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Update On Cardiogenic Shock
28 Plays6 years ago
Cardiogenic shock (CS) is a common cause of mortality, and its management remains challenging despite significant advances in treatment options.
In this episode of Critical Matters, we discuss basic concepts, a new proposed classification, and updates on the medical management of patients with cardiogenic shock.
Our guest is Dr. Steve Hollenberg, a practicing cardiologist with dual training in cardiology and critical care medicine. Dr. Hollenberg is a Professor of Medicine at Hackensack Meridian School of Medicine at Seton Hall University and Associate Director of the CTICU at Hackensack Meridian University Hospital.
Additional Resources:
The paramedian lumbar puncture: http://bit.ly/2pk8JUw
Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association: http://bit.ly/2Qdjoey
SCAI clinical expert consensus statement on the classification of cardiogenic shock: http://bit.ly/2XdjeWa
SCAI stages of cardiogenic shock stratify mortality risk: http://bit.ly/2CCzbf9
Books Mentioned in this Episode:
Ulysses by James Joyce: https://amzn.to/2QgIoBW
Gravity’s Rainbow by Thomas Pynchon: https://amzn.to/36Vgjps
The Elements of Style by E. B. White: https://amzn.to/2QdklUa
The Little Prince by Antoine de Saint-Exupéry
https://amzn.to/352frOi
Recommended
Transcript
Introduction to Critical Matters Podcast
00:00:06
Speaker
Welcome to Critical Matters, a sound critical care podcast covering a broad range of topics related to the practice of intensive care medicine.
00:00:14
Speaker
Sound Critical Care provides comprehensive critical care programs to hospitals across the country.
00:00:20
Speaker
To learn more about our programs and career opportunities, visit www.soundphysicians.com.
00:00:27
Speaker
And now your host, Dr. Sergio Zanotti.
Understanding Cardiogenic Shock: Challenges and Management
00:00:32
Speaker
Cardiogenic shock is a common cause of mortality, and its management remains challenging despite significant advances in treatment options.
00:00:40
Speaker
Although the number of specialized cardiovascular intensive care units continues to grow, a large number of patients with cardiogenic shock are still cared for in general medical and surgical ICUs.
00:00:51
Speaker
In today's episode of the podcast, we will discuss some basic concepts, a new proposed classification, and updates on the medical management of patients with cardiogenic shock.
Introducing Dr. Steve Hollenberg: Expertise in Cardiovascular Critical Care
00:01:01
Speaker
Our guest is Dr. Steve Hollenberg.
00:01:03
Speaker
Dr. Hollenberg is a practicing cardiologist with dual training in cardiology and critical care medicine.
00:01:08
Speaker
He is professor of medicine at Hackensack Meridian School of Medicine at Seton Hall University in New Jersey.
00:01:14
Speaker
In addition, he's the associate director of the CTICU at Hackensack Meridian University Hospital.
00:01:20
Speaker
Dr. Hollenberg is a recognized expert in cardiovascular critical care and has published extensively on the topic.
00:01:26
Speaker
He is a dear friend who over the years has taught me a lot
00:01:30
Speaker
first as my attending in the MICU and CCU, then as a research mentor, and finally as a colleague.
00:01:36
Speaker
It's a true pleasure and honor to have him as a guest on Critical Matters.
00:01:39
Speaker
Steve, welcome to the podcast.
00:01:41
Speaker
Thank you.
00:01:42
Speaker
It's a pleasure to be here.
Lumbar Puncture Technique: A Personal Insight
00:01:44
Speaker
So since we're going to talk about cardiogenic shock with a cardiology critical care specialist, I thought the best place to start would be with a paramedian lumbar puncture.
00:01:56
Speaker
You want me to tell you about that?
00:01:59
Speaker
Please.
00:02:00
Speaker
Yes, so when I was a critical care fellow at the NIH, it was multidisciplinary.
00:02:08
Speaker
And one of my colleagues, Bill Hoffman, who's an anesthesiology critical care person who's now in, who's at Mass General for a while and is still in Massachusetts, taught me how to do a paramedian lumbar puncture, which is basically a way of doing a lumbar puncture that's not dependent on getting the patient in position, but rather goes around.
00:02:29
Speaker
And since then, I've never done anything other than the paramedian lumbar puncture.
00:02:35
Speaker
And one of my favorite things and trainees is to say, oh, let me show you how to do a paramedian lumbar puncture.
00:02:42
Speaker
I've probably done more paramedian lumbar punctures than any cardiologist practicing ever in the history of the United States, but I don't do too many of them anymore.
00:02:52
Speaker
Once the house offices learn to do them, then I don't have to do them anymore.
00:02:56
Speaker
And I think that I just wanted to start there and I'll put a link in the show notes because this is something that you taught me when I was an intern and I got to upstage one of my senior fellows on one of my rotations as an intern.
00:03:10
Speaker
And it perhaps was the highest moment of my training.
00:03:13
Speaker
I never felt so empowered.
00:03:16
Speaker
So I want to thank you for that.
00:03:18
Speaker
But I do think it's a nifty technique that a lot of our listeners should learn and we'll put a link in the show notes.
Defining Cardiogenic Shock: Hemodynamics and Clinical Aspects
00:03:25
Speaker
But let's talk about cardiogenic shock, which is really the topic for today.
00:03:29
Speaker
And I would like to start, May, by hearing about your definition of when you were to explain to somebody who's not in medicine, what is cardiogenic shock?
00:03:37
Speaker
What would you tell them?
00:03:38
Speaker
And then maybe tell us what are some more pragmatic or practical definitions that some of the trials have utilized?
00:03:44
Speaker
Well, so the easiest definition, I think this is also the best definition, is
00:03:51
Speaker
inadequate tissue perfusion that is secondary to cardiac dysfunction.
00:03:57
Speaker
So I think that that definition encompasses both of the important aspects.
00:04:03
Speaker
Shock is really a perfusion defect, and cardiogenic shock says that it's the heart that's causing that defect in perfusion.
00:04:13
Speaker
So, but basically it has a hemodynamic definition.
00:04:18
Speaker
And so it's a hemodynamic disease as a recurrent theme over the course of this conversation.
00:04:23
Speaker
So basically that entails hypotension defined either as a blood pressure, systolic blood pressure less than 90 or a mean less than 60 or a drop of 40 millimeters less than the baseline blood pressure.
00:04:38
Speaker
But in any case, hypotension
00:04:40
Speaker
low cardiac output, usually defined as an index less than 2.2, and high filling pressures, defined usually as a wedge pressure greater than either 15 or some people use 18.
00:04:55
Speaker
So basically that's a hemodynamic definition that says that you have a low cardiac output, you have high filling pressures, and the failure of the heart has led to hypotension.
00:05:06
Speaker
So that hemodynamic definition is great and useful for all sorts of reasons, but there's also a clinical definition, and the clinical definition says that you have decreased cardiac output and evidence of tissue hypoperfusion on a clinical basis in the presence of what you think is adequate intravascular volume.
00:05:29
Speaker
So that's sort of, I think, a recognition of the fact is that
00:05:34
Speaker
Although hemodynamics are important, you don't have to have a PA catheter in your patient to recognize cardiogenic shock when you see it.
00:05:42
Speaker
Absolutely.
00:05:43
Speaker
And I think that it's important because, as we've seen with many other syndromes in critical care, people think of different patients when we use the same nomenclature.
00:05:53
Speaker
So cardiac shock, for me, might be something different than somebody else who I'm working with.
00:05:58
Speaker
And I think that getting everybody on the same page is important when we have these multidisciplinary
00:06:04
Speaker
teams caring for these very sick patients.
00:06:08
Speaker
Yeah, I think I agree with that.
00:06:09
Speaker
I also think that it just is sort of an addition.
00:06:13
Speaker
One of the things that goes to cardiogenic shock is that you ought to identify a reason that the patient's in cardiogenic shock.
00:06:19
Speaker
So you might have low blood pressure and you might have low cardiac index.
00:06:25
Speaker
If the patient is hypovolemic, then that's not cardiogenic shock.
00:06:28
Speaker
That's hypovolemic shock with a low cardiac output.
00:06:31
Speaker
So I think it's important to say there's an underlying cause, and we'll get to the causes, I think, relatively soon.
00:06:37
Speaker
But it's important to have some sense of why you think this particular patient is in cardiogenic shock at this particular moment.
Historical and Current Treatments of Cardiogenic Shock
00:06:46
Speaker
And I think that before we jump into the causes, maybe you could just give us a brief overview of what has happened to patients with cardiogenic shock.
00:06:53
Speaker
I think that clearly over the last several decades, the explosion on revascularization and the PCI has changed the landscape, but we still see plenty of patients with cardiogenic shock and maybe that incidence is changing.
00:07:08
Speaker
But what I've always been interested in or has been striking to me is that if you get cardiogenic shock in 2019,
00:07:15
Speaker
it's still pretty bad and maybe as bad as it was 20 years ago.
00:07:19
Speaker
Yeah, maybe not quite as bad as 20 years ago, but I do agree.
00:07:24
Speaker
So if you go all the way back,
00:07:28
Speaker
So if you go all the way back to the point where there was no revascularization for acute myocardial infarction, that is, so we're going to pre-thrombolytic times, we're going back into the 60s and 70s.
00:07:40
Speaker
Treatment of myocardial infarction was basically to put the patient in bed and to give them oxygen and morphine and to hope that they got better.
00:07:50
Speaker
And in that setting, if you got cardiogenic shock, you pretty much died.
00:07:54
Speaker
The heart wasn't coming back.
00:07:55
Speaker
Your blood pressure went down.
00:07:56
Speaker
There was nothing to do about it.
00:07:58
Speaker
And there was a, if you will, a nihilism.
00:08:01
Speaker
Why bother to treat cardiogenic shock no matter what you do?
00:08:04
Speaker
They all die.
00:08:06
Speaker
And so the first really big breakthrough was, and so then with revascularization, with thrombolytic therapy, the thought was that
00:08:18
Speaker
Well, lots of patients with acute MI did better.
00:08:23
Speaker
It turned out patients with cardiogenic shock didn't really do that well with thrombolytic therapy, in part because the lytic therapy didn't get there, in part because they had a lot of other problems.
00:08:35
Speaker
But it didn't really produce a revolution in, really didn't produce an improvement in cardiogenic shock outcomes like you would have thought, the way it produced an improvement in mortality from MI as a whole.
00:08:49
Speaker
And then the shock trial came, and that was sort of a landmark trial
00:08:57
Speaker
that was published by Judy Hockman and her group.
00:09:01
Speaker
And that looked at that randomized patients to percutaneous coronary intervention for cardiogenic shock versus lytic therapy.
00:09:12
Speaker
And interestingly enough, everybody in that trial got intra-aortic balloon pump support because that was felt to be the state of the art.
00:09:22
Speaker
And in that context,
00:09:24
Speaker
the mortality of cardiogenic shock was improved.
00:09:30
Speaker
So there was improvement in mortality from 56% to 49%.
00:09:38
Speaker
So that was much better than the previous results.
00:09:44
Speaker
And so with Rebask, so the dogma, at least in acute coronary syndrome, was that cardiogenic shock was not always fatal.
00:09:50
Speaker
Interestingly enough, there was a parallel trial that people don't really know about called SMASH by a guy named Philippe Urbin.
00:09:57
Speaker
in Europe, and that trial was stopped early because he could only recruit 80 patients.
00:10:03
Speaker
And the recruitment problems changed in the middle of the trial.
00:10:07
Speaker
So at first, he couldn't recruit anybody into the trial because everybody said, why bother to do angioplasty?
00:10:13
Speaker
You know everybody's going to die.
00:10:16
Speaker
And by the time he was trying to finish the trial, everybody said,
00:10:21
Speaker
We can't conscion not doing angioplasty on these patients.
00:10:25
Speaker
We don't want to randomize them not to get angioplasty because everybody knows they need it.
00:10:29
Speaker
So poor Dr. Urban managed to publish his results with 80 patients because that was all he could recruit.
00:10:36
Speaker
And actually, it chose more or less the same thing as the randomized shock trial, although the power is much lower.
00:10:43
Speaker
So that incidence, that mortality stayed at about, say, 60%.
00:10:47
Speaker
It went from 80% to 60% with revascularization.
00:10:51
Speaker
It stayed there for a fair amount of time, and only recently,
00:10:56
Speaker
with support devices has it come down?
00:10:59
Speaker
And the data suggests that the current mortalities are in the 40 to 45% range, depending on patients and settings and causes and such.
Causes and Classification of Cardiogenic Shock
00:11:11
Speaker
So, I mean, I guess you can sort of ask what you think about that number.
00:11:15
Speaker
So on the other hand, 40% is a lot better than 80%.
00:11:18
Speaker
On the other hand, 40% is awfully high mortality for any disease.
00:11:23
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And we certainly have a long way to go.
00:11:25
Speaker
to improve therapy.
00:11:27
Speaker
Absolutely.
00:11:28
Speaker
And maybe this would be a good time to talk about some of the causes.
00:11:31
Speaker
Obviously, the majority are going to be related to acute coronary syndromes, but could you give us maybe a little bit more of a deeper dive into what are other causes or how it relates to acute coronary syndromes?
00:11:42
Speaker
Sure.
00:11:42
Speaker
So there actually are a couple of causes.
00:11:45
Speaker
And as you allude to, the best data are with acute coronary syndromes.
00:11:49
Speaker
And the best data actually come from the shock trial registry.
00:11:53
Speaker
So the shock randomized trial was 300 patients, but there were fairly stringent eligibility criteria.
00:11:59
Speaker
And if you didn't make it in and you had to have pump failure, cardiogenic shock.
00:12:03
Speaker
So if you had some other cause or this or that,
00:12:06
Speaker
You didn't make it into the trial.
00:12:08
Speaker
So they kept those patients in a registry.
00:12:10
Speaker
And that registry, and so the data on causes in acute MI probably come from the shock trial registry and suggest that about three quarters of patients with acute coronary syndrome have cardiogenic shock from pump failure.
00:12:24
Speaker
And the other quarter have a smattering of causes, including mechanical causes of shock that we're probably going to get to in a little bit, and right ventricular infarction, and this and that.
00:12:36
Speaker
But it's certainly the most common cause of acute cardiogenic shock.
00:12:41
Speaker
There are other causes that are worthwhile, and some of the therapies that have been most developed most thoroughly in acute coronary syndromes have been translated to those other settings.
00:12:55
Speaker
The other more common setting and one that's somewhat, it's a different setting is end-stage heart failure.
00:13:02
Speaker
So if you have had a heart failure for a long time and you finally begin to worsen, then you're going to have a heart failure.
00:13:12
Speaker
then you can have cardiogenic shock sort of at the latter part of that stage.
00:13:18
Speaker
So in end-stage heart failure with hypotension and cardiogenic shock in those patients, have a different discussion about support, but it's also, it's support and you have to think about whether you have
00:13:30
Speaker
an end game in that setting.
00:13:33
Speaker
Myocarditis of various flavors can present with cardiogenic shock, and those patients, again, are really good candidates for support because many of those patients will improve if you only support them through the acute phase.
00:13:47
Speaker
In myocarditis is stress cardiomyopathy, sometimes known as Takasubo cardiomyopathy or Takasubo syndrome.
00:13:57
Speaker
I actually prefer stress cardiomyopathy
00:14:00
Speaker
as a term, but that's a story for another day.
00:14:03
Speaker
And then, as I'm learning in my world now, post-bypass.
00:14:08
Speaker
There is an incidence of cardiogenic shock.
00:14:10
Speaker
The heart is not perfused, or you go on bypass, it's a stress to the heart, and there's an incidence of cardiogenic shock post-bypass.
00:14:19
Speaker
Again, another setting where commonly mechanical support is employed in an attempt to tie patients through to recovery.
00:14:26
Speaker
So it is mostly acute coronary syndromes, but there are other settings in which cardiogenic shock can occur.
00:14:34
Speaker
And my understanding is that those other settings are driving an increase in the number of cardiogenic shock that we're seeing today.
00:14:41
Speaker
I presume mostly due to like increased surgeries, but also the patients with heart failure that we now can treat for much longer periods of time.
00:14:50
Speaker
Yes, that's exactly right.
00:14:51
Speaker
You'd expect with the idea would be with widespread use of early revascularization for acute coronary syndromes, mortality goes down and you'd expect the incidence of cardiogenic shock to go down, but it hasn't.
00:15:04
Speaker
And I think the reason you're exactly right about the reason.
00:15:08
Speaker
One of the reasons is that
00:15:10
Speaker
Some of these patients with acute coronary syndromes, instead of having mortality, are survivors, but they're survivors with left ventricular dysfunction, and that's driving an increase in late heart failure after acute coronary syndromes.
00:15:23
Speaker
But you're right, there's a lot more surgery, and in fact, I guess...
00:15:28
Speaker
not only is there more surgery, but because the interventional cardiologists are picking off the low-risk patients that are going to cardiac surgery, now the people in the operating room are higher risk and they have a higher incidence of trouble afterwards.
00:15:43
Speaker
Excellent.
00:15:44
Speaker
So I think that many of us who have read about cardiogenic shock have seen a figure that has several arrows and many loops that I think...
00:15:56
Speaker
It still is being utilized and actually we'll link it to the show notes.
00:16:00
Speaker
But I think that this was a creation you did maybe for a paper in the annals in the 90s.
00:16:06
Speaker
Is that correct?
00:16:07
Speaker
That's exactly right.
00:16:09
Speaker
And there are some people, you know, on that paper.
00:16:11
Speaker
But Dr. Perillo told me that I had to spend a lot of time making a beautiful figure.
00:16:19
Speaker
because people would be using that figure for a long time afterwards.
00:16:23
Speaker
And in this, as in many things, Dr. Perillo is absolutely correct.
00:16:28
Speaker
So the idea of that figure was that LV dysfunction, ischemia begets LV dysfunction and LV dysfunction begets ischemia, and that has the potential for a vicious cycle, and in fact, a death cycle, a death spiral.
00:16:46
Speaker
if uncorrected.
00:16:47
Speaker
So you have myocardial dysfunction, your blood pressure is low, your coronary perfusion pressure, which relies on your aortic diastolic pressure, which is low, and your LDN diastolic pressure, which is high, and so the gradient for coronary perfusion goes down.
00:17:04
Speaker
And so when that happens, coronary perfusion goes down, you wind up with ischemia.
00:17:08
Speaker
Ischemia causes left ventricular dysfunction.
00:17:11
Speaker
Left ventricular dysfunction causes cardiac output to drop and your blood pressure to drop, and that
00:17:16
Speaker
causes more ischemia, and you get in big trouble.
00:17:20
Speaker
And so that was the idea of that figure.
00:17:23
Speaker
There are sort of additions to that figure.
00:17:26
Speaker
Judy Hochman likes to refer to that figure as the classic description of cardiogenic shock, by which she means the old, now outmoded description.
00:17:35
Speaker
And what
00:17:36
Speaker
What her group added to that was the notion that in some patients there was an inflammatory component that causes inappropriate vasodilation and further contributes to hypotension.
00:17:47
Speaker
And I think that's correct.
00:17:48
Speaker
And I also think that that's of a piece of a certain final common pathway in all forms of shock, which is that eventually inflammation and refractory vasodilation can occur.
00:18:01
Speaker
And so it sort of all gets down into at least a similar pathway at the end.
00:18:06
Speaker
Excellent.
00:18:07
Speaker
So I think that what I would like to do, Steve, next is for you to tell us a little bit about classification, clinical classification of cardiogenic shock.
00:18:15
Speaker
And specifically, I wanted to hear from you in terms of a recent publication this year that you were part of with a Skype on a consensus conference statement talking about maybe a better way of thinking about these patients in terms of a spectrum and how we should communicate
00:18:36
Speaker
within each other when we're talking about cardiogenic shock patients.
00:18:40
Speaker
Yeah, I'm glad you asked.
00:18:42
Speaker
It's an interesting and I think a valuable effort.
00:18:45
Speaker
So the idea was that, so as you sort of alluded to, cardiogenic shock comes in a lot of flavors, but people just refer to cardiogenic shock and if you lump them all into one category, particularly with respect to severity, then it becomes a little difficult to select treatments and it also becomes difficult to compare outcomes.
00:19:10
Speaker
And this is particularly important in clinical trials and also in retrospective analyses.
00:19:16
Speaker
So people, particularly in the mechanical support world, they say, well, now we're doing better than we used to.
00:19:23
Speaker
And the question is, are you selecting patients, particularly in retrospective, look, are you selecting patients of equivalent severity?
00:19:30
Speaker
but it's also important in planning clinical trials.
00:19:32
Speaker
So if you do a clinical trial and the patients are all too sick to begin with, then it won't work.
00:19:38
Speaker
And if they're not sick enough, then it will do well, but your therapy won't benefit them because they were all going to do well no matter what.
00:19:44
Speaker
So some way of trying to standardize the risk in patients with cardiogenic shock was useful.
00:19:51
Speaker
So they came up with the
00:19:53
Speaker
five category.
00:19:54
Speaker
It's a little too cute for me, but it sort of works as an A, B, C, D, E category, and it's a pyramid going from a broad base on the bottom to a narrow base at the top.
00:20:04
Speaker
And so the A is for at risk.
00:20:06
Speaker
Those are patients who aren't in cardiogenic shock, but at least you ought to worry that they might
00:20:11
Speaker
that they might wind up in cardiogenic shock.
00:20:13
Speaker
And in the context of being in, say, a small hospital without a lot of resources, those are the patients that, particularly acute myocardial infarction, that you might think about transferring to the hub center just in case they get in trouble.
00:20:29
Speaker
I don't know that all those patients have to be transferred, but it's least at worst thinking about that.
00:20:34
Speaker
The second phase is beginning cardiogenic shock.
00:20:36
Speaker
That is, they're hypotensive.
00:20:38
Speaker
They're often tachycardic, but they do not present with hypoperfusion.
00:20:43
Speaker
So perfusion is still normal.
00:20:45
Speaker
They don't quite meet the definition of hypoperfusion and shock, but they're getting there.
00:20:50
Speaker
The blood pressure's lowish.
00:20:52
Speaker
The heart rate is highish.
00:20:53
Speaker
And these are the people you really should be worried about, the people you should be getting in, getting too early to try to keep them from coming to phase C, which is classic
00:21:04
Speaker
Cardiogenic shock, sort of the definition I gave you before.
00:21:06
Speaker
Hypoperfusion, requiring support with either vasopressor drugs or mechanical support.
00:21:15
Speaker
And then D is deteriorating.
00:21:17
Speaker
Those are patients who are deteriorating despite what you're doing.
00:21:20
Speaker
And those are patients where you need to think hard about whether there's more to do or whether there isn't any more to do.
00:21:26
Speaker
And then E is a category of patients in extremis, that is patients in cardiogenic shock who just had a cardiac arrest or just crashed and you're pumping on the chest.
00:21:35
Speaker
And that's a different scenario.
00:21:37
Speaker
And again, if you include those sorts of patients in, would say, classic cardiogenic shock, you're going to wind up with two really different populations.
00:21:47
Speaker
And I think that what I find very useful in this framework also relates to the fact that a single patient, let's say Mr. Johnson,
00:21:55
Speaker
usually during the hospital stay might go through all of these maybe and progress it.
00:22:00
Speaker
So it's a very dynamic and fluid classification that really, I mean, has patients moving from one category to another as you deteriorate, but also hopefully as we intervene and maybe are successful.
00:22:14
Speaker
Yeah, I think that's correct.
00:22:16
Speaker
And one thing that they also put in that's worth mentioning is that the category has what's called an arrest modifier.
00:22:25
Speaker
There's sort of a little subscript A. And that is to say that if you had a cardiac arrest at any point in your hospitalization,
00:22:33
Speaker
you do worse.
00:22:34
Speaker
So this was a theoretical classification, but there are actually now data.
00:22:39
Speaker
It's a very nice paper by Jake Jentzer at the Mayo Clinic and his colleagues that looked at a database and looked at and classified patients into this classification and looked at outcomes.
00:22:53
Speaker
And what it shows in
00:22:57
Speaker
It's gratifying is that, in fact, this classification from A to E does predict mortality with an increasing mortality as you go down the scheme from at risk to beginning to extremis.
00:23:09
Speaker
And in addition, they looked at patients with cardiac arrest, and cardiac arrest confers a worse prognosis in terms of mortality at each of the stages.
00:23:18
Speaker
So it's a recent paper out in the Journal of the American College of Cardiology, and it's at least initial validation of this classification in the setting of acute coronary syndromes.
00:23:30
Speaker
And I'll link that paper to the show notes, but I do think that, again, like you said, this has been at least validated with one paper, but also I think it's a very useful framework just to think of patients at the bedside.
00:23:43
Speaker
And I find it very interesting.
00:23:45
Speaker
The other thing that is in this paper that I would like to hear a little bit more from you, Steve, is they talk about three domains in terms of thinking about these patients, which I think are also good in terms of how we manage and evaluate these patients, which are basically the physical exam, biomarkers, and hemodynamics.
Assessing Cardiogenic Shock: Exams, Biomarkers, and Hemodynamics
00:24:07
Speaker
Yeah, so, and I think that's a,
00:24:10
Speaker
It's important, and I think one of the important things is that when you have three domains, you have the possibility that things get a little messy.
00:24:18
Speaker
You have one from column A and one from column B, but I think all those three things are important.
00:24:24
Speaker
So you have your clinical examination, you have whether somebody's in shock, and that's basically the examination to evaluate perfusion.
00:24:33
Speaker
do you have adequate perfusion?
00:24:36
Speaker
Remember, cardiac output is just a number.
00:24:38
Speaker
The question is whether that cardiac output is enough to provide the tissues with enough supply of nutrients for them to function.
00:24:45
Speaker
So you have the clinical signs of inadequate perfusion.
00:24:50
Speaker
And then you have laboratory values.
00:24:53
Speaker
And basically, you're looking at signs of global perfusion, prominently things like lactate, but also the usual suspects with respect to cardiogenic shock, arterial blood gases, degree of acidosis, renal function, CBCs and platelets and all that.
00:25:10
Speaker
And then finally and importantly, you have hemodynamics, and cardiogenic shock is a hemodynamic disease.
00:25:19
Speaker
The Swann-Gans catheter was basically invented to characterize cardiogenic shock, and so we're probably not going to get into a big debate about PA catheters, but if you ever use a PA catheter, this is the setting that you're going to use it in.
00:25:37
Speaker
And I think that that is something I wanted to dive into because obviously over the last several decades, the PA catheter has taken quite a beating.
00:25:45
Speaker
But I know that there's even some recent small studies that suggest that maybe in cartogenic shock populations, there is value.
00:25:52
Speaker
And like you said, that's why it was invented in the first place.
00:25:56
Speaker
But why don't we talk a little bit about the hemodynamic profiles of a cartogenic shock?
00:26:01
Speaker
I think that in general, people have always thought of volume status and peripheral circulation as
00:26:06
Speaker
determining different phenotypes that then have a very typical hemodynamic profile, but starting maybe with a very traditional cold and wet, which is I think the classic would be a category C cartogenic shock.
00:26:22
Speaker
But maybe you can explore a little bit more, not only that, but some of the other variants that we might see and why it's important.
00:26:29
Speaker
Right.
00:26:30
Speaker
So you're alluding to the original hemodynamic classification followed a clinical classification.
00:26:40
Speaker
So if you were warm and dry, then you had a good cardiac output and you had low filling pressures.
00:26:49
Speaker
If you were cold and dry,
00:26:51
Speaker
Then you had a low cardiac output, but you had low filling pressures.
00:26:57
Speaker
And those patients actually might improve their cardiac output if you give them fluid resuscitation.
00:27:01
Speaker
There aren't that many of those patients, but they're there.
00:27:03
Speaker
If you're warm and wet, that's sort of classic pulmonary edema.
00:27:06
Speaker
Your output's okay, but you have crackles on exam.
00:27:10
Speaker
And classic cardiogenic shock is cold and wet.
00:27:14
Speaker
It goes to the hemodynamic definition, low cardiac output.
00:27:18
Speaker
and elevated filling pressure.
00:27:19
Speaker
So that's sort of the classic thing.
00:27:21
Speaker
And people have sort of said, well, you know, if I've got pulmonary edema and cardiogenic shock, I already know the wedge pressure is high.
00:27:31
Speaker
Why is it so important to do a hemodynamic assessment?
00:27:35
Speaker
So I have an answer for that.
00:27:36
Speaker
And the answer for that is that I want to treat cardiac output and I want to know what the cardiac output is and I want to follow that.
00:27:43
Speaker
the effects of my therapy.
00:27:45
Speaker
But actually, the hemodynamics of cardiogenic shock have now sort of shifted into a different two-by-two category, looking at right ventricular output and left ventricular output.
00:27:59
Speaker
and the notion that you can have univentricular dysfunction.
00:28:03
Speaker
So you can have normal.
00:28:04
Speaker
So down on the bottom left would be normal right ventricular output and normal left ventricular filling pressures.
00:28:10
Speaker
If you have normal left ventricular filling pressures and high right ventricular filling pressures, then you have RV infarction and isolated right ventricular failure.
00:28:18
Speaker
And if you have normal right ventricular pressures, but high left ventricular pressures, then you have isolated left ventricular failure.
00:28:25
Speaker
And that's what
00:28:26
Speaker
most people think about when they think about cold and wet and cardiogenic shock.
00:28:30
Speaker
But what has come to the fore is the notion that ventricles, the left ventricle doesn't really fail alone very much.
00:28:38
Speaker
And many of these patients with cardiogenic shock, in fact, have biventricular failure.
00:28:43
Speaker
failure of both the right and the left ventricle.
00:28:46
Speaker
And if you don't do a hemodynamic assessment, you won't find that.
00:28:49
Speaker
You won't know that they have right.
00:28:51
Speaker
You'll know that they have left ventricular failure from the crackles on exam, but you won't know whether they have the right ventricular failure, and you won't know about the output.
00:28:59
Speaker
So the whole notion of increased hemodynamic assessment is not only to assess cardiac output and response to therapy, but also to look at right ventricular and left ventricular function.
00:29:12
Speaker
And part of the drivers of that is at least the potential availability of right ventricular mechanical support devices now.
00:29:19
Speaker
So now that there's something to do about the right ventricle, maybe it makes some sense to try to diagnose that problem.
00:29:26
Speaker
Excellent.
00:29:27
Speaker
And I think that
00:29:28
Speaker
Along those same lines, one of the things you mentioned earlier, Steve, was related to making sure that when you have cardiogenic shock or you identify cardiogenic shock, you figure out why the patient has cardiogenic shock.
00:29:40
Speaker
I think that a lot of times in other shock syndromes such as sepsis, we might not find a source and we'll treat them.
00:29:45
Speaker
But like you said, in cardiogenic shock, there are specific interventions that might be helpful that have identified the right cause we could implement.
00:29:55
Speaker
And what are the things that in somebody who you are seeing for the first time, maybe in the context of an ED consultation and you're suspecting cardiogenic shock that you would say are important in getting to that answer as to why?
00:30:08
Speaker
Sure.
00:30:08
Speaker
So to go back a little bit, so one of the things, so you want a clinical examination for perfusion.
00:30:14
Speaker
You want to look at capillary refill and you want to see whether they look sick and what does this patient look sick?
00:30:21
Speaker
It's probably the most important thing of all.
00:30:23
Speaker
And tachycardia and crackles and estries and murmurs and urine output and capillary refill, all that part of the clinical exam.
00:30:32
Speaker
You want to get the usual suspects, and that's an arterial blood gas.
00:30:38
Speaker
So just a little bit side.
00:30:41
Speaker
At least in this context, there's sort of a fad for venous blood gases in some emergency departments.
00:30:47
Speaker
That may be okay in some settings, but this is not one of them.
00:30:49
Speaker
You want to know what the pH is in the arterial system.
00:30:52
Speaker
You want to know what the PCO2 is in the arterial system.
00:30:55
Speaker
And you want to know what the PO2 is in the arterial system, not in the venous blood in the forearm.
00:31:00
Speaker
So you want a blood gas, you want electrolytes and CBC and troponins, which aren't very useful right away, but you might as well get them.
00:31:08
Speaker
And you want to follow, and you want to lactate.
00:31:10
Speaker
Maybe that one number isn't important, but the trend of the lactate is important.
00:31:14
Speaker
I think you want a chest x-ray.
00:31:16
Speaker
In this setting, this is not time to save money by not getting a chest x-ray.
00:31:20
Speaker
Just get a chest x-ray.
00:31:22
Speaker
You never know.
00:31:23
Speaker
Don't mistake the pulmonary edema for pneumonia, but it might not be pulmonary edema.
00:31:27
Speaker
It might be a pneumonia.
00:31:28
Speaker
It might be something else.
00:31:29
Speaker
You never know what you might find.
00:31:31
Speaker
And I think pretty much everybody with a suspected diagnosis of cardiogenic shock ought to have an echocardiogram.
00:31:40
Speaker
I also think it's important to say that that echocardiogram should be fairly comprehensive at some point.
00:31:47
Speaker
So you want overall left ventricular function, you want regional wall motion abnormalities, you want a Doppler exam to look for mechanical causes of cardiogenic shock, papillary muscle rupture, an acute ventricular septal defect, and maybe free wall rupture.
00:32:05
Speaker
You might find something else.
00:32:06
Speaker
You might find right ventricular failure, you might be looking at a pulmonary embolism that you didn't know about.
00:32:11
Speaker
You might be looking at an aortic dissection.
00:32:14
Speaker
So I think it's fine.
00:32:16
Speaker
There's a lot of this ED quick scan echocardiogram.
00:32:20
Speaker
That's fine.
00:32:21
Speaker
And it's no problem doing that, looking at a heart that's not pumping and saying, okay, I know at least to a first approximation what you're doing, what I'm dealing with.
00:32:30
Speaker
But I do think it's worth following that up with a really good comprehensive echocardiography sooner rather than later.
00:32:38
Speaker
And it's pretty much universal in cardiogenic shock.
00:32:42
Speaker
And I think that's a very valid point.
00:32:44
Speaker
I think something important to remind our audience that, like you said, we're really trying to get information that goes beyond just a fast hemodynamic assessment, and that information might have significant implications.
00:32:55
Speaker
So I do agree.
00:32:56
Speaker
I think that these patients should have, at the minimum, their echocardiography ordered in the ED, but hopefully they get it as soon as possible before they even leave the ED in most instances.
Fluid Management and Differential Diagnosis in Cardiogenic Shock
00:33:08
Speaker
So,
00:33:09
Speaker
Let's talk about treatment and maybe just start with fluids, which would be counterintuitive maybe in these cardiogenic shock patients, but sometimes might be useful in how you approach it.
00:33:19
Speaker
Yeah, so I don't think it's entirely unreasonable.
00:33:23
Speaker
There is that small population that's actually cold and dry.
00:33:28
Speaker
I don't think it's unreasonable to give a bolus of fluid to somebody who's hypotensive in your emergency department, but I'd be a little careful.
00:33:35
Speaker
If they're really frothing out of the lungs and their saturation is 89%, this is not the time to give them a liter and see what happens.
00:33:43
Speaker
Give them 250 cc's and see if they look better.
00:33:47
Speaker
And if they look better at 250 cc's, give them another 250 cc's, but carefully.
00:33:53
Speaker
And so it's also, you ought to think twice before you start doing 30 cc's per kilo sepsis resuscitation in these patients.
00:34:03
Speaker
Just if you think it's cardiogenic shock, maybe you should put on the brakes and get a little more information before you start doing that.
00:34:10
Speaker
But I don't think a little bit of fluid is always the wrong thing to do.
00:34:15
Speaker
Is there any value for you up front when you're trying to figure out in the BMP, which almost every patient I see has measured anyways, in terms of how you would apply it to these populations?
00:34:28
Speaker
Well, yes and no.
00:34:30
Speaker
I mean, I suppose if you get a BNP and it's high, it suggests that something's going on with the heart.
00:34:37
Speaker
It depends a little bit on what you already know about the patient.
00:34:40
Speaker
So if you already know that somebody, some of these patients in cardiogenic shock may have an abnormal ventricle to begin with, and if that happens, then your BNP is going to be abnormal to start with, and it isn't going to help you very much.
00:34:52
Speaker
But
00:34:53
Speaker
It's, and of course, BMPs can be higher and stuff like pulmonary embolism, et cetera, et cetera.
00:34:59
Speaker
But I don't think it's entirely unreasonable.
00:35:01
Speaker
I just think it's not especially helpful once you get your echo and figure out what's going on.
00:35:12
Speaker
And I think the other thing that we mentioned earlier related to making sure you differentiate between sepsis and
00:35:19
Speaker
septic shock and cardiogenic shock.
00:35:21
Speaker
But if I recall, Steve, in the shock trial originally, 19% or 20% of the patients had cardiogenic shock and were probably infected as well.
00:35:30
Speaker
So I guess that's a subset of patients that might occur, in which case, obviously, you're going to have to balance how you treat them.
00:35:36
Speaker
Yeah, it's a little tricky.
00:35:38
Speaker
They didn't really prove that a lot of those people had actual infection.
00:35:43
Speaker
What they had was vasodilation from inflammation that looked a lot, it was a sepsis-like picture.
00:35:50
Speaker
So I think that gets a little bit tricky of whether it's an actual infection or whether it's inflammation and consequent vasodilation.
00:36:00
Speaker
So there certainly are some people who are infected.
00:36:04
Speaker
And certainly worthwhile looking for infection.
00:36:06
Speaker
And some people with chronic heart failure can certainly get tipped over by infection.
00:36:10
Speaker
But I just, I'm a little cautious about that.
00:36:13
Speaker
So to me, it's a little, I'm a little cautious about an x-ray reading that calls pneumonia on somebody with pulmonary edema.
00:36:21
Speaker
If you've got sputum and a white count and it looks like pneumonia, then it probably is.
00:36:25
Speaker
But if you don't have sputum and you don't have a white count, the only thing you have going for pneumonia is an x-ray reading that says it looks like pneumonia.
00:36:32
Speaker
I'd think twice about that.
00:36:35
Speaker
And I think that's a great point.
00:36:36
Speaker
And that's where the echo obviously can also be very, very helpful in understanding the whole picture.
Airway Management and Medications in Cardiogenic Shock
00:36:44
Speaker
What about how do you deal with the airway or with ventilatory support in these patients?
00:36:49
Speaker
And I think that there's
00:36:50
Speaker
maybe a miss and the blurry line between what is decompensated heart failure, pulmonary edema and true cardiogenic shock.
00:37:01
Speaker
Yeah.
00:37:01
Speaker
So I have a little bias about this too.
00:37:03
Speaker
And so we'll talk about, maybe we should talk about it in two different contexts.
00:37:07
Speaker
So if you've got somebody with an acute coronary syndrome,
00:37:11
Speaker
And they come in and they're hypoxemic and breathing fast.
00:37:16
Speaker
And so they're in pulmonary edema.
00:37:19
Speaker
You've got them sitting bolt upright and you're giving them, you're ventilating them however you're ventilating them.
00:37:24
Speaker
To me, you have to think about what you're about to do.
00:37:27
Speaker
So you're about to take them to the cardiac catheterization laboratory and you're about to lay them flat.
00:37:32
Speaker
And when you do that, they are not going to like it.
00:37:34
Speaker
And I don't know whether, you probably have, I don't know whether all of your listeners have ever seen somebody trying to intubate somebody in a cardiac catheterization laboratory, but it gets ugly sometimes.
00:37:44
Speaker
So to me, if you're close to, and you're also using a lot of energy with ventilation, trying to breathe 35 times a minute.
00:37:52
Speaker
So if you're close to intubation in the ED and you're about to take somebody to the cath lab, my bias is to just go ahead and intubate them.
00:37:59
Speaker
There's nothing easier than extubating somebody who used to be in pulmonary edema but who is now not in pulmonary edema.
00:38:06
Speaker
And I don't see that there's much of a downside in extubating them, decreasing their work of breathing, making sure that their oxygenation is okay.
00:38:13
Speaker
With acute heart failure, it's a little fuzzy.
00:38:15
Speaker
BiPAP can sometimes tide these people over.
00:38:18
Speaker
But, again, I think you ought to watch these people, and you ought to have a low threshold for mechanical ventilation in this setting, particularly if you think you have somewhere to go in terms of reversing this.
00:38:30
Speaker
And I agree.
00:38:30
Speaker
I think that having been called to the cath lab emergently on multiple occasions, I always would have rather done it elsewhere or even before they got up there.
00:38:40
Speaker
It's a lot easier than trying to wrestle through the C-arm and trying to contort in different ways to get to the patient.
00:38:48
Speaker
So I think it's an important point of really having a low threshold for proceeding and securing the airway in these patients.
00:38:56
Speaker
You turn to them and you say, can I please have the Yankauer suction catheter in your cath lab?
00:39:01
Speaker
People say, what?
00:39:03
Speaker
Yeah, exactly.
00:39:04
Speaker
What about any, I know that there's no specific trials and modes of mechanical ventilation, but any comments that you have in general for these cardiogenic shock when they are on mechanical ventilation?
00:39:15
Speaker
I guess my bias is PEEP is good for heart failure, so particularly left-sided heart failure.
00:39:20
Speaker
So remember that PEEP decreases preload and actually also decreases afterload because you're putting, you're increasing the pressure in the chest and the distal aorta is outside the chest.
00:39:31
Speaker
So you're in fact helping the blood get from the aorta to out of the aorta.
00:39:35
Speaker
So my bias in ventilating them is to really, if you're given a lot of PEEP with BiPAP when you ventilate them, you probably ought to
00:39:43
Speaker
ought to give them PEEP.
00:39:44
Speaker
The only caveat is that if you have biventricular failure and your right ventricle is failing, then you need to be a little bit careful about too much PEEP.
00:39:51
Speaker
But in general, PEEP is good for these patients.
00:39:56
Speaker
And what about vasoactive drugs?
00:39:58
Speaker
Specifically, I guess we can start with vasopressors.
00:40:01
Speaker
This has been studied.
00:40:02
Speaker
I think that there's some still prevailing misconceptions of what are better catecholamines for septic shock.
00:40:09
Speaker
But just give us your take on
00:40:12
Speaker
basal oppressors and then maybe we can talk about inotropes and how you use it.
00:40:16
Speaker
Yeah, so the world has shifted a little bit.
00:40:19
Speaker
It used to be that the go-to drug in patients with bad ventricles was dopamine.
00:40:25
Speaker
in the days when a lot of people used a lot of dopamine.
00:40:28
Speaker
And so the SOAP trial, looking at comparing dopamine and norepinephrine, was done to look at that comparison in a number of settings.
00:40:39
Speaker
But there was a pre-specified subgroups of patients with shock.
00:40:43
Speaker
And so they pre-specified among the pre-specified subgroups was cardiogenic shock because the
00:40:49
Speaker
The thought beforehand was if dopamine was better in any group, it would be in the patients with cardiogenic shock.
00:40:56
Speaker
So as you probably know, that's the opposite of the way it turned out.
00:41:00
Speaker
For the trial as a whole, there was really no significant difference between dopamine and norepinephrine, although there were more.
00:41:06
Speaker
arrhythmias with dopamine.
00:41:07
Speaker
But in the subgroup of patients with cardiogenic shock, norepinephrine was in fact better.
00:41:12
Speaker
And so that to me has changed the landscape.
00:41:14
Speaker
I'm more inclined to reach for norepinephrine as my first choice in that population.
00:41:20
Speaker
One caveat is that the cardiogenic shock population in that trial was not especially well-defined.
00:41:26
Speaker
It was fairly heterogeneous.
00:41:28
Speaker
And so
00:41:29
Speaker
I don't know that this, you could argue that it's not entirely clear that that applies to all subsets, but I do think norepinephrine is a reasonable first choice.
00:41:39
Speaker
The other thing about the patients with acute coronary syndromes are predisposed to tachyarrhythmias.
00:41:46
Speaker
So if you're in trouble with tachyarrhythmias,
00:41:48
Speaker
then either adding something like phenylephrine, which isn't really an especially good, it has no inotropic effect and isn't really an especially great vasopressor.
00:41:59
Speaker
But once in a while, if you're really looking at BT and BT and BT, a little bit of phenylephrine added to norepinephrine is sometimes useful.
00:42:08
Speaker
Vasopressin may be in that setting, although it's a pretty good coronary vasoconstrictor and not something that you'd really like to do if you could avoid it.
00:42:18
Speaker
And what about inotrope support, Steve?
00:42:20
Speaker
What is your go-to drug and how do you look at that?
00:42:23
Speaker
Yeah, so in cardiogenic shock, usually dobutamine is a first choice in my practice, mostly because of the short half-life.
00:42:34
Speaker
Dobutamine, as you probably know, it has beta-2 effects, but it also has beta-1 effects, but it also has alpha-1.
00:42:43
Speaker
1 and beta 2 effects, so the alpha effects are vasoconstrictive, the beta 2 effects are vasodilatory.
00:42:49
Speaker
They usually cancel themselves out, and at the same resistance, if you increase cardiac output, you'll increase blood pressure.
00:42:56
Speaker
So, dibutamine is not a vasopressor, it's an inotrope, but it's usually a reasonable first choice.
00:43:01
Speaker
It is more arrhythmogenic than something like milrinone.
00:43:04
Speaker
The problem is milrinone is a vasodilator and can make your blood pressure worse.
00:43:09
Speaker
And milrinone also has a longer half-life.
00:43:12
Speaker
So if you get in trouble with milrinone, you get in trouble for a longer time than if you get in trouble with dopamine.
00:43:18
Speaker
In Europe, they have levosimendan.
00:43:20
Speaker
Hasn't really been improved in clinical trials, even in Europe, and it's not available in the U.S., so I don't have any experience whatsoever with that, but there are those who believe in levosimendan.
00:43:33
Speaker
But we could use a new inotrope or two.
00:43:36
Speaker
And are there any other evasoactive drugs that you have sometimes utilized?
00:43:41
Speaker
I mean, there are obviously some pulmonary evasodilators that sometimes might be helpful.
00:43:45
Speaker
I know that there's not a lot of evidence behind them, but any other drugs that you might want to mention?
00:43:51
Speaker
Yeah, I think there are no data about pulmonary vasodilators.
00:43:55
Speaker
I think if you're getting into the notion, if you're in the world of right-sided failure and you want an isolated right-sided vasodilator, you can think about something like inhaled pristocybin or inhaled nitric oxide.
00:44:10
Speaker
The data for
00:44:12
Speaker
The data in left heart failure and in acute coronary syndromes for some of the drugs used for pulmonary hypertension, the endothelial antagonists, and the possible diesterase inhibitors are either nonexistent or negative.
00:44:23
Speaker
So I really don't think that they have a role there.
00:44:27
Speaker
So before we go into the mechanical devices and PCI, the role of both of these, I think, is obviously critical and has really changed the landscape.
00:44:36
Speaker
I wanted to ask you a little bit about CRRT.
00:44:39
Speaker
I did notice that in the AHA guidelines and many other guidelines, they specifically talk about CRRT and cartogenic shock.
00:44:47
Speaker
I haven't seen any large trials, but I just wanted to take your impression in terms of how do you utilize it.
00:44:53
Speaker
It's something you adopt early and in who?
00:44:56
Speaker
Yeah, so I think it is useful.
00:44:58
Speaker
So, you know, the challenge is often you get acute kidney injury and cardiogenic shock and you have no urine output and you keep pouring fluid in and pouring fluid in or not, but
00:45:11
Speaker
If it's not going anywhere, you'd kind of like to control the volume, particularly when you have right-sided dysfunction or as we've talked about in some of the support devices when the right side is stressed.
00:45:24
Speaker
So trying to keep fluid volume in a reasonable state is a good idea.
00:45:29
Speaker
Dialysis itself often not well-tolerated.
00:45:33
Speaker
You take all that blood, you stick it in the dialysis machine, and the blood pressure goes down, then you need more vasopressor support.
00:45:39
Speaker
So some of the continuous modalities are very useful, whether that's CBVH or whether the nephrologists think they can do the same with what they call SLED, the acronym SLO, SLO, continuous, something.
00:45:57
Speaker
I can't remember what SLED stands for.
00:45:59
Speaker
But SLED is six hours of slow hemoperfusion.
00:46:04
Speaker
But I think that those are underutilized and should be utilized more often.
00:46:09
Speaker
I'll have to confess that we don't do CBVH just now.
00:46:13
Speaker
Stay tuned.
00:46:13
Speaker
In two months, we're hoping to start.
00:46:15
Speaker
But I think it can be useful.
00:46:17
Speaker
And again, I think earlier is better.
Mechanical Support and Intervention Strategies
00:46:20
Speaker
Excellent.
00:46:20
Speaker
So let's talk about mechanical devices.
00:46:22
Speaker
And I think that this is really something that has really changed the landscape.
00:46:26
Speaker
And then we can finish the treatment discussion with just, I mean, what are the current recommendations for PCI so that
00:46:33
Speaker
our audience is aware.
00:46:35
Speaker
But in terms of mechanical devices, Steve, when are you thinking of these?
00:46:39
Speaker
I guess anybody who's a C, you start thinking about it.
00:46:43
Speaker
Yeah.
00:46:44
Speaker
For sure.
00:46:45
Speaker
Yes, B's for sure.
00:46:46
Speaker
And C's for sure, D's for sure, that's where you're going with D. C is failing, you're going for a mechanical support device.
00:46:55
Speaker
And so the old classic is the intra-aortic balloon pump.
00:47:00
Speaker
It's easily available, it's inserted in the femoral artery.
00:47:07
Speaker
And so it's readily available in all sorts of hospitals.
00:47:11
Speaker
The challenge with the balloon pump is that it doesn't really, so it increases diastolic pressure, which is good for coronary perfusion, except that it doesn't really do that if you have a pinhole of a stenosis.
00:47:23
Speaker
And it decreases afterload when that balloon deflates, but it turns out that only raises cardiac output by 500 cc's or so.
00:47:30
Speaker
It's not really a great way to raise cardiac output.
00:47:32
Speaker
And in fact, in a randomized control trial, comparing a balloon pump to no balloon pump, there was no benefit, actually, to randomized control trials.
00:47:41
Speaker
So the balloon pump, if a balloon pump is all you have, that's okay, but most people with other choices have gone to those other choices.
00:47:50
Speaker
So, the axial flow pump, they actually, there are two of them.
00:47:55
Speaker
One is the PHP, but the more common one is called the impella.
00:48:00
Speaker
And that's an axial flow pump that goes across the aortic valve and using the principle of Archimedes screw, the rotor spins and it sucks the blood from the left ventricle, from the
00:48:13
Speaker
inlet cannula and left ventricle to the outflow cannula and the aorta.
00:48:18
Speaker
And so it's doing much of the pump function of the heart.
00:48:21
Speaker
So it unloads the left ventricle and also increases its output.
00:48:26
Speaker
That's relatively easy to put in the cath lab because it's a femoral approach and the interventional cardiologists are used to going, putting a wire across the aortic valve, putting it in.
00:48:37
Speaker
And so it's a good device.
00:48:42
Speaker
And there have been registry data suggesting that if you use these devices, in particular, if you use them early, outcomes are better than historical controls.
00:48:52
Speaker
The caveat there is there are no randomized trial, and the outcome of registry data are quite dependent on patient selection.
00:49:02
Speaker
So if you use it in patients who ultimately would have done well without it, it's going to look good.
00:49:06
Speaker
And if you use it in patients who wouldn't have done well except for the device, then it's an appropriate use of that device.
00:49:13
Speaker
But at least the data, many of the data suggest that if you use this
00:49:18
Speaker
technology in appropriately selected patients, your mortality can go into the 25% range, which is pretty good.
00:49:25
Speaker
The Tandem Heart is a slightly more complicated device that relies on external pump.
00:49:31
Speaker
It's sort of a little clever device.
00:49:32
Speaker
It goes through a transeptal puncture into the left atrium, and it takes oxygenated blood out of the left atrium, and it pumps it back into the arterial circulation.
00:49:44
Speaker
That's a good support device.
00:49:49
Speaker
And actually works very well.
00:49:51
Speaker
It's a little more complicated to insert.
00:49:53
Speaker
You have to have institutional expertise, but in institutions that are good at that, the results are pretty good and to some extent comparable to the Impella.
00:50:00
Speaker
Again, really no randomized trials that suggest efficacy.
00:50:05
Speaker
And then the other thing that can be done and that can be done at most places is full-on VA ECMO.
00:50:11
Speaker
cannula, blood, one cannula in the femoral vein, one cannula in the femoral artery, blood comes out of the femoral vein, goes through an oxygenator, goes into the femoral artery.
00:50:20
Speaker
That is a, it's important to recognize that's a circulatory support device that raises blood pressure and raises cardiac output.
00:50:28
Speaker
But in fact, that actually is not a left ventricular support device.
00:50:31
Speaker
You're taking blood out of the venous circulation, you're putting it back in the arterial circulation into the aorta.
00:50:37
Speaker
And if anything, you're increasing the afterload of the left ventricle.
00:50:41
Speaker
So there's now a movement to sort of vent the left ventricle.
00:50:46
Speaker
If the left ventricle isn't pumping, you want to vent it so it doesn't blow up, and there are any number of ways to do that.
00:50:53
Speaker
In the operating room, you can put a left atrial vent.
00:50:56
Speaker
You can put in an impeller device, the so-called ecapella configuration, and some people use a balloon pump.
00:51:05
Speaker
The other thing to talk about with these devices may be expense.
00:51:09
Speaker
The balloon pump is not entirely expensive.
00:51:12
Speaker
I don't know, it probably runs $500 or $600.
00:51:15
Speaker
ECMO is not stunningly expensive.
00:51:16
Speaker
It's a couple of thousand dollars.
00:51:18
Speaker
Impella and Tandem Heart are expensive.
00:51:20
Speaker
We're talking $25,000 to $30,000 at current prices.
00:51:25
Speaker
And the other thing I wanted to ask you about, which I think is also a rationale that I sometimes hear our interventional cardiologists use,
00:51:33
Speaker
is this whole concept of CPO, cardiac power output, and how that may make the Impella, especially the 5.0 more attractive?
00:51:45
Speaker
Correct.
00:51:46
Speaker
So the cardiac power output is a hemodynamic measure.
00:51:50
Speaker
And basically that says how much work is the heart doing?
00:51:53
Speaker
So it's basically very simple.
00:51:56
Speaker
It's cardiac output times mean arterial pressure.
00:51:59
Speaker
So how much is it pumping and what is the heart pumping against and then you divide by a fudge factor of 451 to make the units work.
00:52:08
Speaker
And so that cardiac output, the sort of magic number there is 0.6.
00:52:12
Speaker
So, you know, Sergio, if you have a cardiac output of five liters and a mean arterial pressure of, say, 80, then you're probably doing okay.
00:52:26
Speaker
But if you have a cardiac output of four and a mean arterial pressure of 60, then you're not.
00:52:31
Speaker
So people have used that number as sort of a cutoff, and there are registry data that suggests that if you look at your lactate and your cardiac power output after initiation of mechanical support,
00:52:48
Speaker
So that's relatively shortly after.
00:52:51
Speaker
If your lactate is still high and your cardiac output is low, you're in big trouble.
00:52:56
Speaker
And if your lactate is coming down and your cardiac output is high, you do well and one or the other is sort of intermediate.
00:53:02
Speaker
So I think that's actually a good marker.
00:53:05
Speaker
It essentially says, how much work is the heart together with my mechanical support device doing?
00:53:10
Speaker
How well am I supporting the circulation?
00:53:12
Speaker
And that's, again, another motivation.
00:53:14
Speaker
So if you're going to calculate a cardiac power output,
00:53:17
Speaker
then you do that with a cardiac output.
00:53:19
Speaker
I should mention there's another hemodynamic index that is useful in the context of right ventricular pressure, and that's called the pulmonary artery pulsatility index, initials PAPI, P-A-P-I, and that's basically the pulse pressure in the pulmonary circulation divided by the right atrial pressure.
00:53:39
Speaker
So if your pulse pressure is high and your right atrial pressure is low, then that number is high.
00:53:45
Speaker
And if your pulse pressure is low, suggesting your right ventricle isn't pumping, and your right atrial pressure is high, suggesting your right ventricular pressures are high, then that number, that PAPI is low and that's trouble.
00:53:58
Speaker
Excellent.
00:53:59
Speaker
And I think that to kind of finalize the treatment discussion, could you tell us just what the current state or what does a
00:54:08
Speaker
critical care physician need to know about PCI and cardiogenic shock?
00:54:13
Speaker
So they need to know the sooner is better and they need to know that to call somebody.
00:54:18
Speaker
It turns out the shock trial actually accepted people out to 18 hours.
00:54:24
Speaker
So to me, whatever time it is, you ought to be going to the cath lab.
00:54:29
Speaker
And the landscape of what to do at PCI for the interventional cardiologist has changed a little bit.
00:54:38
Speaker
So it used to be
00:54:40
Speaker
that you did the culprit artery and then you stopped.
00:54:43
Speaker
And then for a while there was a little bit of data suggesting that multivessel PCI in the setting of MI is better than just doing the single vessel.
00:54:51
Speaker
And then there was something called the culprit shock trial, which randomized patients to multivessel PCI versus single vessel PCI.
00:54:58
Speaker
And the people who had single vessel culprit PCI did better in that trial.
00:55:03
Speaker
And so the pendulum has sort of switched to just doing the culprit artery.
00:55:09
Speaker
I also think there is a school of thought, there's now a trial as well, looking at impella support before PCI.
00:55:18
Speaker
It's kind of a little scary concept, and the idea is that the ventricle, if you support the ventricle with a support device for half an hour before you even do the PCI, that the heart is in better shape and it recovers better after you actually do your PCI.
00:55:33
Speaker
That is being tested in the clinical trial.
00:55:36
Speaker
The pilot trial suggested that that was in fact safe.
00:55:39
Speaker
So you're asking the interventional cardiologist to just look at the patient for half an hour and not even do an angiogram.
00:55:44
Speaker
But the patients looked okay and were awaiting results of that trial, probably be a good 12 to 18 months before then.
00:55:52
Speaker
But I think that you need to go to the cath lab, you need to think about a support device, you need to revascularize, and if you don't have that in your institution where you are,
00:56:02
Speaker
then you really ought to send the patient to an institution where that's an option.
00:56:06
Speaker
And the other question I had regarding PCI, Steve, is I know that if you have a non-STEMI, right, you're much less likely to go to the cath lab immediately.
00:56:17
Speaker
However, if you have a non-STEMI and cardiogenic shock, it's a different story, right?
00:56:22
Speaker
That's correct.
00:56:22
Speaker
So to me, cardiogenic shock, the shock trial did not distinguish by STEMI or non-STEMI.
00:56:27
Speaker
If you've got a patient in cardiogenic shock, it no longer matters whether you have ST elevation or not.
00:56:32
Speaker
They're in trouble with a closed artery and you need to go to the cath lab and try to open that artery.
00:56:37
Speaker
Excellent.
00:56:38
Speaker
So the last question I have regarding cardiogenic shock was just if you could just give us a very brief overview, a reminder.
Complications in Acute Coronary Syndrome Leading to Cardiogenic Shock
00:56:47
Speaker
on some of the mechanical complications associated with acute coronary syndrome that might lead to a cardiogenic shock, which used to be much more common before early reperfusion, but these days still appear, and sometimes they appear after surgery, and maybe the timing has changed, but I still think it's important to have that clinical suspicion and understand what's happening.
00:57:09
Speaker
Yeah, I think that is true.
00:57:11
Speaker
And it's the other thing to say about that.
00:57:13
Speaker
They are much less common with early reperfusion, but sometimes you'll see patients who have late reperfusion for whatever reason.
00:57:20
Speaker
They've been having pain for three days, and they didn't see anybody, and you're finally seeing them late.
00:57:24
Speaker
And those people really are at risk for complications of acute myocardial infarction and sometimes actually present with them four days after what, in retrospect, you think was the index event.
00:57:35
Speaker
So basically three...
00:57:37
Speaker
three important complications.
00:57:39
Speaker
First is papillary muscle rupture.
00:57:42
Speaker
That is, you have an infarct and the papillary muscle ruptures, you get torrential mitral regurgitation, you wind up in cardiogenic shock and pulmonary edema.
00:57:50
Speaker
And basically, you need to go to the operating room and you need to replace that valve as soon as you can.
00:57:56
Speaker
That's not a situation which you can wait around.
00:57:59
Speaker
You support the patient as you can, some with an intra-artic balloon pump or not.
00:58:03
Speaker
If you're in an institution without surgery, you get them to an institution with surgery and you try to replace that valve.
00:58:10
Speaker
Acute ventricular septal defect, again, comes in two flavors.
00:58:16
Speaker
It comes in with an anterior MI where the defect is in the anterior septal wall and inferior MI where it's down in the inferior wall.
00:58:26
Speaker
And again, that gets a little bit tricky.
00:58:29
Speaker
The mortality, even with surgery, is high.
00:58:31
Speaker
And interestingly enough, the ones that are inferior MIs are harder.
00:58:36
Speaker
And the reason is that even if the infarct is smaller and the rest of the ventricle is okay, that's down at the apex of the heart and it's dead and it's mushy and your surgeon has a real challenge trying to put that all together.
00:58:48
Speaker
So they would like to wait and see if it scars in and becomes an easier operation.
00:58:54
Speaker
The challenge is that patients may not do very well while they're waiting.
00:58:58
Speaker
It's a tough clinical problem.
00:59:00
Speaker
And the last problem is free wall rupture.
00:59:02
Speaker
That is rupture out into the pericardium, occasionally into the thoracic cavity, usually into the pericardium.
00:59:10
Speaker
If it's free rupture out into the thoracic cavity, that's probably not survivable.
00:59:16
Speaker
But into the pericardium, and classically you see sort of a pseudoaneurysm.
00:59:21
Speaker
Classically it's an elderly hypertensive patient, more women than men,
00:59:27
Speaker
who just sort of look gray and start vomiting and they look awful.
00:59:31
Speaker
If you think about this after MI and you get an echocardiogram and you see tamponade which doesn't belong, then you may have the diagnosis and you need to go as quickly to the operating room as you can.
00:59:44
Speaker
The other thing to mention about that is that pericardiosynthesis in that setting is a double-edged sword.
00:59:49
Speaker
So if you take away the fluid that is plugging the hole in the heart, you may wind up with a bigger hole in the heart.
00:59:57
Speaker
So you ought to think twice before doing pericardiocentesis and you ought to have a chat with your surgeon and maybe you should go straight to the operating room and maybe pericardiocentesis raises the blood pressure and buys you a little bit of time, but you ought to think twice about doing that.
01:00:12
Speaker
Excellent.
01:00:13
Speaker
So I think we could keep talking about a lot of these topics, Steve, but I want to be very respectful of your time.
01:00:19
Speaker
And one of the things we do at the podcast is end the episode and
01:00:24
Speaker
with some questions that tap into the wisdom of our guests that are unrelated to the topic we spoke of.
01:00:30
Speaker
Would that be okay?
01:00:32
Speaker
Sure.
01:00:33
Speaker
So the first question relates to books.
01:00:36
Speaker
And I wonder if there's a book that has influenced you the most or if there's a book that you have gifted often to others.
01:00:42
Speaker
So I have, I guess actually probably the, so if we go back to childhood, I read a book called Microbe Hunters by Paul De Cruyff, which just had all these guys figuring out this cool microbiology stuff and really got me interested in science.
01:01:00
Speaker
And then further along in my training, probably two books, both novels, Ulysses by James Joyce, really a new concept of how to write and the importance of the common man and Gravity's Rainbow, which just has this wonderful
01:01:20
Speaker
different odd perspective way of looking at the world.
01:01:24
Speaker
None of those books are books that I have commonly gifted.
01:01:27
Speaker
And actually, there's the one I probably most commonly gifted and the best one I gift.
01:01:33
Speaker
So the one I probably most commonly gifted is a book called The Elements of Style about how to write because I think writing is most important.
01:01:42
Speaker
And I used to give it to the new fellows when they came.
01:01:46
Speaker
But if I had to give one book, it would probably be Sant Exuperee's Little Prince, which is just a wonderful, wonderful book.
01:01:55
Speaker
Excellent.
01:01:56
Speaker
And I do think that one of the things that I mentioned at the intro that you have really taught me a lot of things, but one of the things that has been imprinted in my thought process is that good writing reflects organized thinking.
01:02:12
Speaker
disorganized writing reflects disorganized thinking and how important it really is to put that effort when we write things and making sure that we're expressing things in an organized way.
01:02:22
Speaker
Yeah, I couldn't agree more.
01:02:25
Speaker
So the second question relates to things you believe in to be true that you think most other people or many people don't believe to be true.
01:02:35
Speaker
Yeah, so I guess I've really been, at least in my clinical practice, I always think that understanding the physiology and understanding the pathophysiology, both on a broad level and in an individual patient, is really important, not only in this setting, but also to improve your own practice.
01:02:56
Speaker
And I guess I've thought about this.
01:02:59
Speaker
There are sort of two ways of looking at the world.
01:03:02
Speaker
One way is to say that, and this is what I think most people think is that if you only understood something well enough, then you could make it simple.
01:03:12
Speaker
I think most people believe that.
01:03:15
Speaker
And I actually sort of have a different view, which I think I picked up at Hopkins, where they have some really very, very great physiologists.
01:03:26
Speaker
And at least what I've come to believe is that the harder you look at something, in fact, the more complicated and complex it gets.
01:03:36
Speaker
And I think that is true.
01:03:37
Speaker
And I think that also, I mean, the more we understand about something, the more we know that we really don't understand it at all, right?
01:03:44
Speaker
Yeah, it's a different way of putting the same thought.
01:03:47
Speaker
Excellent.
01:03:48
Speaker
So the final question is related to what would you want every intensivist or listener to listen to us in this episode to know?
01:03:56
Speaker
Right.
01:03:56
Speaker
So I'm going to give you one of my favorite quotes.
01:04:00
Speaker
And that quote is,
01:04:03
Speaker
Good judgment comes from experience and experience comes from bad judgment.
01:04:09
Speaker
So what that means to me is that really, really to get good at practicing medicine, the part is practicing.
01:04:19
Speaker
You have to go to the bedside, you have to try stuff, you have to see what works and you also have to see what doesn't work.
01:04:26
Speaker
You have to get yourself into trouble and then you have to get yourself out of trouble, hopefully.
01:04:32
Speaker
And that it's really there's sort of there's a tendency to look at studies and data and think of, if you will, the electronic patient.
01:04:45
Speaker
And it's a real patient in front of you.
01:04:49
Speaker
And looking at them and talking to them provides insights that you just can't get any other way.
01:04:56
Speaker
And I think that's a great place to stop.
01:04:58
Speaker
Steve, thank you so much for your time and for sharing your expertise and thoughts with us.
01:05:02
Speaker
And I look forward to having you back on Critical Matters soon.
01:05:05
Speaker
It's been a genuine pleasure.
01:05:07
Speaker
Thank you for having me.
01:05:09
Speaker
Thank you for listening to Critical Matters, a sound critical care podcast.
01:05:14
Speaker
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01:05:19
Speaker
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01:05:25
Speaker
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