put more stock in the venous oxygen saturation than the cardiac output anyways, because that at least gives me some idea of what the supply-demand balance is for the patient, recognizing that venous oxygen saturations have numerous caveats that you always have to think about.
Speaker: So you alluded to mechanical circulatory support, and this is, of course, the most exciting aspect of the care of patients with cardiogenic shock.
Speaker: The
Speaker: The premise behind mechanical circulatory support is very sound.
Speaker: You have a condition where low cardiac output is the problem.
Speaker: You have evidence that inotropes and vasopressors can cause major, potentially life-threatening toxicity, and also in many cases are not effective.
Speaker: So how can you restore adequate cardiac output to the organs to get them to recover if the drugs you're using are
Speaker: aren't doing it?
Speaker: And the answer obviously would be mechanical circulatory support.
Speaker: And we've had mechanical circulatory support in the form of a balloon pump for like pushing 50 years, I think.
Speaker: The problem is, is that we have been uniformly incapable of demonstrating that mechanical circulatory support improves survival when compared to medical therapy alone.
Speaker: And this was, we showed this in 2012 with the balloon pump.
Speaker: And then more recently with ECMO.
Speaker: So at the European Society of Cardiology meeting this week, they presented the results of the ECLS shock trial, which is the largest and most rigorously performed study examining advanced mechanical circulatory support in patients with cardiogenic shock.
Speaker: It was more than 400 patients.
Speaker: They all had acute MI and were getting revascularized, and they couldn't find any benefit whatsoever
Speaker: of early ECMO versus medical therapy alone.
Speaker: And so I think that this is an area where we as a field need to really think about and make sure that we draw the right conclusions.
Speaker: And it's all about tailored therapy.
Speaker: So it's not about do the same thing to everybody.
Speaker: It's identify patients who are likely to benefit from the therapy and
Speaker: and then apply the right therapy tailored to who that patient is, what their hemodynamics are, what their phenotype is, et cetera.
Speaker: And so the key here is to do this in a multidisciplinary way.
Speaker: So this is not just me standing there at the bedside by myself and saying, gosh, let's do this.
Speaker: This is me collaborating with, you know, potentially a heart surgeon, a heart failure transplant cardiologist, and, you know,
Speaker: potentially other team members to really think about where is this patient in their shock journey?
Speaker: Where is this patient in their overall heart related health journey and what options are realistic for them?
Speaker: What outcomes are realistic for them?
Speaker: What type of a device would be adequate to meet their needs?
Speaker: And are they a candidate for that device?
Speaker: And there's a lot of data points that can swirl into this and doing it in an algorithmic manner is a bit tough, which is why doing it as a shock team approach is probably the most important.
Speaker: And one of the key things that we always have to think about is, OK, so how are we getting this patient off temporary mechanical support?
Speaker: So a key factor that people sometimes forget about is that MCS is nothing more than a bridge.
Speaker: You're taking a patient from a terrible situation, you know, bad cardiogenic shock, and you're bringing them to something hopefully better.
Speaker: In an ideal situation, it's recovery of myocardial function and liberation.
Speaker: But in many cases, it's, you know, transition to either a durable mechanical support device like an LVAD or maybe heart transplant.
Speaker: And particularly with the increasing prevalence of heart failure related cardiogenic shock, patients with end stage cardiomyopathy,
Speaker: you know, the exit strategy is crucially important.
Speaker: And so I think that being a candidate for advanced therapies is probably the most important variable that predicts outcomes, you know, favorable outcomes in cardiogenic shock.
Speaker: You have a patient who's
Speaker: not going to be a candidate for advanced therapies due to age comorbidities or other factors, that's a person who's very, very likely to have a bad outcome.
Speaker: On the other hand, you have a person who is a candidate for those therapies and has an exit strategy.
Speaker: They're much more likely to do well because if they don't recover, they have somewhere to go.
Speaker: So in terms of the evidence, there is no evidence that says that any individual patient must or must not receive any specific device.
Speaker: And so this is where your clinical judgment comes in.
Speaker: I think that using invasive hemodynamic data is important because if you find that the patient has isolated right ventricular failure, putting in a left ventricular assist device won't help them.
Speaker: Likewise, if the patient has isolated left ventricular failure,
Speaker: probably all you need is a left ventricular assist device.
Speaker: The key factor being if they have horrendous pulmonary failure, then they may need pulmonary support as well.
Speaker: So in terms of the different devices we use, the balloon pump is the most commonly used.
Speaker: It's cheapest, it's smallest, it's safest.
Speaker: It doesn't do much.
Speaker: It probably has better effects in patients with chronic cardiomyopathy
Speaker: In them, you can see an average increase in cardiac output in the 0.5 to 1 liter range.
Speaker: And a pretty sizable number of patients will have some increase in cardiac output, and some people will be super responders who really get a lot better.
Speaker: In the setting of acute MI, it's not really clear if a balloon pump improves hemodynamics meaningfully more than medical therapy alone.
Speaker: The one exception being that if someone has mechanical complication like ventricular septal rupture or mitral valve rupture, we think that the balloon pump
Speaker: And the key way that the balloon pump actually works is by offloading the ventricle.
Speaker: So it's the only therapy that will raise the blood pressure and simultaneously lower the LV afterload because it dissociates those two things, which is good, but of course will be less useful if someone's requiring lots and lots of vasopressors and has high peripheral vascular tone because of that.
Speaker: So when do I use the balloon pump?
Speaker: Well, I probably use it a bit more than I should, given the limited evidence base and the lack of benefit demonstrated in acute MI patients.
Speaker: I will use it in patients who have no other option.
Speaker: I'll use it as a therapeutic trial if I don't think it's going to hurt the patient, or I'll use it if the patient has, and this is acute MI specifically, or I'll use it in a patient with a mechanical complication.
Speaker: If the I'm much more likely to use it in patients with milder forms of shock, if you're already on three pressers, there's no reason to think the balloon pump and its modest hemodynamic effects are going to be the answer.
Speaker: But if the person's maybe on a little bit of something, and I think that that getting them off that would be advantageous because maybe it's causing toxicity, then I'll try it.
Speaker: On the other hand, for patients with heart failure, cardiogenic shock, we're much more liberal with balloon pumps.
Speaker: And if you have the ability to place them via an axillary approach, which requires a skilled hand, then it's actually very advantageous because the patient can remain ambulatory as a sort of a bridging strategy to the next step.
Speaker: So the key thing is,
Speaker: When a person is doing well on vasopressors and inotropes, I'm not usually thinking about MCS.
Speaker: But if the patient is having toxicity or failure to achieve hemodynamic goals, then I am.
Speaker: Now, the more advanced devices would be percutaneous ventricular assist devices.
Speaker: So the most commonly used is the impella device, which the most commonly used one is a left ventricular device.
Speaker: There's also right ventricular device.
Speaker: There's a couple sizes.
Speaker: The key thing with these devices is they definitely have more horsepower and they definitely will improve hemodynamics to a greater extent than the balloon pump.
Speaker: The incremental benefit and the added effect depends on what device you use and a lot of other factors.
Speaker: The problem is that because these are larger, the risk of complications is substantially higher.
Speaker: And that's been convincingly and consistently demonstrated that these devices definitely cause more complications than a balloon pump.
Speaker: The problem is that the evidence base supporting the efficacy of these devices for improving outcomes is really thin.
Speaker: There's some small trials, none of which have shown a consistent benefit for improving survival.
Speaker: So these devices, again, have to be thought of in a comprehensive strategy of person is doing badly on medical therapy.
Speaker: If we can stabilize their hemodynamics and recover their organs, they are likely to be a candidate for recovery or advanced heart failure therapies, transplant VAD.
Speaker: In that situation, it's reasonable to try one of these, you know, one of these percutaneous vads.
Speaker: But you have to respect the fact that the risk of complications is can be very substantial, particularly when being done in situations where the level of experience is fairly low.
Speaker: Now, the higher highest level of support is ECMO.
Speaker: And ECMO is an amazing device.
Speaker: It can provide full cardiac support, full pulmonary support.
Speaker: You can use it in patients who are in cardiac arrest and preserve and restore their organ function.
Speaker: It's very, very impressive.
Speaker: And so if a person has refractory circulatory failure that doesn't respond to anything else, ECMO is pretty much your only option, assuming low cardiac output is the problem.
Speaker: It can be used for left ventricular support, right ventricular support, biventricular support, as well as heart and lung support.
Speaker: So many institutions are using ECMO as a default for any bad cardiogenic shock case because the acquisition cost of the different parts, the disposables, is less than for most percutaneous VADs, which tend to be fairly expensive.
Speaker: The problem is we have yet to prove that using ECMO as a routine strategy improves survival.
Speaker: That's that new study, and again,
Speaker: prior smaller studies have been shown the same results.
Speaker: And there's definitely an increased risk of complications with ECMO.
Speaker: You know, ECMO, particularly when done in lower volume centers or less experienced hands, a lot of things can go wrong.
Speaker: Even with very experienced centers, you know, the need for vascular repairs and things is fairly frequent.
Speaker: So in my practice, I
Speaker: still believe that appropriate application of these devices can be beneficial, even if they're not appropriate for all patients.
Speaker: But I really try to be selective and think about patients who have a next step option.
Speaker: And so if I have somebody who looks like they might be a candidate for VAT or transplant, even if I don't know for certain, I call that bridge to decision and I feel comfortable thinking about doing mechanical circulatory support in kind of a tailored way.
Speaker: you know, based on what the patient's hemodynamic needs are and their hemodynamic phenotype.
Speaker: At my center, we tend to do, we have a surgeon who's very experienced in doing the larger bore surgical access Impela 5.5 device.
Speaker: So for patients with isolated or predominant LV failure as a bridge, we have been doing that more often.
Speaker: It tends to work well in the right patients.
Speaker: A lot of other patients end up getting ECMO.
Speaker: Um,
Speaker: ECMO has a lot of important advantages and disadvantages that are probably, you know, a bit outside of the scope of this discussion.
Speaker: There are a lot of novel approaches to ECMO that allow you to unload the left ventricle, which are very potentially advantageous.
Speaker: But again, it's all about, is the patient likely to do well enough with medical therapy, in which case don't bother with the mechanical support, or is the patient likely to be a candidate for an advanced therapy where, you
Speaker: making sure that they have adequate hemodynamic support becomes your highest priority to avoid end organ failure that would, you know, preclude next steps.
Speaker: And I think, Jake, that...
Speaker: Two of the most important aspects of the discussion on mechanical secretarial support is the need to have a multidisciplinary approach.
Speaker: And I would encourage our critical care colleagues to lean in and participate because we do have things to add from more of a holistic view.
Speaker: I can see how the interventional cardiologist with the patient on the table or the CT surgeon who did a procedure,
Speaker: might have, obviously, for the right reasons, a biased view of what needs to be done, right?
Speaker: And I think that being part of that discussion and trying to tailor that to the individual patient is extremely important.
Speaker: But also the exit strategy, and you mentioned just to reemphasize that,
Speaker: sometimes um decision timing is a is an exit strategy right somebody you're not sure or you might think there might be some stunning or some reversibility giving that patient a bit of time in the right context and with the right discussion is also part of that decision uh for for exit strategy and in addition i guess it would be a destination therapy or a transplant as the other big bridges right
Speaker: Absolutely.
Speaker: You know, one of the things that I personally struggle with is anticipating which patients will have myocardial recovery and when that may occur.
Speaker: A lot of patients with acute myocardiogenate shock have sort of acute on chronic ischemia, and their heart sometimes acts more like a hibernating myocardium than sort of acute ischemia.
Speaker: And the reason that that matters is that hibernating myocardium
Speaker: often has incomplete recovery and it can be delayed by weeks to months.
Speaker: And so if you revascularize somebody and you are planning on supporting them for a week to see if they recover, that only makes sense if the thing you revascularized is likely to recover in a week.
Speaker: And
Speaker: I'm not personally familiar with a lot of literature looking at this in the setting of cardiogenic shock.
Speaker: It's much more well-defined in chronic cardiomyopathy or clear acute MI.
Speaker: And so it remains an area of controversy and uncertainty.
Speaker: And I've, I've been in situations where, you know,
Speaker: you have to ask, are we really going to support this person for a month?
Speaker: Is that a logical thing for them knowing that after a month they may be in the exact same spot?
Speaker: And that's, that's why those multidisciplinary teams are so crucial because I don't, I don't know all there is about chronic cardiomyopathies, but my heart failure colleagues, they might.
Speaker: And, and working with them is going to be much better than just trying to figure it out all on my own.
Speaker: For sure.
Speaker: And I think that as you said, Jake, this is really a evolving and dynamic field.
Speaker: A lot of very interesting trials on their way.
Speaker: So definitely we'll love to have you back when those come out and we can talk in more detail about what we've learned.
Speaker: I think there's some of these topics that we could take on their own for another hour.
Speaker: But really, I appreciate the comprehensive overview that you've provided.
Speaker: Is there anything else you want to add to the topic of cartagenic shock before we go to our closing questions?
Speaker: You know, one of the things we talked about in the paper that you referenced that is always challenging is right ventricular predominant shock.
Speaker: In my experience, patients with, you know, critical pulmonary hypertension progress to cartagenic shock are some of the most
Speaker: quite frankly, terrifying patients to care for because very small perturbations in the wrong direction can make them, you know, spiral down and crash in sometimes irrecoverable ways.
Speaker: I think what's really interesting about these patients is that
Speaker: You know, we spend all of our time thinking about left ventricular preload, left ventricular afterload, all these things.
Speaker: And those are completely irrelevant for these patients.
Speaker: They need you need to think about RV afterload.
Speaker: And so, you know, I talked a little bit about the respiratory therapy side of it and ventilation.
Speaker: But, you know, there's a lot of very unique drugs and now an expanding number of drugs that can be used for these patients.
Speaker: I think the key thing is to lower the RV afterload.
Speaker: after load.
Speaker: And there's a lot of ways to do that in a, in a, you know, hyper emergency.
Speaker: Sometimes inhaled nitric oxide is the quickest thing you can do before you start thinking about some of these more complex pH therapies, making sure that we don't harm the patient, right?
Speaker: If you have high ventilator pressures and things like that, sometimes that can, you know, make things worse rather than better.
Speaker: A lot of these patients will need some sort of inotropic support.
Speaker: Milrinone tends to work well in this situation because it can have a little bit of pulmonary vasodilation, which is nice.
Speaker: Supporting the systemic blood pressure, sometimes we'll use vasopressin for these patients because it tends not to constrict the pulmonary vessels.
Speaker: So the combination of milrinone and vasopressin we often talk about.
Speaker: And then really trying to optimize the RV volume status.
Speaker: The RV is funny, and a normal RV and a sick RV behave very differently.
Speaker: So if you have a sick, chronically diseased, or acutely injured RV, it's going to need a little bit higher filling pressure than normal.
Speaker: to function properly.
Speaker: So if a patient who has, you know, RV predominant shock has a central venous pressure of three, that's probably not enough for them and they may need some volume back.
Speaker: Although in my experience, most of these patients are already volume overloaded and the problem is the opposite, which is if you have, if you over distend the RV with fluid, it loses the mechanical advantage and stops working as well.
Speaker: And so actually you may be in a situation where you diurese the patient
Speaker: to bring their filling pressure back down to like the low teens, the 10 to 12 range is often optimal.
Speaker: And you're diuresing them while they're on pressers.
Speaker: And in some of these patients, that actually gets them a lot better.
Speaker: And so I think these patients are very, very challenging.
Speaker: I tend to put a pulmonary artery catheter in all of these patients.
Speaker: And because as you monitor them, you know, sometimes...
Speaker: Having the pulmonary artery pressure go up or down gives you a clue to what else is going on because one of the first things that will change that is the cardiac output.
Speaker: So if I have a person who has pulmonary hypertension and RV predominant shock and I think they're getting worse and I see their pulmonary artery pressure go down, I sometimes view that as an alarm signal that their cardiac output is dropping.
Speaker: Likewise, if I put them on inotropes and their pulmonary artery pressure goes up, sometimes I actually view that as a win because now their RV is able to generate more pressure.
Speaker: But these patients are super complicated, super interesting.
Speaker: And you can actually get this phenotype, as you know, from ARDS with, you know, with true core pulmonale.
Speaker: And that is a uniquely complex challenge.
Speaker: But I think...
Speaker: You know, with a sort of systematic approach and a very thoughtful approach, you know, you can bail these patients out and have some fairly dramatic turnarounds because as the RV starts to get better, sometimes it progressively just gets, you know, a lot better through like an upward spiral as you do all the right things.
Speaker: I think that's a, and thanks for covering that as well, because you are right.
Speaker: You do touch that in the paper.
Speaker: And I think it's a very specific type of patient, but that they pose significant challenges for management and not recognizing them.
Speaker: We can, a lot of times cause harm with our usual approach.
Speaker: So thanks for covering that.
Speaker: So we'd like to finish the podcast, Jake, with asking some questions unrelated to the clinical topic that kind of tap into your wisdom.
Speaker: Would that be okay?
Speaker: Okay.
Speaker: Um, if I have any left, I'll be happy to share it.
Speaker: So the first question relates to books.
Speaker: Are there any books that have influenced you significantly or books that you have gifted often to other people?
Speaker: Yeah.
Speaker: So this is, I love to read and I read a lot.
Speaker: Um, a lot of the stuff that I read is, is of course, you know, has a limited nutritional value, so to speak.
Speaker: Um, you know, one of the, you know, so I, I have a son and he's 12 and so he's starting to read, uh, Tolkien, uh,
Speaker: And so one of the books that I, you know, that he's reading now is The Hobbit.
Speaker: And so I'm really trying to get him to read the Lord of the Rings series because I actually thought that was dramatically better than The Hobbit.
Speaker: So that would be more of a fun and enjoyment reading, you know, something I really like to do outdoor stuff and the way that Tolkien describes the environment.
Speaker: you know, even though it's obviously fantasy, I think it really resonates with me about how important preserving our natural environment is.
Speaker: And, you know, as an outdoors person really resonates with me a lot.
Speaker: From the standpoint of sort of professional related reading, I think one of the books that impacted me a lot was The House of God.
Speaker: And I think that there's a lot of, quite frankly, a lot of bad stuff in that book.
Speaker: But what I think it
Speaker: helps me understand is that a lot of the struggles that I've felt as a physician in the modern healthcare system are not new.
Speaker: They've been around for a long time.
Speaker: And I think that the ways that the author deals with them in that book are pretty dysfunctional and give me insights about kind of what to avoid.
Speaker: And, you know, I think
Speaker: And so that is sort of a counterexample of what not to do.
Speaker: But it really emphasizes for me that being compassionate is so important and is the core of what makes a good physician.
Speaker: And as an intensivist, dealing with death a lot, finding ways to
Speaker: maintain my own inner strength in the face of that potential despair is, you know, very challenging.
Speaker: And I think with the burnout that a lot of us struggle with, I think it's really important to remember that it that if you let it get you, it can you know, it can get very bad.
Speaker: Absolutely.
Speaker: And I think that we'll reference all these books.
Speaker: And it's interesting because the House of God, obviously, is a book that maybe younger generations have not encountered.
Speaker: But you're right.
Speaker: It has a lot of themes that are relevant today.
Speaker: Right.
Speaker: So none of these challenges are brand new.
Speaker: As a lot of times we tend to think.
Speaker: that it's all about this year or last year, right?
Speaker: Post COVID or they've been around for a long time.
Speaker: So definitely we'll reference all those books and the show notes.
Speaker: The second question relates to what is something that you believe to be true in medicine or life that other people don't believe or act as they don't believe.
Speaker: You know,
Speaker: I think the, this is going to be a bit dark and I hope you'll see why.
Speaker: I think that a lot of people forget that death is inevitable for all of us.
Speaker: And as physicians, sometimes the only control we have is how the patient's experience of death goes.
Speaker: And this is essentially allowing a death with dignity, you know, a humane death for patients who are
Speaker: you know, aren't, aren't going to make it.
Speaker: And I think as someone who deals with death a lot in my practice, I really try to advise families that if we're at a situation where, you know, death becomes imminent and, and inevitable, um,
Speaker: that sometimes our best option is to focus on dignity and comfort to allow someone to pass away in the way that they want, rather than to try to struggle and fight to get the last few days or last few hours or last few minutes of unpleasantness when things become inevitable.
Speaker: And I think that for a critical care audience, this is always an important reminder
Speaker: And something that we tend to understand, I believe, Jake, a little bit better than some of our colleagues in other specialties.
Speaker: And I think that there are two important things to take home here.
Speaker: One is that we can help others in medicine understand this.
Speaker: But most importantly, like you mentioned, there is always something that is within our control that can make the life of a patient and their family a little bit better.
Speaker: And in these circumstances, I think more than ever, we need to be at the bedside and help this natural stage of life be as dignified as possible.
Speaker: So absolutely, I love that.
Speaker: And I think it's a great answer.
Speaker: The last question relates to what would you want everybody listening to us today to know could be a quote, a fact or a thought.
Speaker: So there was a quote painted on the wall of one of the intensive care units at Pitt where I did fellowship.
Speaker: And I honestly forget the attribution, but essentially the paraphrase is, the job of the physician is to entertain the patient while nature cures the disease.
Speaker: I probably misquoted it, but I think the sentiment is there.
Speaker: Many things that we do as physicians, we feel are going to imminently change the disease state.
Speaker: And sometimes that is true and sometimes that is not true.
Speaker: And I think we have to have humility to realize that so much of what drives our patients good or bad outcomes is out of our hands.
Speaker: And it has a lot to do with their remaining inherent capacity to recover.
Speaker: And our job in the ICU is to create a state where the patient has a chance to recover.
Speaker: And that's particularly true for cardiogenic shock, where we basically have failed to demonstrate
Speaker: that any individual therapy applied routinely to all patients improves survival.
Speaker: So that doesn't mean that what we do isn't valuable.
Speaker: It doesn't mean that trying different things to help the patient is futile, but it does mean that we have to have the humility to realize that some of our patients are going to get better no matter what we do, and some of our patients are going to get worse no matter what we do.
Speaker: And we just have to make sure that we don't impede the healing process of
Speaker: You know, by doing things that are not necessary or not appropriate or not beneficial.
Speaker: And, you know, we have to treat ourselves with empathy if despite our best efforts, all the best care we can provide, you know, the patient is one of the unfortunate somewhere in one in every three people that doesn't survive cardiogenic shock.
Speaker: I think this is a perfect place to stop.
Speaker: Once again, Jake, I really want to thank you for sharing your expertise with us and giving us your time.
Speaker: And I look forward to having you back on the podcast.
Speaker: Maybe when some of these trials give us a shed some light on the way forward.
Speaker: And thank you again.
Speaker: Well, it was my pleasure.
Speaker: Sorry, I'm a bit long winded, but hopefully hopefully chock full of information for the interested audience.
Speaker: Absolutely.
Speaker: Thank you.
Speaker: You're very welcome.
Speaker: My pleasure.
Speaker: Have a good day.
Speaker: Thank you for listening to Critical Matters, a sound podcast.
Speaker: Make sure to subscribe to Critical Matters on Apple or Google Podcasts and share with your network.
Speaker: Sounds transforming the way critical care is provided in hospitals across the country.
Speaker: To learn more, visit www.soundphysicians.com.
