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Cardiogenic Shock Update
22 Plays2 years ago
In this episode, Dr. Zanotti discusses advances in the management of cardiogenic shock. His guest is Dr. Jacob Jentzer, 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, MN. As the Director of Cardiac Intensive Care Unit Research at Mayo Clinic, he is active in Intensive Care Unit patient outcomes research, with a particular focus on the outcomes of patients with cardiogenic shock and cardiac arrest.
Additional Resources
Concise Definitive Review: Advances in the Management of Cardiogenic Shock. Jentzer JC et al. Crit Care Medicine 2023: https://pubmed.ncbi.nlm.nih.gov/37184336/
SCAI clinical expert consensus statement on the classification of cardiogenic shock. Baran DA, et al.: https://www.ncbi.nlm.nih.gov/pubmed/31104355
SCAI stages of cardiogenic shock stratify mortality risk. Jentzer JC et al.: https://www.ncbi.nlm.nih.gov/pubmed/?term=SCAI+stages+of+cardiogenic+shock+stratify+mortality+risk
Advances in the Staging and Phenotyping of Cardiogenic Shock: Part 1. Jentzer JC, et al. JACC Advances 2022: https://www.jacc.org/doi/10.1016/j.jacadv.2022.100120
Machine Learning Approaches for Phenotyping in Cardiogenic Shock and Critical Illness: Part 2. Jentzer JC, et al. JACC Advances 2023: https://www.jacc.org/doi/10.1016/j.jacadv.2022.100126
Extracorporeal Life Support in Infarct-Related Cardiogenic Shock. ECLS-SHOCK Investigators. New Eng J of Med 2023: https://pubmed.ncbi.nlm.nih.gov/37634145/
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Transcript
Introduction to the Podcast and Host
00:00:06
Speaker
Welcome to Critical Matters, a sound podcast covering a broad range of topics related to the practice of intensive care medicine.
00:00:14
Speaker
Sound provides comprehensive critical care programs to hospitals across the country.
00:00:19
Speaker
To learn more about our programs and career opportunities, visit www.soundphysicians.com.
Introduction to Dr. Jacob Jenser
00:00:26
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And now, your host, Dr. Sergio Zanotti.
00:00:34
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Cardiogenic shock represents a final pathway for many patients with cardiovascular disease.
00:00:39
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It is an important reason for admission to the intensive care unit, and although its mortality has improved over time, it still remains high.
00:00:47
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In this episode of the podcast, we will discuss advances in the management of cardiogenic shock.
00:00:52
Speaker
Our guest is Dr. Jacob Jenser.
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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.
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He's the director of cardiac intensive care unit research at Mayo Clinic.
00:01:07
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He is active in cardiac intensive care unit and looking at outcomes of patients with cardiogenic shock and cardiac arrest.
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Dr. Jenser has numerous publications, including a recent concise definitive review in critical care medicine entitled Advances in the Management of Cardiogenic
Advances in Cardiogenic Shock Management
00:01:25
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Shock.
00:01:25
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Jake, welcome to Critical Matters.
00:01:28
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Thank you.
00:01:28
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It's terrific to be here.
00:01:30
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Well, like I said at the beginning, we were talking ahead of time.
00:01:34
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This is obviously a topic you're very passionate of.
00:01:38
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You work exclusively in a cardiac unit.
00:01:43
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You dedicate a lot of your time to studying cardiogenic shock and treating patients with cardiogenic shock and advanced patients.
00:01:49
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support for cardiogenic shock.
00:01:51
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But it's also, it's a common problem in ICUs all over the country.
00:01:54
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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.
00:02:04
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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
00:02:13
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face more and more of these patients.
00:02:15
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So I think it's a perfect topic for us to cover today in the podcast.
00:02:19
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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?
Evolving Definition of Cardiogenic Shock
00:02:34
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Absolutely.
00:02:35
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You know, the way that you define cardiogenic shock to some extent depends on what the whole purpose is.
00:02:40
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And most of the definitions you see in the literature are based on research and randomized trial enrollment.
00:02:46
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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.
00:03:01
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But we've been using pulmonary artery catheters less and less and less.
00:03:04
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And so as the result, the definitions clinically have evolved.
00:03:09
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And this is not just a research thing.
00:03:11
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This is a clinical thing.
00:03:13
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So the most common presentation of cardiogenic shock is a patient who presents with blood pressure.
00:03:19
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clinical evidence of hypoperfusion and low cardiac output and is in pulmonary edema.
00:03:25
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And that's what most of us see in practice.
00:03:27
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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.
00:03:39
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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.
00:03:52
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And so really, the newer definitions emphasize the presence of hypoperfusion, and that can be defined in lots of different ways.
00:03:59
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And some
00:04:00
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Some definitions are a little bit more restrictive and require multiple different things.
00:04:06
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Others are a little bit more liberal.
00:04:08
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But the kinds of things that we see clinically at the bedside would be cold and model extremities with delayed capillary refill.
00:04:16
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We often an elevated lactate level.
00:04:19
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Also other biomarkers, evidence of acute kidney injury, acute liver injury.
00:04:24
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And there's a lot of other things that experienced intensivists will recognize as evidence of hypoperfusion.
00:04:30
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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.
00:04:46
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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.
Normotensive Cardiogenic Shock
00:04:59
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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,
00:05:11
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is really the patients who are early in the disease state who still are able to preserve their peripheral vascular tone.
00:05:17
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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.
00:05:28
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And these are patients who over time typically lose that ability to preserve their blood pressure and become hypotensive.
00:05:35
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And so I think that's the real evolution is a focus on hypoperfusion
00:05:39
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really more so than the actual exact hemodynamic numbers, particularly the blood pressure.
00:05:46
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And I think that it's no different than maybe other states of shock, right?
00:05:49
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We're moving away from absolute numbers and really thinking about what's the impact on end organ perfusion and organ function.
00:05:57
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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.
00:06:08
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Absolutely.
00:06:09
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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.
00:06:21
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I'm a little bit older, have some white hair.
00:06:24
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And when I was in training, the reasons why patients came to a cardiac unit in shock were
00:06:31
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where almost exclusively or more commonly due to cardiac ischemia.
00:06:36
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How is that changing today in your practice?
00:06:39
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So this is really important.
00:06:41
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I think that there are two trends that are superimposed on
Epidemiology Shifts in Cardiogenic Shock
00:06:45
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each other.
00:06:45
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The first is we are recognizing and diagnosing cardiogenic shock more often.
00:06:51
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So the prevalence in epidemiologic studies and the incidents are going up.
00:06:55
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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.
00:07:06
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I think it's both.
00:07:07
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So that's the first thing is we're seeing more and more and more.
00:07:10
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But the excess that we're seeing is increasingly due to other causes of cardiogenic shock besides acute myocardial infarction.
00:07:19
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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.
00:07:28
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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.
00:07:39
Speaker
But we haven't really seen that in practice.
00:07:42
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but the proportion of cardiogenic shock cases that are due to acute MI has dropped fairly dramatically.
00:07:49
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And this is something that I think to some extent differs by centers.
00:07:53
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
00:08:11
Speaker
of the overall population of cardiogenic shock cases is due to end stage cardiomyopathy.
00:08:17
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.
00:08:29
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And we're seeing more and more of these patients.
00:08:31
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They numerically outnumber acute MI cases in most tertiary ICUs.
00:08:38
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That's been shown both at Mayo Clinic and in the larger critical care cardiology trials network, which is a multicenter CCU database.
00:08:46
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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.
00:08:57
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And those patients really differ in a lot of ways from patients without acute MI who are now more numerous.
Modern Coronary Care Units
00:09:05
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And I think it also speaks, Jake, to the evolution of CCUs, right?
00:09:08
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Back when I was a resident, it was mostly acute MIs.
00:09:13
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And now a lot of the tertiary care and high-powered CCUs have a lot of devices.
00:09:18
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There's a lot of cardiogenic shock.
00:09:20
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There's a lot of complex disease.
00:09:22
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And I would say higher acuity overall.
00:09:26
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Yeah, that's absolutely true.
00:09:28
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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,
00:09:37
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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.
00:09:47
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They never come to the intensive care unit at all.
00:09:49
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So the patients that do come to the intensive care unit predominantly have circulatory failure, either chronic or acute.
00:09:56
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And that spectrum of cardiogenic shock is most of our patients nowadays.
00:10:01
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Some are on the milder spectrum where they don't really have cardiogenic shock and then all the way up to full on
00:10:07
Speaker
shock, which is another topic I think we'll discuss later.
00:10:10
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But it really does parallel cardiac ICU care in general.
00:10:14
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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.
00:10:24
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Perfect.
00:10:25
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And you did mention spectrum.
00:10:26
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So I think that's a good lead way to our next topic, which is classification and prognostication of cardiogenic shock.
Introduction to the SKY Shock Classification
00:10:34
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So I understand that over the last couple of years, there's really a new severity staging classification for cardiogenic shock.
00:10:42
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
00:10:56
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Absolutely.
00:10:57
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So this has been a particular area of interest in research for me for the past several years.
00:11:03
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This, what we call it, SKY, short for the Society of Cardiovascular Angiography Intervention, shock classification.
00:11:09
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And this was introduced back in 2019.
00:11:12
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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.
00:11:23
Speaker
And even
00:11:25
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patients meeting a very clear, very narrow research definition of cardiogenic shock will present with a fairly wide spectrum of illness.
00:11:33
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And in many cases, there's not a clear cut point between who absolutely is in shock and who absolutely isn't in shock.
00:11:42
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And there's these intermediate or pre-shock states that exist.
00:11:46
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And so what they did, based on expert consensus, is they sat down and they said, look,
00:11:51
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.
00:12:00
Speaker
And some of them will and some of them won't.
00:12:02
Speaker
And many of those who will, will proceed through first a pre-shock state of impending hemodynamic decompensation or early hemodynamic decompensation.
00:12:12
Speaker
And then we'll go to a standard classical form of shock, which
00:12:17
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.
00:12:24
Speaker
And those patients who deteriorate are in many ways very, very different.
00:12:28
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And some of them will deteriorate but then be stabilized, and some will deteriorate to the point of circulatory collapse.
00:12:35
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And within the patients who have over unquestioned cardiogenic shock, there's this whole severity of illness.
00:12:42
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.
00:12:53
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.
00:13:00
Speaker
But essentially, the grading system goes from A to E,
00:13:04
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.
00:13:13
Speaker
And so they're hemodynamically stable.
00:13:15
Speaker
They have normal perfusion, normal hemodynamics, normal blood pressure.
00:13:19
Speaker
And most of those patients, of course, are going to be fine.
00:13:22
Speaker
But some of them are going to deteriorate and develop worsening hemodynamic state.
00:13:28
Speaker
And so the first hemodynamic compromise state is called stage B or beginning cardiogenic shock.
00:13:34
Speaker
But these patients, they don't yet have cardiogenic shock.
00:13:37
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I classify them as pre-shock.
00:13:39
Speaker
And so they have some form of hemodynamic compromise, which could be hypotension.
00:13:42
Speaker
It could be compensatory tachycardia.
00:13:45
Speaker
It could be low cardiac output or other things.
00:13:49
Speaker
hemodynamic abnormalities, but despite that, the patient is still compensated enough to have adequate end-organ perfusion.
00:13:56
Speaker
And so they haven't developed shock because in this construct, shock means end-organ hypoperfusion due to circulatory failure.
00:14:04
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.
00:14:11
Speaker
And so shock or classic shock is defined as stage C,
00:14:16
Speaker
And patients in stage C have end-organ hypoperfusion due to circulatory failure.
00:14:23
Speaker
And importantly, it needs some sort of a higher level intervention, which doesn't mean just a little bit of fluids.
00:14:29
Speaker
This means even after fluid resuscitation, the patient still has hypoperfusion and they require inotropes, vasopressors, or MCS.
00:14:39
Speaker
And again,
00:14:40
Speaker
Most of these patients will stabilize with that initial intervention, but not all of them do.
00:14:44
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Some of them deteriorate to what we call stage D for, of course, deterioration.
00:14:49
Speaker
And these are patients who are worsening despite that initial therapy.
00:14:52
Speaker
The most common thing would be somebody who has a rising lactate or rising vasopressor and inutrope requirements.
00:15:00
Speaker
And so these patients, again, are, you know, sicker.
00:15:04
Speaker
And some of them do get stabilized with that escalating therapy.
00:15:09
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.
00:15:20
Speaker
So these are typically patients with actual or impending circulatory collapse.
00:15:25
Speaker
These patients may be pericode.
00:15:26
Speaker
They may be on very massive doses of vasopressors.
00:15:29
Speaker
They may have a code card at bedside.
00:15:30
Speaker
You know, these patients do not, you know, they don't stay in stage E for very long.
00:15:36
Speaker
Either you stabilize them or they, you know, crash and burn.
Application of SKY Classification in Clinical Practice
00:15:39
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.
00:15:53
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.
00:16:01
Speaker
This means I have a patient who is clearly in cardiogenic shock.
00:16:05
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.
00:16:18
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.
00:16:24
Speaker
And so when I tell you
00:16:25
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.
00:16:30
Speaker
You're not looking at somebody on six vasopressors.
00:16:33
Speaker
You're not looking at someone who's, you know, got a lactate at 20.
00:16:36
Speaker
You're not looking at someone who's, you know, crashing and burning right in front of your eyes.
00:16:41
Speaker
On the other hand, if I tell you, man, I have this guy coming in hot, he's a stage E shock.
00:16:46
Speaker
You know, we've been bolusing him with small doses of vasopressors.
00:16:49
Speaker
He's on three drips.
00:16:51
Speaker
I'm thinking about what's the next step because we better do something now.
00:16:55
Speaker
And those are two very different looking patients who both have cardiogenic shock.
00:17:00
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.
00:17:07
Speaker
It's actually for communication.
00:17:08
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.
00:17:23
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.
00:17:30
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.
00:17:38
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.
00:17:50
Speaker
But that's not what it's about.
00:17:52
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.
00:18:04
Speaker
And as long as you and I have a shared understanding of what this means,
00:18:08
Speaker
You and I will be on the same page.
00:18:10
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.
00:18:26
Speaker
Excellent.
00:18:28
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.
00:18:40
Speaker
So I could see, for example, that somebody just got admitted to my ICU and I walk into the bedside.
00:18:46
Speaker
and they don't look as sick as many of my other patients.
00:18:49
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
00:19:03
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?
00:19:11
Speaker
So I believe that it also helps us maybe think about these patients earlier and to pay more attention.
00:19:17
Speaker
Absolutely.
00:19:18
Speaker
And I think that, you know, translating this from the research arena, right?
00:19:24
Speaker
to the clinical arena has been a little bit difficult because a lot of the research definitions are just too complicated.
00:19:29
Speaker
You just can't do them at the bedside.
00:19:31
Speaker
But one of the things that some of my colleagues have done at Mayo Clinic is we've leveraged the electronic health record.
00:19:38
Speaker
And so I can't remember all the criteria for all of these things, but the computer can.
00:19:43
Speaker
And the computer can automatically import the data into an algorithm, and it can say, based on the rules that we defined,
00:19:50
Speaker
This person meets this stage.
00:19:52
Speaker
And so we're using that in practice as an early warning system.
00:19:56
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.
00:20:06
Speaker
This person is sick.
00:20:07
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.
00:20:14
Speaker
Oh, they're on three pressers now.
00:20:15
Speaker
Oh, you know, all these things.
00:20:17
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.
00:20:31
Speaker
Maybe it's a little bit low or maybe sometimes it's low and sometimes it's not.
00:20:34
Speaker
So it's kind of borderline.
00:20:36
Speaker
But then, you know, you realize, gosh, their lactate's five.
00:20:40
Speaker
Something is going on here that is not manifested in their blood pressure.
00:20:44
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
00:20:59
Speaker
Either my fellow or my advanced practice provider from the CICU will go to assess the patient at bedside.
00:21:05
Speaker
Then they'll talk to the team.
00:21:06
Speaker
They'll say, gosh, you know, what's going on here?
00:21:07
Speaker
Is this a patient who actually doesn't have cardiogenic shock?
00:21:10
Speaker
They actually have sepsis.
00:21:12
Speaker
Is this a patient who actually has impending or developing cardiogenic shock who now they're better off in the ICU?
00:21:19
Speaker
And I think that that is one of the first ways we've been able to leverage this directly.
00:21:25
Speaker
Ideally, the goal would be that you could come up with treatment algorithms by sky stage.
00:21:33
Speaker
Unfortunately, I don't think we have enough evidence yet to definitely do that.
00:21:39
Speaker
But I think that's what we hope for in the future.
00:21:41
Speaker
The idea being if you have worse shock, you need a more intensive intervention.
00:21:46
Speaker
This is, you know, sort of has face validity, but hasn't yet been studied.
00:21:51
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
00:22:06
Speaker
how sick the patient is, right?
00:22:08
Speaker
So if I call them, I think they have cardiogenic shock.
00:22:10
Speaker
Like you said, a lot of times that can mean many things for many people.
00:22:13
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.
00:22:27
Speaker
Absolutely.
00:22:28
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.
00:22:38
Speaker
And
00:22:39
Speaker
and, you know, I had looked at the SERS criteria because we, you know, did that back then.
00:22:44
Speaker
And, you know, the patient met SERS criteria and had suspected infection.
00:22:48
Speaker
And I said, this patient meets criteria for sepsis.
00:22:51
Speaker
They were on the ward.
00:22:52
Speaker
They didn't have septic shock.
00:22:54
Speaker
So I talked to the surgery resident and I said, look, you know, this person has, and I forget what it was.
00:22:58
Speaker
Maybe it was a gallbladder for the sake of discussion.
00:23:01
Speaker
Let's say that what it was.
00:23:01
Speaker
And I said, this person is septic
00:23:04
Speaker
You know, they have evidence of cholecystitis.
00:23:06
Speaker
I think that they need to go to the OR.
00:23:09
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.
00:23:16
Speaker
They said the patient's not septic.
00:23:19
Speaker
And I said, yes, they are.
00:23:20
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.
00:23:27
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.
00:23:41
Speaker
You know, they only viewed sepsis as septic shock and critical illness.
00:23:45
Speaker
And this is the same kind of an idea that if we had been talking the same language,
00:23:51
Speaker
it would have been easier to communicate.
00:23:52
Speaker
If I said, this person has sepsis without septic shock, this is why, this is what it means.
00:23:58
Speaker
And they said, oh, SERS criteria, of course, I understand that.
00:24:01
Speaker
Now we know that there's better ways to define sepsis, of course, but...
00:24:06
Speaker
In the context of cardiogenic shock, it's really the same type of a discussion.
00:24:09
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.
00:24:28
Speaker
And they might say, oh, a person's not really in cardiogenic shock because you stabilized them.
00:24:31
Speaker
But if you're talking the same language and you say, I have stage C, this is what it is.
00:24:35
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.
00:24:45
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
00:24:58
Speaker
levels of aggressiveness.
00:25:00
Speaker
So I think you're absolutely right.
00:25:01
Speaker
It's all about communication.
00:25:03
Speaker
Perfect.
00:25:04
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?
00:25:15
Speaker
Absolutely.
00:25:16
Speaker
So phenotypes of cardiogenic shock is a complex topic that I'm really interested in.
00:25:21
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
Phenotypes of Cardiogenic Shock
00:25:35
Speaker
what it comes down to is there are many different patterns that come up in large cardiogenic shock populations.
00:25:45
Speaker
And some of these are basic things like the cause.
00:25:48
Speaker
We talked about acute MI versus non, you know, versus all the other things.
00:25:52
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.
00:26:02
Speaker
And that's, and that example of acute MI versus non-acute MI, those patients look and act very differently.
00:26:07
Speaker
They need different treatment pathways.
00:26:09
Speaker
Their ability to compensate and how that looks is very, very different.
00:26:13
Speaker
And so,
00:26:15
Speaker
That's one way to think about it, but there's a lot of other ways.
00:26:18
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.
00:26:27
Speaker
So one way would be looking at the pattern of ventricular dysfunction.
00:26:31
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.
00:26:40
Speaker
And so you can think about it in terms of the etiology.
00:26:43
Speaker
You can think about it in terms of the ventricular dysfunction.
00:26:45
Speaker
You can also look at it in terms of hemodynamics, which may reflect, you know, is the patient vasodilated?
00:26:51
Speaker
Do they have right-sided or left-sided congestion?
00:26:52
Speaker
And that's something that's been described for many years as well.
00:26:56
Speaker
The really exciting aspect of phenotypes, though, is where you start getting into biomarkers and patterns of
00:27:05
Speaker
actual underlying pathophysiologic processes that might potentially define different treatment strategies.
00:27:14
Speaker
And we're at the very, very early phases of this.
00:27:17
Speaker
But one really exciting paper that came out a few years ago used machine learning and the admission laboratory values.
00:27:25
Speaker
And they said, look,
00:27:27
Speaker
What we do, what we're finding is patterns of laboratory values that are kind of different in three separate groups.
00:27:35
Speaker
And you have one group that really doesn't have a lot of laboratory abnormalities.
00:27:40
Speaker
And it turns out that those same patients are younger, healthier at baseline and less sick.
00:27:46
Speaker
Their shock is less severe and they look quite a bit different on paper than the other two groups.
00:27:54
Speaker
The second group is
00:27:56
Speaker
again, has a different pattern of laboratory values.
00:27:59
Speaker
In particular, they have really bad kidney function.
00:28:02
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.
00:28:10
Speaker
But they're
00:28:12
Speaker
population demographics in that group is quite a bit different.
00:28:14
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.
00:28:24
Speaker
And so they have, you know, they're congested and they have renal dysfunction and you could call them a cardiorenal phenotype.
00:28:31
Speaker
But then the sickest group and the most complex group have lots of extensive laboratory abnormalities.
00:28:37
Speaker
Their lactate's really high.
00:28:38
Speaker
Their kidneys are doing poorly.
00:28:40
Speaker
Their liver's doing poorly.
00:28:42
Speaker
And they have a lot of other abnormalities that go along with that.
00:28:45
Speaker
Their hemodynamics are terrible.
00:28:47
Speaker
They have a lot of right-sided congestion, which may contribute to the other organ dysfunctions.
00:28:52
Speaker
And then their hemodynamic compromise is worse.
00:28:55
Speaker
And so they were labeled the hemometabolic group.
00:28:58
Speaker
And so these different patterns of lab abnormalities identify groups that have other characteristics that are quite a lot different.
00:29:06
Speaker
And their prognosis was quite a lot different, even when you had looked at their shock severity.
00:29:11
Speaker
And so this is something that is really in its infancy, but it emphasizes that these different groups look different and act different.
00:29:19
Speaker
And it's possible that applying a treatment to one group or the other might yield a different result.
00:29:25
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.
00:29:40
Speaker
And so now that we're getting into some of these targeted biologics, the hope is that if you can identify a phenotype,
00:29:47
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.
00:30:05
Speaker
And so this is something that is extremely crude, but it mirrors what we're trying to figure out in sepsis and ARDS.
00:30:13
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
00:30:26
Speaker
groups within the ARDS population that are more or less likely to respond to steroids or anti-inflammatory therapies or things like that.
00:30:35
Speaker
And so this is a research field right now.
00:30:39
Speaker
It is not ready for prime time.
00:30:41
Speaker
It is not ready for clinical practice.
00:30:43
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
00:30:54
Speaker
a phenotype of cardiogenic shock for each patient, probably with different parameters, and then eventually link that to different treatment strategies.
00:31:05
Speaker
And like you mentioned, this is also being investigated in other disease processes relevant to critical care like sepsis and ARDS.
00:31:12
Speaker
And I think it is in its infancy, but definitely a very exciting development that hopefully will bring better therapies to the bedside.
00:31:22
Speaker
So with that, let's talk about therapy.
Early Identification and Evaluation in Cardiogenic Shock
00:31:25
Speaker
Let's talk about management of cardiogenic shock and kind of where are we today and what's updated in this respect.
00:31:32
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?
00:31:43
Speaker
Absolutely.
00:31:44
Speaker
You know, I think that the early identification is always a challenge in critical illness because most critical illness syndromes,
00:31:54
Speaker
although they might have a defined starting point, that occurs an unknown amount of time before you see the patient.
00:32:01
Speaker
So when you're dealing with acute myocardial infarction,
00:32:04
Speaker
It's often a lot easier to define the onset, although not always.
00:32:08
Speaker
You know, some people, they were fine yesterday.
00:32:10
Speaker
This morning, they had chest pain, clearly have an acute infarct, and you can define the time of onset.
00:32:15
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.
00:32:23
Speaker
And you're not really sure when it actually started.
00:32:25
Speaker
All you know is that it's been going on for 12, 24 hours.
00:32:28
Speaker
And unfortunately, those are some of the folks we get who, because they didn't get treatment, end up in cardiogenic shock.
00:32:34
Speaker
But with some of these other things like heart failure, it is really hard to define the time of onset.
00:32:40
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.
00:32:50
Speaker
And that congestion really starts to compromise their end organs and their cardiac function.
00:32:56
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.
00:33:03
Speaker
So early identification is tough.
00:33:05
Speaker
I think the key things are to recognize things that are in retrospect obvious, but recognizing at the time of.
00:33:14
Speaker
Patient has an elevated anion gap and, you know, check a lactate in that situation.
00:33:19
Speaker
Patient has, you know, for example, a heart rate that's higher than their systolic blood pressure, you know, that classic shock index.
00:33:28
Speaker
Even if they're not overtly hypotensive, the fact that they're having that tachycardia as compensation, think about that.
00:33:36
Speaker
Look at patients who are at risk, identify those stage A's and figure out among them who they're
00:33:43
Speaker
is actually in stage B, but you didn't realize it.
00:33:46
Speaker
And among those stage B's who might actually be in stage C and you didn't realize it.
00:33:50
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.
00:34:04
Speaker
You're not going to find that in a medical chart.
00:34:06
Speaker
You have to see the patient.
00:34:08
Speaker
you know, thinking, you know, checking that lactate in the, in a situation where you're have reason to be suspicious.
00:34:15
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.
00:34:30
Speaker
And the,
00:34:34
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.
00:34:41
Speaker
And so you have to sort of do it in a focused manner.
00:34:43
Speaker
You know, what's the LV function?
00:34:45
Speaker
What's the RV function?
00:34:46
Speaker
Is there evidence of major valve disease that could be the cause?
00:34:49
Speaker
Is there evidence of a pericardial effusion that could be causing tamponade?
00:34:53
Speaker
And then...
00:34:54
Speaker
If you're facile with it, at least some assessment of the hemodynamics.
00:34:58
Speaker
The most important thing usually is to look at the volume status.
00:35:02
Speaker
Volume status by echo continues to be a bit of a controversial area.
00:35:06
Speaker
Simply looking at the inferior vena cava in a sort of gross way, a 2D isn't always all there is to it.
00:35:13
Speaker
But again, it can give you a general idea.
00:35:16
Speaker
Other, of course, urgent diagnostic tests you're going to think about, the 12-lead EKG, right?
00:35:21
Speaker
You obviously want to identify patients who have acute ischemia that might be a treatable and reversible cause of your cardiogenic shock.
00:35:30
Speaker
Your chest X-ray, remember the tension pneumothorax is going to mirror and mimic cardiogenic shock shock.
00:35:36
Speaker
very closely and can be very hard to differentiate just simply at the bedside without looking at that.
00:35:43
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.
00:35:52
Speaker
Comprehensive laboratory workup, specifically focusing on your cardiac biomarkers and other evidence of hypoperfusion and end organ injury.
00:36:02
Speaker
I think with a lot of critical illness syndromes,
00:36:05
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?
00:36:11
Speaker
So airway breathing circulation, right?
00:36:13
Speaker
That's a, always a good way to think about your critically ill patient.
00:36:17
Speaker
Um, uh, and then I always think about D for damage control, which is essentially your end organ dysfunction.
00:36:23
Speaker
How do you reverse it?
00:36:25
Speaker
And then E for etiology.
00:36:27
Speaker
And so, you know, I, I,
00:36:28
Speaker
You don't always go through that in a, you know, in a stepwise sequential manner.
00:36:35
Speaker
You're often doing it simultaneously, thinking about, you know, multiple aspects, but you want to cover all the key management aspects there.
00:36:45
Speaker
Perfect.
00:36:46
Speaker
And obviously you mentioned you wear both hats.
00:36:48
Speaker
You're an intensivist and you're also a cardiologist.
00:36:51
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.
00:37:00
Speaker
Could you just tell us how you think about initial respiratory support in these patients?
00:37:05
Speaker
Absolutely.
00:37:06
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.
00:37:13
Speaker
And
00:37:14
Speaker
You know, that obviously can cause very severe respiratory failure.
00:37:18
Speaker
And of course, if you're hypoxic and having respiratory distress, then
00:37:24
Speaker
that added workload on your respiratory system actually can use a very sizable proportion of your cardiac output.
00:37:32
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.
00:37:46
Speaker
So, uh, that's, you know, so respiratory support is really part and parcel of care for these patients.
00:37:52
Speaker
Um,
00:37:53
Speaker
As with any other patient, you have to use your judgment, right?
00:37:56
Speaker
Some of these patients, a lot of them actually are comatose after cardiac arrest, and those patients need a definitive airway.
00:38:02
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.
00:38:06
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.
00:38:13
Speaker
Of course, intubating any patient who's hemodynamically compromised is, you know, risky proposition.
00:38:19
Speaker
These patients often will...
00:38:22
Speaker
have worsening hypotension after getting sedation, as many other critically ill patients with circulatory failure will.
00:38:31
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.
00:38:42
Speaker
We often talk about using a hemodynamically stable agent like etomidate or ketamine, but all of the drugs that can be used
00:38:50
Speaker
can cause major hemodynamic compromise.
00:38:53
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.
00:38:58
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,
00:39:11
Speaker
and to be patient.
00:39:12
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.
00:39:19
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.
00:39:24
Speaker
They clearly need sedation analgesia for their safety and comfort.
00:39:29
Speaker
And you give some, but it just doesn't work.
00:39:31
Speaker
And the reason is that it, that you're
00:39:34
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
00:39:56
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.
00:40:07
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.
00:40:17
Speaker
But what you hope is that you don't have to intubate the patient, right?
00:40:21
Speaker
You hope that you can get away with non-invasive support.
00:40:23
Speaker
And so if a patient is, um,
00:40:26
Speaker
you know, as a candidate for non-invasive support, sometimes that can be really effective.
00:40:30
Speaker
We know that administering positive pressure can be really, really good for the left ventricle and for patients with pulmonary edema.
00:40:37
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.
00:40:50
Speaker
And so it functionally reduces the preload pressure and the afterload pressure on the left ventricle.
00:40:57
Speaker
And so sometimes that's enough to really help the patient's ventricle.
00:41:02
Speaker
And there's evidence that it can actually increase cardiac output.
00:41:05
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.
00:41:20
Speaker
beneficial in the setting of LV failure.
00:41:22
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.
00:41:36
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.
00:41:45
Speaker
And so when I have a patient who has, you know, critical pulmonary hypertension,
00:41:50
Speaker
I try at all costs to avoid intubating them.
00:41:53
Speaker
And indeed, I'll usually try to do Optiflow or, you know, excuse me, high flow nasal cannula.
00:42:01
Speaker
as an alternative to positive pressure.
00:42:04
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.
00:42:11
Speaker
But if you can avoid intubation in those patients, it often is hemodynamically beneficial.
00:42:16
Speaker
If you're stuck and the person is failing, they're profoundly hypoxic.
00:42:20
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.
00:42:27
Speaker
This is one of those all hands on deck situations.
00:42:30
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.
00:42:42
Speaker
And so I try to find the best airway person and I try to do it in the most controlled manner possible.
00:42:47
Speaker
If you're able to do and you have time to do.
00:42:50
Speaker
you know, an awake fiber optic intubation with, you know, minimal sedation and, you know, local anesthetic, that's ideal.
00:42:57
Speaker
Can't always do that.
00:42:59
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.
00:43:15
Speaker
Perfect.
00:43:16
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.
00:43:27
Speaker
Absolutely.
Use of Vasopressors and Inotropes
00:43:28
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.
00:43:37
Speaker
So the only clinical trial that we have in the field of cardiogenic shock is
00:43:44
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.
00:43:54
Speaker
And so one of the core tenets of cardiogenic shock care is to identify and treat acute myocardial infarction.
00:44:03
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,
00:44:12
Speaker
is a person who probably needs a coronary angiogram.
00:44:15
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.
00:44:27
Speaker
But even patients who it's not clear whether they truly are having an acute MI
00:44:34
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.
00:44:44
Speaker
So I'm a big advocate for early coronary angiography.
00:44:48
Speaker
So I'm going to just put in a plug for that and we'll kind of move on.
00:44:51
Speaker
The key thing there is that if you do find an occluded artery, a culprit artery,
00:44:56
Speaker
That's what you treat.
00:44:57
Speaker
You don't go around looking for other things to treat.
00:45:00
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.
00:45:08
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.
00:45:16
Speaker
And culprit PCI is associated with better outcomes, which is different than what we expected.
00:45:21
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.
00:45:29
Speaker
So as we think about treatment, you have to, you know, it's all a spectrum.
00:45:33
Speaker
And so some of this, of course, is going to be started in the cath lab.
00:45:38
Speaker
In terms of invasive hemodynamic monitoring, having accurate measurement of the blood pressure is probably the most important thing.
00:45:45
Speaker
And so I'm a big advocate for placing an arterial line.
00:45:48
Speaker
I know that that hasn't been well demonstrated to improve survival outcomes in other critically ill populations.
00:45:54
Speaker
But in particular, patients with low cardiac output, I find that the non-invasive outcomes
00:46:01
Speaker
assessment of blood pressure tends to be fairly inaccurate.
00:46:03
Speaker
You end up with these frequent blood pressure checks that lead to these numbers that are kind of nonsensical.
00:46:08
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.
00:46:18
Speaker
The more complex question is whether these patients all need a pulmonary artery catheter.
00:46:22
Speaker
So as a cardiologist, as a critical care cardiologist, I am very familiar and comfortable with the pulmonary catheter.
00:46:29
Speaker
I do it a lot.
00:46:31
Speaker
You know, it's, you know, generally a quick and easy procedure in experienced hands.
00:46:36
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.
00:46:46
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.
00:46:53
Speaker
And there is a randomized trial going on now that's actually trying to answer this question, so that'll be helpful.
00:46:58
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.
00:47:06
Speaker
So if you have an accurate evaluation of the patient's blood pressure,
00:47:11
Speaker
You have some way to evaluate the patient's cardiac output and its effect on the end organs.
00:47:16
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?
00:47:25
Speaker
Does the patient have abnormal vasodilation?
00:47:27
Speaker
If you can figure all those things out with less invasive means, I'm not convinced that a pulmonary artery catheter adds much.
00:47:33
Speaker
However, it can be very difficult to figure things out with less invasive means, and so
00:47:39
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.
00:47:46
Speaker
So I tend to place a PA catheter early.
00:47:49
Speaker
I have a bias towards that.
00:47:51
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.
00:47:59
Speaker
But until then, I am more likely to do a PA catheter than not.
00:48:06
Speaker
And
00:48:07
Speaker
I feel strongly that a PA catheter should be placed when things aren't going well.
00:48:13
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.
00:48:27
Speaker
I might say, you know what, this is treatment success.
00:48:30
Speaker
Let's let the dust settle and, you know, see if we can avoid an extra invasive procedure.
00:48:36
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.
00:48:54
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.
00:49:04
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.
00:49:13
Speaker
Um, and so therefore currently standard of care is medical therapy.
00:49:17
Speaker
And so I personally start with vasopressors because I believe that critical hypotension is the primary problem.
00:49:27
Speaker
If your blood pressure is too low, your organs cannot auto regulate.
00:49:31
Speaker
They're going to get hypoperfused regardless of your cardiac output.
00:49:34
Speaker
And even worse, your heart may become hypoperfused and may get stunning from global ischemia just driven by hypotension.
00:49:43
Speaker
So getting the patient's blood pressure up is the key priority.
00:49:48
Speaker
And so the question is, how do you do this most effectively and most safely?
00:49:53
Speaker
And now let's be clear.
00:49:55
Speaker
No one knows what the proper blood pressure goals are for patients with cardiogenic shock.
00:49:59
Speaker
I typically would say a map of 65 is probably...
00:50:03
Speaker
reasonable like we would for most patients.
00:50:06
Speaker
Some patients, you might be a little bit more liberal and go sort of 60 to 65.
00:50:11
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.
00:50:22
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.
00:50:31
Speaker
And so we always so the guidelines for many years said you use dopamine.
00:50:36
Speaker
which has very powerful beta agonist activity at adrenergic beta receptors that increases heart rate, cardiac output, stroke volume, all those things.
00:50:48
Speaker
And so we thought that you had to do that because you had to raise the cardiac output.
00:50:52
Speaker
But it turns out that at the doses that are required for vasopressor effects โ
00:50:58
Speaker
Dopamine causes horrendous toxicity, particularly in patients with cardiogenic shock.
00:51:03
Speaker
And the real issue is arrhythmias.
00:51:04
Speaker
And so a sick heart with cardiogenic shock is going to be extremely prone to arrhythmias.
00:51:08
Speaker
If the patient develops an arrhythmia, it can be fatal or can really compromise their cardiovascular function.
00:51:14
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.
00:51:26
Speaker
So then they said, well, maybe dopamine is an outlier.
00:51:28
Speaker
Maybe it's maybe it's, you know, maybe epinephrine, which is a little bit more direct.
00:51:33
Speaker
And maybe that's better.
00:51:35
Speaker
Turns out, no, it's not.
00:51:37
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.
00:51:46
Speaker
That.
00:51:47
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.
00:51:56
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.
00:52:04
Speaker
And importantly, you see more arrhythmias, more toxicity and more bad outcomes.
00:52:08
Speaker
So epinephrine is not a great option either.
00:52:11
Speaker
So based on those studies, I would say that norepinephrine is the safest option.
00:52:16
Speaker
first line drug as a vasopressor for cardiogenet shock, and that's where I start.
00:52:20
Speaker
I start norepinephrine.
00:52:21
Speaker
I figure out what's the lowest dose that will get me to an adequate mean arterial pressure to support the organs.
00:52:27
Speaker
I try to avoid overtreatment, and that's kind of my first line approach.
00:52:33
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.
00:52:46
Speaker
And so those aren't drugs that I tend to use as a first line.
00:52:49
Speaker
That being said, if you're in an emergency situation, you have to use what you've got.
00:52:53
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.
00:53:01
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.
00:53:10
Speaker
So once I have started norepinephrine and I have it at an adequate dose to get a reasonable blood pressure,
00:53:16
Speaker
Then I'll usually add an inotrope to try and increase the cardiac output with the primary goal of reversing end-organ hypoperfusion.
00:53:25
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.
00:53:37
Speaker
There's only a cardiac output that's either adequate to meet the metabolic demands of the body or one that's inadequate.
00:53:42
Speaker
And of course, if you have 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.
00:53:53
Speaker
So really, I try to focus on the end organ perfusion to lactate, urine output, clinical exam.
00:54:00
Speaker
So if I start a patient on an inotrope and those things get better and get back to normal,
00:54:05
Speaker
and then I measure the cardiac output and realize that it's still low, I actually might not worry about it.
00:54:10
Speaker
I might say, you know what, that's fine.
00:54:12
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.
00:54:23
Speaker
Tricky situation, of course, is if the cardiac output looks normal and the end organ perfusion looks bad.
00:54:28
Speaker
And then you have to decide, is raising the blood pressure going to help?
00:54:33
Speaker
Is raising the cardiac output further going to help?
00:54:35
Speaker
And there's a little bit of trial and error involved.
00:54:38
Speaker
The question is, what inotropes should you use?
00:54:40
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.
00:54:50
Speaker
Now, my personal bias is towards Dubutamine because it has better pharmacokinetics.
00:54:54
Speaker
It kicks in faster.
00:54:56
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.
00:55:04
Speaker
So that's my bias, as I prefer that.
00:55:06
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.
00:55:19
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?
00:55:27
Speaker
You know, if I'm using high doses of dopamine, I know it's toxic, I know it's harmful.
00:55:31
Speaker
But what about those low doses, like two to five mics per kilo per minute?
00:55:35
Speaker
I will use that sometimes if, for example, dobutamine causes the patient to vasodilate too much.
00:55:42
Speaker
I might switch over to dopamine and see if it can get me that inotropic effect without the vasodilation.
00:55:48
Speaker
But it doesn't work quite as well as dobutamine, so I don't use it as first line.
00:55:51
Speaker
And epinephrine, again, same logic.
00:55:53
Speaker
Again, 0.0 something, 0.02, 0.05 of epinephrine sometimes can give you that inotropic effect without causing a ton of toxicity.
00:56:00
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.
00:56:10
Speaker
Perfect.
00:56:12
Speaker
Interestingly, one last thing I would mention is there is a randomized trial trying to decide if
00:56:16
Speaker
inotropes added to vasopressors even have any advantage.
00:56:20
Speaker
And so we'll see that's the do re mi to study.
00:56:22
Speaker
And we'll see if that actually see what that happened, what that result turns out to be.
00:56:26
Speaker
So I think it's going to be thought provoking either way.
00:56:29
Speaker
But I think, like you mentioned, a couple of important points to reemphasize.
00:56:36
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?
00:56:51
Speaker
I mean, regardless of what's next,
00:56:53
Speaker
We got to get that as good as we can for each individual patient.
00:56:59
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.
00:57:21
Speaker
Absolutely.
00:57:22
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.
00:57:39
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.
00:57:50
Speaker
The
00:57:52
Speaker
The premise behind mechanical circulatory support is very sound.
00:57:56
Speaker
You have a condition where low cardiac output is the problem.
00:58:01
Speaker
You have evidence that inotropes and vasopressors can cause major, potentially life-threatening toxicity, and also in many cases are not effective.
00:58:12
Speaker
So how can you restore adequate cardiac output to the organs to get them to recover if the drugs you're using are
00:58:21
Speaker
aren't doing it?
00:58:23
Speaker
And the answer obviously would be mechanical
Mechanical Circulatory Support Strategies
00:58:25
Speaker
circulatory support.
00:58:25
Speaker
And we've had mechanical circulatory support in the form of a balloon pump for like pushing 50 years, I think.
00:58:33
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.
00:58:47
Speaker
And this was, we showed this in 2012 with the balloon pump.
00:58:52
Speaker
And then more recently with ECMO.
00:58:54
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.
00:59:13
Speaker
It was more than 400 patients.
00:59:15
Speaker
They all had acute MI and were getting revascularized, and they couldn't find any benefit whatsoever
00:59:22
Speaker
of early ECMO versus medical therapy alone.
00:59:27
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.
00:59:38
Speaker
And it's all about tailored therapy.
00:59:41
Speaker
So it's not about do the same thing to everybody.
00:59:44
Speaker
It's identify patients who are likely to benefit from the therapy and
00:59:50
Speaker
and then apply the right therapy tailored to who that patient is, what their hemodynamics are, what their phenotype is, et cetera.
00:59:56
Speaker
And so the key here is to do this in a multidisciplinary way.
01:00:01
Speaker
So this is not just me standing there at the bedside by myself and saying, gosh, let's do this.
01:00:08
Speaker
This is me collaborating with, you know, potentially a heart surgeon, a heart failure transplant cardiologist, and, you know,
01:00:18
Speaker
potentially other team members to really think about where is this patient in their shock journey?
01:00:24
Speaker
Where is this patient in their overall heart related health journey and what options are realistic for them?
01:00:32
Speaker
What outcomes are realistic for them?
01:00:34
Speaker
What type of a device would be adequate to meet their needs?
01:00:40
Speaker
And are they a candidate for that device?
01:00:42
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.
01:00:53
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?
01:01:02
Speaker
So a key factor that people sometimes forget about is that MCS is nothing more than a bridge.
01:01:08
Speaker
You're taking a patient from a terrible situation, you know, bad cardiogenic shock, and you're bringing them to something hopefully better.
01:01:16
Speaker
In an ideal situation, it's recovery of myocardial function and liberation.
01:01:20
Speaker
But in many cases, it's, you know, transition to either a durable mechanical support device like an LVAD or maybe heart transplant.
01:01:29
Speaker
And particularly with the increasing prevalence of heart failure related cardiogenic shock, patients with end stage cardiomyopathy,
01:01:37
Speaker
you know, the exit strategy is crucially important.
01:01:41
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.
01:01:52
Speaker
You have a patient who's
01:01:54
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.
01:02:02
Speaker
On the other hand, you have a person who is a candidate for those therapies and has an exit strategy.
01:02:08
Speaker
They're much more likely to do well because if they don't recover, they have somewhere to go.
01:02:13
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.
01:02:23
Speaker
And so this is where your clinical judgment comes in.
01:02:26
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.
01:02:42
Speaker
Likewise, if the patient has isolated left ventricular failure,
01:02:46
Speaker
probably all you need is a left ventricular assist device.
01:02:49
Speaker
The key factor being if they have horrendous pulmonary failure, then they may need pulmonary support as well.
01:02:56
Speaker
So in terms of the different devices we use, the balloon pump is the most commonly used.
01:03:02
Speaker
It's cheapest, it's smallest, it's safest.
01:03:05
Speaker
It doesn't do much.
01:03:06
Speaker
It probably has better effects in patients with chronic cardiomyopathy
01:03:13
Speaker
In them, you can see an average increase in cardiac output in the 0.5 to 1 liter range.
01:03:19
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.
01:03:27
Speaker
In the setting of acute MI, it's not really clear if a balloon pump improves hemodynamics meaningfully more than medical therapy alone.
01:03:35
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
01:03:43
Speaker
And the key way that the balloon pump actually works is by offloading the ventricle.
01:03:48
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.
01:04:05
Speaker
So when do I use the balloon pump?
01:04:07
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.
01:04:15
Speaker
I will use it in patients who have no other option.
01:04:19
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.
01:04:31
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.
01:04:41
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.
01:04:51
Speaker
On the other hand, for patients with heart failure, cardiogenic shock, we're much more liberal with balloon pumps.
01:04:57
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.
01:05:10
Speaker
So the key thing is,
01:05:13
Speaker
When a person is doing well on vasopressors and inotropes, I'm not usually thinking about MCS.
01:05:19
Speaker
But if the patient is having toxicity or failure to achieve hemodynamic goals, then I am.
01:05:24
Speaker
Now, the more advanced devices would be percutaneous ventricular assist devices.
01:05:30
Speaker
So the most commonly used is the impella device, which the most commonly used one is a left ventricular device.
01:05:36
Speaker
There's also right ventricular device.
01:05:37
Speaker
There's a couple sizes.
01:05:39
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.
01:05:50
Speaker
The incremental benefit and the added effect depends on what device you use and a lot of other factors.
01:05:56
Speaker
The problem is that because these are larger, the risk of complications is substantially higher.
01:06:01
Speaker
And that's been convincingly and consistently demonstrated that these devices definitely cause more complications than a balloon pump.
01:06:10
Speaker
The problem is that the evidence base supporting the efficacy of these devices for improving outcomes is really thin.
01:06:18
Speaker
There's some small trials, none of which have shown a consistent benefit for improving survival.
01:06:24
Speaker
So these devices, again, have to be thought of in a comprehensive strategy of person is doing badly on medical therapy.
01:06:33
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.
01:06:43
Speaker
In that situation, it's reasonable to try one of these, you know, one of these percutaneous vads.
01:06:49
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.
01:07:02
Speaker
Now, the higher highest level of support is ECMO.
01:07:05
Speaker
And ECMO is an amazing device.
01:07:07
Speaker
It can provide full cardiac support, full pulmonary support.
01:07:10
Speaker
You can use it in patients who are in cardiac arrest and preserve and restore their organ function.
01:07:18
Speaker
It's very, very impressive.
01:07:20
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.
01:07:32
Speaker
It can be used for left ventricular support, right ventricular support, biventricular support, as well as heart and lung support.
01:07:38
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.
01:07:51
Speaker
The problem is we have yet to prove that using ECMO as a routine strategy improves survival.
01:07:58
Speaker
That's that new study, and again,
01:08:01
Speaker
prior smaller studies have been shown the same results.
01:08:04
Speaker
And there's definitely an increased risk of complications with ECMO.
01:08:07
Speaker
You know, ECMO, particularly when done in lower volume centers or less experienced hands, a lot of things can go wrong.
01:08:13
Speaker
Even with very experienced centers, you know, the need for vascular repairs and things is fairly frequent.
01:08:20
Speaker
So in my practice, I
01:08:25
Speaker
still believe that appropriate application of these devices can be beneficial, even if they're not appropriate for all patients.
01:08:33
Speaker
But I really try to be selective and think about patients who have a next step option.
01:08:38
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.
01:08:54
Speaker
you know, based on what the patient's hemodynamic needs are and their hemodynamic phenotype.
01:08:59
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.
01:09:08
Speaker
So for patients with isolated or predominant LV failure as a bridge, we have been doing that more often.
01:09:15
Speaker
It tends to work well in the right patients.
01:09:18
Speaker
A lot of other patients end up getting ECMO.
01:09:20
Speaker
Um,
01:09:21
Speaker
ECMO has a lot of important advantages and disadvantages that are probably, you know, a bit outside of the scope of this discussion.
01:09:28
Speaker
There are a lot of novel approaches to ECMO that allow you to unload the left ventricle, which are very potentially advantageous.
01:09:34
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
01:09:50
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.
01:10:00
Speaker
And I think, Jake, that...
01:10:02
Speaker
Two of the most important aspects of the discussion on mechanical secretarial support is the need to have a multidisciplinary approach.
01:10:11
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.
01:10:19
Speaker
I can see how the interventional cardiologist with the patient on the table or the CT surgeon who did a procedure,
01:10:27
Speaker
might have, obviously, for the right reasons, a biased view of what needs to be done, right?
01:10:33
Speaker
And I think that being part of that discussion and trying to tailor that to the individual patient is extremely important.
01:10:40
Speaker
But also the exit strategy, and you mentioned just to reemphasize that,
01:10:46
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
Predicting Myocardial Recovery and Multidisciplinary Care
01:11:02
Speaker
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
01:11:12
Speaker
Absolutely.
01:11:13
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.
01:11:23
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.
01:11:34
Speaker
And the reason that that matters is that hibernating myocardium
01:11:39
Speaker
often has incomplete recovery and it can be delayed by weeks to months.
01:11:44
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.
01:11:58
Speaker
And
01:11:59
Speaker
I'm not personally familiar with a lot of literature looking at this in the setting of cardiogenic shock.
01:12:04
Speaker
It's much more well-defined in chronic cardiomyopathy or clear acute MI.
01:12:11
Speaker
And so it remains an area of controversy and uncertainty.
01:12:16
Speaker
And I've, I've been in situations where, you know,
01:12:20
Speaker
you have to ask, are we really going to support this person for a month?
01:12:23
Speaker
Is that a logical thing for them knowing that after a month they may be in the exact same spot?
01:12:30
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.
01:12:42
Speaker
And, and working with them is going to be much better than just trying to figure it out all on my own.
01:12:49
Speaker
For sure.
01:12:52
Speaker
And I think that as you said, Jake, this is really a evolving and dynamic field.
01:12:57
Speaker
A lot of very interesting trials on their way.
01:13:02
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.
01:13:08
Speaker
I think there's some of these topics that we could take on their own for another hour.
01:13:15
Speaker
But really, I appreciate the comprehensive overview that you've provided.
01:13:20
Speaker
Is there anything else you want to add to the topic of cartagenic shock before we go to our closing questions?
01:13:25
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.
Managing Right Ventricular Shock
01:13:33
Speaker
In my experience, patients with, you know, critical pulmonary hypertension progress to cartagenic shock are some of the most
01:13:40
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.
01:13:52
Speaker
I think what's really interesting about these patients is that
01:13:55
Speaker
You know, we spend all of our time thinking about left ventricular preload, left ventricular afterload, all these things.
01:14:01
Speaker
And those are completely irrelevant for these patients.
01:14:03
Speaker
They need you need to think about RV afterload.
01:14:05
Speaker
And so, you know, I talked a little bit about the respiratory therapy side of it and ventilation.
01:14:11
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.
01:14:18
Speaker
I think the key thing is to lower the RV afterload.
01:14:23
Speaker
after load.
01:14:24
Speaker
And there's a lot of ways to do that in a, in a, you know, hyper emergency.
01:14:28
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?
01:14:37
Speaker
If you have high ventilator pressures and things like that, sometimes that can, you know, make things worse rather than better.
01:14:44
Speaker
A lot of these patients will need some sort of inotropic support.
01:14:47
Speaker
Milrinone tends to work well in this situation because it can have a little bit of pulmonary vasodilation, which is nice.
01:14:55
Speaker
Supporting the systemic blood pressure, sometimes we'll use vasopressin for these patients because it tends not to constrict the pulmonary vessels.
01:15:04
Speaker
So the combination of milrinone and vasopressin we often talk about.
01:15:08
Speaker
And then really trying to optimize the RV volume status.
01:15:13
Speaker
The RV is funny, and a normal RV and a sick RV behave very differently.
01:15:17
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.
01:15:24
Speaker
to function properly.
01:15:26
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.
01:15:36
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.
01:15:48
Speaker
And so actually you may be in a situation where you diurese the patient
01:15:52
Speaker
to bring their filling pressure back down to like the low teens, the 10 to 12 range is often optimal.
01:16:00
Speaker
And you're diuresing them while they're on pressers.
01:16:03
Speaker
And in some of these patients, that actually gets them a lot better.
01:16:06
Speaker
And so I think these patients are very, very challenging.
01:16:10
Speaker
I tend to put a pulmonary artery catheter in all of these patients.
01:16:15
Speaker
And because as you monitor them, you know, sometimes...
01:16:18
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.
01:16:25
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.
01:16:39
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.
01:16:47
Speaker
But these patients are super complicated, super interesting.
01:16:51
Speaker
And you can actually get this phenotype, as you know, from ARDS with, you know, with true core pulmonale.
01:16:59
Speaker
And that is a uniquely complex challenge.
01:17:02
Speaker
But I think...
01:17:05
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.
01:17:23
Speaker
I think that's a, and thanks for covering that as well, because you are right.
01:17:27
Speaker
You do touch that in the paper.
01:17:28
Speaker
And I think it's a very specific type of patient, but that they pose significant challenges for management and not recognizing them.
01:17:37
Speaker
We can, a lot of times cause harm with our usual approach.
01:17:40
Speaker
So thanks for covering that.
01:17:44
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.
Closing Thoughts and Book Recommendations
01:17:52
Speaker
Would that be okay?
01:17:52
Speaker
Okay.
01:17:54
Speaker
Um, if I have any left, I'll be happy to share it.
01:17:57
Speaker
So the first question relates to books.
01:17:59
Speaker
Are there any books that have influenced you significantly or books that you have gifted often to other people?
01:18:06
Speaker
Yeah.
01:18:06
Speaker
So this is, I love to read and I read a lot.
01:18:09
Speaker
Um, a lot of the stuff that I read is, is of course, you know, has a limited nutritional value, so to speak.
01:18:15
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,
01:18:22
Speaker
And so one of the books that I, you know, that he's reading now is The Hobbit.
01:18:26
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.
01:18:33
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.
01:18:44
Speaker
you know, even though it's obviously fantasy, I think it really resonates with me about how important preserving our natural environment is.
01:18:52
Speaker
And, you know, as an outdoors person really resonates with me a lot.
01:18:56
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.
01:19:04
Speaker
And I think that there's a lot of, quite frankly, a lot of bad stuff in that book.
01:19:08
Speaker
But what I think it
01:19:10
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.
01:19:18
Speaker
They've been around for a long time.
01:19:20
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.
01:19:30
Speaker
And, you know, I think
01:19:32
Speaker
And so that is sort of a counterexample of what not to do.
01:19:37
Speaker
But it really emphasizes for me that being compassionate is so important and is the core of what makes a good physician.
01:19:49
Speaker
And as an intensivist, dealing with death a lot, finding ways to
01:19:56
Speaker
maintain my own inner strength in the face of that potential despair is, you know, very challenging.
01:20:02
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.
01:20:11
Speaker
Absolutely.
01:20:12
Speaker
And I think that we'll reference all these books.
01:20:15
Speaker
And it's interesting because the House of God, obviously, is a book that maybe younger generations have not encountered.
01:20:22
Speaker
But you're right.
01:20:25
Speaker
It has a lot of themes that are relevant today.
01:20:30
Speaker
Right.
01:20:30
Speaker
So none of these challenges are brand new.
01:20:34
Speaker
As a lot of times we tend to think.
01:20:36
Speaker
that it's all about this year or last year, right?
01:20:39
Speaker
Post COVID or they've been around for a long time.
01:20:42
Speaker
So definitely we'll reference all those books and the show notes.
01:20:46
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.
01:20:57
Speaker
You know,
01:20:59
Speaker
I think the, this is going to be a bit dark and I hope you'll see why.
01:21:03
Speaker
I think that a lot of people forget that death is inevitable for all of us.
01:21:09
Speaker
And as physicians, sometimes the only control we have is how the patient's experience of death goes.
01:21:19
Speaker
And this is essentially allowing a death with dignity, you know, a humane death for patients who are
01:21:28
Speaker
you know, aren't, aren't going to make it.
01:21:29
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,
01:21:46
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.
01:22:10
Speaker
And I think that for a critical care audience, this is always an important reminder
01:22:16
Speaker
And something that we tend to understand, I believe, Jake, a little bit better than some of our colleagues in other specialties.
01:22:24
Speaker
And I think that there are two important things to take home here.
01:22:27
Speaker
One is that we can help others in medicine understand this.
01:22:32
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.
01:22:42
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.
01:22:53
Speaker
So absolutely, I love that.
01:22:56
Speaker
And I think it's a great answer.
01:22:59
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.
01:23:08
Speaker
So there was a quote painted on the wall of one of the intensive care units at Pitt where I did fellowship.
01:23:15
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.
01:23:26
Speaker
I probably misquoted it, but I think the sentiment is there.
01:23:32
Speaker
Many things that we do as physicians, we feel are going to imminently change the disease state.
01:23:40
Speaker
And sometimes that is true and sometimes that is not true.
01:23:43
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.
01:23:53
Speaker
And it has a lot to do with their remaining inherent capacity to recover.
01:23:59
Speaker
And our job in the ICU is to create a state where the patient has a chance to recover.
01:24:05
Speaker
And that's particularly true for cardiogenic shock, where we basically have failed to demonstrate
01:24:10
Speaker
that any individual therapy applied routinely to all patients improves survival.
01:24:16
Speaker
So that doesn't mean that what we do isn't valuable.
01:24:18
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.
01:24:33
Speaker
And we just have to make sure that we don't impede the healing process of
01:24:38
Speaker
You know, by doing things that are not necessary or not appropriate or not beneficial.
01:24:44
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.
01:25:00
Speaker
I think this is a perfect place to stop.
01:25:02
Speaker
Once again, Jake, I really want to thank you for sharing your expertise with us and giving us your time.
01:25:08
Speaker
And I look forward to having you back on the podcast.
01:25:10
Speaker
Maybe when some of these trials give us a shed some light on the way forward.
01:25:15
Speaker
And thank you again.
01:25:16
Speaker
Well, it was my pleasure.
01:25:18
Speaker
Sorry, I'm a bit long winded, but hopefully hopefully chock full of information for the interested audience.
01:25:24
Speaker
Absolutely.
01:25:25
Speaker
Thank you.
01:25:26
Speaker
You're very welcome.
01:25:27
Speaker
My pleasure.
01:25:27
Speaker
Have a good day.
01:25:30
Speaker
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01:25:33
Speaker
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01:25:39
Speaker
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01:25:44
Speaker
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