Transcript
Speaker: Welcome to Critical Matters, a sound critical care podcast covering a broad range of topics related to the practice of intensive care medicine.
Speaker: Sound Critical Care provides comprehensive critical care programs to hospitals across the country.
Speaker: To learn more about our programs and career opportunities, visit www.soundphysicians.com.
Speaker: And now your host, Dr. Sergio Zanotti.
Speaker: Cardiogenic shock is a common cause of mortality, and its management remains challenging despite significant advances in treatment options.
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.
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.
Speaker: Our guest is Dr. Steve Hollenberg.
Speaker: Dr. Hollenberg is a practicing cardiologist with dual training in cardiology and critical care medicine.
Speaker: He is professor of medicine at Hackensack Meridian School of Medicine at Seton Hall University in New Jersey.
Speaker: In addition, he's the associate director of the CTICU at Hackensack Meridian University Hospital.
Speaker: Dr. Hollenberg is a recognized expert in cardiovascular critical care and has published extensively on the topic.
Speaker: He is a dear friend who over the years has taught me a lot
Speaker: first as my attending in the MICU and CCU, then as a research mentor, and finally as a colleague.
Speaker: It's a true pleasure and honor to have him as a guest on Critical Matters.
Speaker: Steve, welcome to the podcast.
Speaker: Thank you.
Speaker: It's a pleasure to be here.
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.
Speaker: You want me to tell you about that?
Speaker: Please.
Speaker: Yes, so when I was a critical care fellow at the NIH, it was multidisciplinary.
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.
Speaker: And since then, I've never done anything other than the paramedian lumbar puncture.
Speaker: And one of my favorite things and trainees is to say, oh, let me show you how to do a paramedian lumbar puncture.
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.
Speaker: Once the house offices learn to do them, then I don't have to do them anymore.
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.
Speaker: And it perhaps was the highest moment of my training.
Speaker: I never felt so empowered.
Speaker: So I want to thank you for that.
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.
Speaker: But let's talk about cardiogenic shock, which is really the topic for today.
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?
Speaker: What would you tell them?
Speaker: And then maybe tell us what are some more pragmatic or practical definitions that some of the trials have utilized?
Speaker: Well, so the easiest definition, I think this is also the best definition, is
Speaker: inadequate tissue perfusion that is secondary to cardiac dysfunction.
Speaker: So I think that that definition encompasses both of the important aspects.
Speaker: Shock is really a perfusion defect, and cardiogenic shock says that it's the heart that's causing that defect in perfusion.
Speaker: So, but basically it has a hemodynamic definition.
Speaker: And so it's a hemodynamic disease as a recurrent theme over the course of this conversation.
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.
Speaker: But in any case, hypotension
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.
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.
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.
Speaker: So that's sort of, I think, a recognition of the fact is that
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.
Speaker: Absolutely.
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.
Speaker: So cardiac shock, for me, might be something different than somebody else who I'm working with.
Speaker: And I think that getting everybody on the same page is important when we have these multidisciplinary
Speaker: teams caring for these very sick patients.
Speaker: Yeah, I think I agree with that.
Speaker: I also think that it just is sort of an addition.
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.
Speaker: So you might have low blood pressure and you might have low cardiac index.
Speaker: If the patient is hypovolemic, then that's not cardiogenic shock.
Speaker: That's hypovolemic shock with a low cardiac output.
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.
Speaker: But it's important to have some sense of why you think this particular patient is in cardiogenic shock at this particular moment.
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.
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.
Speaker: But what I've always been interested in or has been striking to me is that if you get cardiogenic shock in 2019,
Speaker: it's still pretty bad and maybe as bad as it was 20 years ago.
Speaker: Yeah, maybe not quite as bad as 20 years ago, but I do agree.
Speaker: So if you go all the way back,
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.
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.
Speaker: And in that setting, if you got cardiogenic shock, you pretty much died.
Speaker: The heart wasn't coming back.
Speaker: Your blood pressure went down.
Speaker: There was nothing to do about it.
Speaker: And there was a, if you will, a nihilism.
Speaker: Why bother to treat cardiogenic shock no matter what you do?
Speaker: They all die.
Speaker: And so the first really big breakthrough was, and so then with revascularization, with thrombolytic therapy, the thought was that
Speaker: Well, lots of patients with acute MI did better.
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.
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.
Speaker: And then the shock trial came, and that was sort of a landmark trial
Speaker: that was published by Judy Hockman and her group.
Speaker: And that looked at that randomized patients to percutaneous coronary intervention for cardiogenic shock versus lytic therapy.
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.
Speaker: And in that context,
Speaker: the mortality of cardiogenic shock was improved.
Speaker: So there was improvement in mortality from 56% to 49%.
Speaker: So that was much better than the previous results.
Speaker: And so with Rebask, so the dogma, at least in acute coronary syndrome, was that cardiogenic shock was not always fatal.
Speaker: Interestingly enough, there was a parallel trial that people don't really know about called SMASH by a guy named Philippe Urbin.
Speaker: in Europe, and that trial was stopped early because he could only recruit 80 patients.
Speaker: And the recruitment problems changed in the middle of the trial.
Speaker: So at first, he couldn't recruit anybody into the trial because everybody said, why bother to do angioplasty?
Speaker: You know everybody's going to die.
Speaker: And by the time he was trying to finish the trial, everybody said,
Speaker: We can't conscion not doing angioplasty on these patients.
Speaker: We don't want to randomize them not to get angioplasty because everybody knows they need it.
Speaker: So poor Dr. Urban managed to publish his results with 80 patients because that was all he could recruit.
Speaker: And actually, it chose more or less the same thing as the randomized shock trial, although the power is much lower.
Speaker: So that incidence, that mortality stayed at about, say, 60%.
Speaker: It went from 80% to 60% with revascularization.
Speaker: It stayed there for a fair amount of time, and only recently,
Speaker: with support devices has it come down?
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.
Speaker: So, I mean, I guess you can sort of ask what you think about that number.
Speaker: So on the other hand, 40% is a lot better than 80%.
Speaker: On the other hand, 40% is awfully high mortality for any disease.
Speaker: And we certainly have a long way to go.
Speaker: to improve therapy.
Speaker: Absolutely.
Speaker: And maybe this would be a good time to talk about some of the causes.
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?
Speaker: Sure.
Speaker: So there actually are a couple of causes.
Speaker: And as you allude to, the best data are with acute coronary syndromes.
Speaker: And the best data actually come from the shock trial registry.
Speaker: So the shock randomized trial was 300 patients, but there were fairly stringent eligibility criteria.
Speaker: And if you didn't make it in and you had to have pump failure, cardiogenic shock.
Speaker: So if you had some other cause or this or that,
Speaker: You didn't make it into the trial.
Speaker: So they kept those patients in a registry.
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.
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.
Speaker: But it's certainly the most common cause of acute cardiogenic shock.
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.
Speaker: The other more common setting and one that's somewhat, it's a different setting is end-stage heart failure.
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.
Speaker: then you can have cardiogenic shock sort of at the latter part of that stage.
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
Speaker: an end game in that setting.
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.
Speaker: In myocarditis is stress cardiomyopathy, sometimes known as Takasubo cardiomyopathy or Takasubo syndrome.
Speaker: I actually prefer stress cardiomyopathy
Speaker: as a term, but that's a story for another day.
Speaker: And then, as I'm learning in my world now, post-bypass.
Speaker: There is an incidence of cardiogenic shock.
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.
Speaker: Again, another setting where commonly mechanical support is employed in an attempt to tie patients through to recovery.
Speaker: So it is mostly acute coronary syndromes, but there are other settings in which cardiogenic shock can occur.
Speaker: And my understanding is that those other settings are driving an increase in the number of cardiogenic shock that we're seeing today.
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.
Speaker: Yes, that's exactly right.
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.
Speaker: And I think the reason you're exactly right about the reason.
Speaker: One of the reasons is that
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.
Speaker: But you're right, there's a lot more surgery, and in fact, I guess...
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.
Speaker: Excellent.
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...
Speaker: It still is being utilized and actually we'll link it to the show notes.
Speaker: But I think that this was a creation you did maybe for a paper in the annals in the 90s.
Speaker: Is that correct?
Speaker: That's exactly right.
Speaker: And there are some people, you know, on that paper.
Speaker: But Dr. Perillo told me that I had to spend a lot of time making a beautiful figure.
Speaker: because people would be using that figure for a long time afterwards.
Speaker: And in this, as in many things, Dr. Perillo is absolutely correct.
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.
Speaker: if uncorrected.
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.
Speaker: And so when that happens, coronary perfusion goes down, you wind up with ischemia.
Speaker: Ischemia causes left ventricular dysfunction.
Speaker: Left ventricular dysfunction causes cardiac output to drop and your blood pressure to drop, and that
Speaker: causes more ischemia, and you get in big trouble.
Speaker: And so that was the idea of that figure.
Speaker: There are sort of additions to that figure.
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.
Speaker: And what
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.
Speaker: And I think that's correct.
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.
Speaker: And so it sort of all gets down into at least a similar pathway at the end.
Speaker: Excellent.
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.
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
Speaker: within each other when we're talking about cardiogenic shock patients.
Speaker: Yeah, I'm glad you asked.
Speaker: It's an interesting and I think a valuable effort.
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.
Speaker: And this is particularly important in clinical trials and also in retrospective analyses.
Speaker: So people, particularly in the mechanical support world, they say, well, now we're doing better than we used to.
Speaker: And the question is, are you selecting patients, particularly in retrospective, look, are you selecting patients of equivalent severity?
Speaker: but it's also important in planning clinical trials.
Speaker: So if you do a clinical trial and the patients are all too sick to begin with, then it won't work.
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.
Speaker: So some way of trying to standardize the risk in patients with cardiogenic shock was useful.
Speaker: So they came up with the
Speaker: five category.
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.
Speaker: And so the A is for at risk.
Speaker: Those are patients who aren't in cardiogenic shock, but at least you ought to worry that they might
Speaker: that they might wind up in cardiogenic shock.
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.
Speaker: I don't know that all those patients have to be transferred, but it's least at worst thinking about that.
Speaker: The second phase is beginning cardiogenic shock.
Speaker: That is, they're hypotensive.
Speaker: They're often tachycardic, but they do not present with hypoperfusion.
Speaker: So perfusion is still normal.
Speaker: They don't quite meet the definition of hypoperfusion and shock, but they're getting there.
Speaker: The blood pressure's lowish.
Speaker: The heart rate is highish.
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
Speaker: Cardiogenic shock, sort of the definition I gave you before.
Speaker: Hypoperfusion, requiring support with either vasopressor drugs or mechanical support.
Speaker: And then D is deteriorating.
Speaker: Those are patients who are deteriorating despite what you're doing.
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.
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.
Speaker: And that's a different scenario.
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.
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,
Speaker: usually during the hospital stay might go through all of these maybe and progress it.
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.
Speaker: Yeah, I think that's correct.
Speaker: And one thing that they also put in that's worth mentioning is that the category has what's called an arrest modifier.
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,
Speaker: you do worse.
Speaker: So this was a theoretical classification, but there are actually now data.
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.
Speaker: And what it shows in
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.
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.
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.
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.
Speaker: And I find it very interesting.
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.
Speaker: Yeah, so, and I think that's a,
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.
Speaker: You have one from column A and one from column B, but I think all those three things are important.
Speaker: So you have your clinical examination, you have whether somebody's in shock, and that's basically the examination to evaluate perfusion.
Speaker: do you have adequate perfusion?
Speaker: Remember, cardiac output is just a number.
Speaker: The question is whether that cardiac output is enough to provide the tissues with enough supply of nutrients for them to function.
Speaker: So you have the clinical signs of inadequate perfusion.
Speaker: And then you have laboratory values.
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.
Speaker: And then finally and importantly, you have hemodynamics, and cardiogenic shock is a hemodynamic disease.
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.
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.
Speaker: But I know that there's even some recent small studies that suggest that maybe in cartogenic shock populations, there is value.
Speaker: And like you said, that's why it was invented in the first place.
Speaker: But why don't we talk a little bit about the hemodynamic profiles of a cartogenic shock?
Speaker: I think that in general, people have always thought of volume status and peripheral circulation as
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.
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.
Speaker: Right.
Speaker: So you're alluding to the original hemodynamic classification followed a clinical classification.
Speaker: So if you were warm and dry, then you had a good cardiac output and you had low filling pressures.
Speaker: If you were cold and dry,
Speaker: Then you had a low cardiac output, but you had low filling pressures.
Speaker: And those patients actually might improve their cardiac output if you give them fluid resuscitation.
Speaker: There aren't that many of those patients, but they're there.
Speaker: If you're warm and wet, that's sort of classic pulmonary edema.
Speaker: Your output's okay, but you have crackles on exam.
Speaker: And classic cardiogenic shock is cold and wet.
Speaker: It goes to the hemodynamic definition, low cardiac output.
Speaker: and elevated filling pressure.
Speaker: So that's sort of the classic thing.
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.
Speaker: Why is it so important to do a hemodynamic assessment?
Speaker: So I have an answer for that.
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.
Speaker: the effects of my therapy.
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.
Speaker: and the notion that you can have univentricular dysfunction.
Speaker: So you can have normal.
Speaker: So down on the bottom left would be normal right ventricular output and normal left ventricular filling pressures.
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.
Speaker: And if you have normal right ventricular pressures, but high left ventricular pressures, then you have isolated left ventricular failure.
Speaker: And that's what
Speaker: most people think about when they think about cold and wet and cardiogenic shock.
Speaker: But what has come to the fore is the notion that ventricles, the left ventricle doesn't really fail alone very much.
Speaker: And many of these patients with cardiogenic shock, in fact, have biventricular failure.
Speaker: failure of both the right and the left ventricle.
Speaker: And if you don't do a hemodynamic assessment, you won't find that.
Speaker: You won't know that they have right.
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.
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.
Speaker: And part of the drivers of that is at least the potential availability of right ventricular mechanical support devices now.
Speaker: So now that there's something to do about the right ventricle, maybe it makes some sense to try to diagnose that problem.
Speaker: Excellent.
Speaker: And I think that
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.
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.
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.
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?
Speaker: Sure.
Speaker: So to go back a little bit, so one of the things, so you want a clinical examination for perfusion.
Speaker: You want to look at capillary refill and you want to see whether they look sick and what does this patient look sick?
Speaker: It's probably the most important thing of all.
Speaker: And tachycardia and crackles and estries and murmurs and urine output and capillary refill, all that part of the clinical exam.
Speaker: You want to get the usual suspects, and that's an arterial blood gas.
Speaker: So just a little bit side.
Speaker: At least in this context, there's sort of a fad for venous blood gases in some emergency departments.
Speaker: That may be okay in some settings, but this is not one of them.
Speaker: You want to know what the pH is in the arterial system.
Speaker: You want to know what the PCO2 is in the arterial system.
Speaker: And you want to know what the PO2 is in the arterial system, not in the venous blood in the forearm.
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.
Speaker: And you want to follow, and you want to lactate.
Speaker: Maybe that one number isn't important, but the trend of the lactate is important.
Speaker: I think you want a chest x-ray.
Speaker: In this setting, this is not time to save money by not getting a chest x-ray.
Speaker: Just get a chest x-ray.
Speaker: You never know.
Speaker: Don't mistake the pulmonary edema for pneumonia, but it might not be pulmonary edema.
Speaker: It might be a pneumonia.
Speaker: It might be something else.
Speaker: You never know what you might find.
Speaker: And I think pretty much everybody with a suspected diagnosis of cardiogenic shock ought to have an echocardiogram.
Speaker: I also think it's important to say that that echocardiogram should be fairly comprehensive at some point.
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.
Speaker: You might find something else.
Speaker: You might find right ventricular failure, you might be looking at a pulmonary embolism that you didn't know about.
Speaker: You might be looking at an aortic dissection.
Speaker: So I think it's fine.
Speaker: There's a lot of this ED quick scan echocardiogram.
Speaker: That's fine.
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.
Speaker: But I do think it's worth following that up with a really good comprehensive echocardiography sooner rather than later.
Speaker: And it's pretty much universal in cardiogenic shock.
Speaker: And I think that's a very valid point.
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.
Speaker: So I do agree.
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.
Speaker: So,
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.
Speaker: Yeah, so I don't think it's entirely unreasonable.
Speaker: There is that small population that's actually cold and dry.
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.
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.
Speaker: Give them 250 cc's and see if they look better.
Speaker: And if they look better at 250 cc's, give them another 250 cc's, but carefully.
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.
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.
Speaker: But I don't think a little bit of fluid is always the wrong thing to do.
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?
Speaker: Well, yes and no.
Speaker: I mean, I suppose if you get a BNP and it's high, it suggests that something's going on with the heart.
Speaker: It depends a little bit on what you already know about the patient.
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.
Speaker: But
Speaker: It's, and of course, BMPs can be higher and stuff like pulmonary embolism, et cetera, et cetera.
Speaker: But I don't think it's entirely unreasonable.
Speaker: I just think it's not especially helpful once you get your echo and figure out what's going on.
Speaker: And I think the other thing that we mentioned earlier related to making sure you differentiate between sepsis and
Speaker: septic shock and cardiogenic shock.
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.
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.
Speaker: Yeah, it's a little tricky.
Speaker: They didn't really prove that a lot of those people had actual infection.
Speaker: What they had was vasodilation from inflammation that looked a lot, it was a sepsis-like picture.
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.
Speaker: So there certainly are some people who are infected.
Speaker: And certainly worthwhile looking for infection.
Speaker: And some people with chronic heart failure can certainly get tipped over by infection.
Speaker: But I just, I'm a little cautious about that.
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.
Speaker: If you've got sputum and a white count and it looks like pneumonia, then it probably is.
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.
Speaker: I'd think twice about that.
Speaker: And I think that's a great point.
Speaker: And that's where the echo obviously can also be very, very helpful in understanding the whole picture.
Speaker: What about how do you deal with the airway or with ventilatory support in these patients?
Speaker: And I think that there's
Speaker: maybe a miss and the blurry line between what is decompensated heart failure, pulmonary edema and true cardiogenic shock.
Speaker: Yeah.
Speaker: So I have a little bias about this too.
Speaker: And so we'll talk about, maybe we should talk about it in two different contexts.
Speaker: So if you've got somebody with an acute coronary syndrome,
Speaker: And they come in and they're hypoxemic and breathing fast.
Speaker: And so they're in pulmonary edema.
Speaker: You've got them sitting bolt upright and you're giving them, you're ventilating them however you're ventilating them.
Speaker: To me, you have to think about what you're about to do.
Speaker: So you're about to take them to the cardiac catheterization laboratory and you're about to lay them flat.
Speaker: And when you do that, they are not going to like it.
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.
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.
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.
Speaker: There's nothing easier than extubating somebody who used to be in pulmonary edema but who is now not in pulmonary edema.
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.
Speaker: With acute heart failure, it's a little fuzzy.
Speaker: BiPAP can sometimes tide these people over.
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.
Speaker: And I agree.
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.
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.
Speaker: So I think it's an important point of really having a low threshold for proceeding and securing the airway in these patients.
Speaker: You turn to them and you say, can I please have the Yankauer suction catheter in your cath lab?
Speaker: People say, what?
Speaker: Yeah, exactly.
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?
Speaker: I guess my bias is PEEP is good for heart failure, so particularly left-sided heart failure.
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.
Speaker: So you're in fact helping the blood get from the aorta to out of the aorta.
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
Speaker: ought to give them PEEP.
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.
Speaker: But in general, PEEP is good for these patients.
Speaker: And what about vasoactive drugs?
Speaker: Specifically, I guess we can start with vasopressors.
Speaker: This has been studied.
Speaker: I think that there's some still prevailing misconceptions of what are better catecholamines for septic shock.
Speaker: But just give us your take on
Speaker: basal oppressors and then maybe we can talk about inotropes and how you use it.
Speaker: Yeah, so the world has shifted a little bit.
Speaker: It used to be that the go-to drug in patients with bad ventricles was dopamine.
Speaker: in the days when a lot of people used a lot of dopamine.
Speaker: And so the SOAP trial, looking at comparing dopamine and norepinephrine, was done to look at that comparison in a number of settings.
Speaker: But there was a pre-specified subgroups of patients with shock.
Speaker: And so they pre-specified among the pre-specified subgroups was cardiogenic shock because the
Speaker: The thought beforehand was if dopamine was better in any group, it would be in the patients with cardiogenic shock.
Speaker: So as you probably know, that's the opposite of the way it turned out.
Speaker: For the trial as a whole, there was really no significant difference between dopamine and norepinephrine, although there were more.
Speaker: arrhythmias with dopamine.
Speaker: But in the subgroup of patients with cardiogenic shock, norepinephrine was in fact better.
Speaker: And so that to me has changed the landscape.
Speaker: I'm more inclined to reach for norepinephrine as my first choice in that population.
Speaker: One caveat is that the cardiogenic shock population in that trial was not especially well-defined.
Speaker: It was fairly heterogeneous.
Speaker: And so
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.
Speaker: The other thing about the patients with acute coronary syndromes are predisposed to tachyarrhythmias.
Speaker: So if you're in trouble with tachyarrhythmias,
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.
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.
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.
Speaker: And what about inotrope support, Steve?
Speaker: What is your go-to drug and how do you look at that?
Speaker: Yeah, so in cardiogenic shock, usually dobutamine is a first choice in my practice, mostly because of the short half-life.
Speaker: Dobutamine, as you probably know, it has beta-2 effects, but it also has beta-1 effects, but it also has alpha-1.
Speaker: 1 and beta 2 effects, so the alpha effects are vasoconstrictive, the beta 2 effects are vasodilatory.
Speaker: They usually cancel themselves out, and at the same resistance, if you increase cardiac output, you'll increase blood pressure.
Speaker: So, dibutamine is not a vasopressor, it's an inotrope, but it's usually a reasonable first choice.
Speaker: It is more arrhythmogenic than something like milrinone.
Speaker: The problem is milrinone is a vasodilator and can make your blood pressure worse.
Speaker: And milrinone also has a longer half-life.
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.
Speaker: In Europe, they have levosimendan.
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.
Speaker: But we could use a new inotrope or two.
Speaker: And are there any other evasoactive drugs that you have sometimes utilized?
Speaker: I mean, there are obviously some pulmonary evasodilators that sometimes might be helpful.
Speaker: I know that there's not a lot of evidence behind them, but any other drugs that you might want to mention?
Speaker: Yeah, I think there are no data about pulmonary vasodilators.
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.
Speaker: The data for
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.
Speaker: So I really don't think that they have a role there.
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.
Speaker: I wanted to ask you a little bit about CRRT.
Speaker: I did notice that in the AHA guidelines and many other guidelines, they specifically talk about CRRT and cartogenic shock.
Speaker: I haven't seen any large trials, but I just wanted to take your impression in terms of how do you utilize it.
Speaker: It's something you adopt early and in who?
Speaker: Yeah, so I think it is useful.
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
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.
Speaker: So trying to keep fluid volume in a reasonable state is a good idea.
Speaker: Dialysis itself often not well-tolerated.
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.
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.
Speaker: I can't remember what SLED stands for.
Speaker: But SLED is six hours of slow hemoperfusion.
Speaker: But I think that those are underutilized and should be utilized more often.
Speaker: I'll have to confess that we don't do CBVH just now.
Speaker: Stay tuned.
Speaker: In two months, we're hoping to start.
Speaker: But I think it can be useful.
Speaker: And again, I think earlier is better.
Speaker: Excellent.
Speaker: So let's talk about mechanical devices.
Speaker: And I think that this is really something that has really changed the landscape.
Speaker: And then we can finish the treatment discussion with just, I mean, what are the current recommendations for PCI so that
Speaker: our audience is aware.
Speaker: But in terms of mechanical devices, Steve, when are you thinking of these?
Speaker: I guess anybody who's a C, you start thinking about it.
Speaker: Yeah.
Speaker: For sure.
Speaker: Yes, B's for sure.
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.
Speaker: And so the old classic is the intra-aortic balloon pump.
Speaker: It's easily available, it's inserted in the femoral artery.
Speaker: And so it's readily available in all sorts of hospitals.
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.
Speaker: And it decreases afterload when that balloon deflates, but it turns out that only raises cardiac output by 500 cc's or so.
Speaker: It's not really a great way to raise cardiac output.
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.
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.
Speaker: So, the axial flow pump, they actually, there are two of them.
Speaker: One is the PHP, but the more common one is called the impella.
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
Speaker: inlet cannula and left ventricle to the outflow cannula and the aorta.
Speaker: And so it's doing much of the pump function of the heart.
Speaker: So it unloads the left ventricle and also increases its output.
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.
Speaker: And so it's a good device.
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.
Speaker: The caveat there is there are no randomized trial, and the outcome of registry data are quite dependent on patient selection.
Speaker: So if you use it in patients who ultimately would have done well without it, it's going to look good.
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.
Speaker: But at least the data, many of the data suggest that if you use this
Speaker: technology in appropriately selected patients, your mortality can go into the 25% range, which is pretty good.
Speaker: The Tandem Heart is a slightly more complicated device that relies on external pump.
Speaker: It's sort of a little clever device.
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.
Speaker: That's a good support device.
Speaker: And actually works very well.
Speaker: It's a little more complicated to insert.
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.
Speaker: Again, really no randomized trials that suggest efficacy.
Speaker: And then the other thing that can be done and that can be done at most places is full-on VA ECMO.
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.
Speaker: That is a, it's important to recognize that's a circulatory support device that raises blood pressure and raises cardiac output.
Speaker: But in fact, that actually is not a left ventricular support device.
Speaker: You're taking blood out of the venous circulation, you're putting it back in the arterial circulation into the aorta.
Speaker: And if anything, you're increasing the afterload of the left ventricle.
Speaker: So there's now a movement to sort of vent the left ventricle.
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.
Speaker: In the operating room, you can put a left atrial vent.
Speaker: You can put in an impeller device, the so-called ecapella configuration, and some people use a balloon pump.
Speaker: The other thing to talk about with these devices may be expense.
Speaker: The balloon pump is not entirely expensive.
Speaker: I don't know, it probably runs $500 or $600.
Speaker: ECMO is not stunningly expensive.
Speaker: It's a couple of thousand dollars.
Speaker: Impella and Tandem Heart are expensive.
Speaker: We're talking $25,000 to $30,000 at current prices.
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,
Speaker: is this whole concept of CPO, cardiac power output, and how that may make the Impella, especially the 5.0 more attractive?
Speaker: Correct.
Speaker: So the cardiac power output is a hemodynamic measure.
Speaker: And basically that says how much work is the heart doing?
Speaker: So it's basically very simple.
Speaker: It's cardiac output times mean arterial pressure.
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.
Speaker: And so that cardiac output, the sort of magic number there is 0.6.
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.
Speaker: But if you have a cardiac output of four and a mean arterial pressure of 60, then you're not.
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,
Speaker: So that's relatively shortly after.
Speaker: If your lactate is still high and your cardiac output is low, you're in big trouble.
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.
Speaker: So I think that's actually a good marker.
Speaker: It essentially says, how much work is the heart together with my mechanical support device doing?
Speaker: How well am I supporting the circulation?
Speaker: And that's, again, another motivation.
Speaker: So if you're going to calculate a cardiac power output,
Speaker: then you do that with a cardiac output.
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.
Speaker: So if your pulse pressure is high and your right atrial pressure is low, then that number is high.
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.
Speaker: Excellent.
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
Speaker: critical care physician need to know about PCI and cardiogenic shock?
Speaker: So they need to know the sooner is better and they need to know that to call somebody.
Speaker: It turns out the shock trial actually accepted people out to 18 hours.
Speaker: So to me, whatever time it is, you ought to be going to the cath lab.
Speaker: And the landscape of what to do at PCI for the interventional cardiologist has changed a little bit.
Speaker: So it used to be
Speaker: that you did the culprit artery and then you stopped.
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.
Speaker: And then there was something called the culprit shock trial, which randomized patients to multivessel PCI versus single vessel PCI.
Speaker: And the people who had single vessel culprit PCI did better in that trial.
Speaker: And so the pendulum has sort of switched to just doing the culprit artery.
Speaker: I also think there is a school of thought, there's now a trial as well, looking at impella support before PCI.
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.
Speaker: That is being tested in the clinical trial.
Speaker: The pilot trial suggested that that was in fact safe.
Speaker: So you're asking the interventional cardiologist to just look at the patient for half an hour and not even do an angiogram.
Speaker: But the patients looked okay and were awaiting results of that trial, probably be a good 12 to 18 months before then.
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,
Speaker: then you really ought to send the patient to an institution where that's an option.
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.
Speaker: However, if you have a non-STEMI and cardiogenic shock, it's a different story, right?
Speaker: That's correct.
Speaker: So to me, cardiogenic shock, the shock trial did not distinguish by STEMI or non-STEMI.
Speaker: If you've got a patient in cardiogenic shock, it no longer matters whether you have ST elevation or not.
Speaker: They're in trouble with a closed artery and you need to go to the cath lab and try to open that artery.
Speaker: Excellent.
Speaker: So the last question I have regarding cardiogenic shock was just if you could just give us a very brief overview, a reminder.
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.
Speaker: Yeah, I think that is true.
Speaker: And it's the other thing to say about that.
Speaker: They are much less common with early reperfusion, but sometimes you'll see patients who have late reperfusion for whatever reason.
Speaker: They've been having pain for three days, and they didn't see anybody, and you're finally seeing them late.
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.
Speaker: So basically three...
Speaker: three important complications.
Speaker: First is papillary muscle rupture.
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.
Speaker: And basically, you need to go to the operating room and you need to replace that valve as soon as you can.
Speaker: That's not a situation which you can wait around.
Speaker: You support the patient as you can, some with an intra-artic balloon pump or not.
Speaker: If you're in an institution without surgery, you get them to an institution with surgery and you try to replace that valve.
Speaker: Acute ventricular septal defect, again, comes in two flavors.
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.
Speaker: And again, that gets a little bit tricky.
Speaker: The mortality, even with surgery, is high.
Speaker: And interestingly enough, the ones that are inferior MIs are harder.
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.
Speaker: So they would like to wait and see if it scars in and becomes an easier operation.
Speaker: The challenge is that patients may not do very well while they're waiting.
Speaker: It's a tough clinical problem.
Speaker: And the last problem is free wall rupture.
Speaker: That is rupture out into the pericardium, occasionally into the thoracic cavity, usually into the pericardium.
Speaker: If it's free rupture out into the thoracic cavity, that's probably not survivable.
Speaker: But into the pericardium, and classically you see sort of a pseudoaneurysm.
Speaker: Classically it's an elderly hypertensive patient, more women than men,
Speaker: who just sort of look gray and start vomiting and they look awful.
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.
Speaker: The other thing to mention about that is that pericardiosynthesis in that setting is a double-edged sword.
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.
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.
Speaker: Excellent.
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.
Speaker: And one of the things we do at the podcast is end the episode and
Speaker: with some questions that tap into the wisdom of our guests that are unrelated to the topic we spoke of.
Speaker: Would that be okay?
Speaker: Sure.
Speaker: So the first question relates to books.
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.
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.
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
Speaker: different odd perspective way of looking at the world.
Speaker: None of those books are books that I have commonly gifted.
Speaker: And actually, there's the one I probably most commonly gifted and the best one I gift.
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.
Speaker: And I used to give it to the new fellows when they came.
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.
Speaker: Excellent.
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.
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.
Speaker: Yeah, I couldn't agree more.
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.
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.
Speaker: And I guess I've thought about this.
Speaker: There are sort of two ways of looking at the world.
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.
Speaker: I think most people believe that.
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.
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.
Speaker: And I think that is true.
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?
Speaker: Yeah, it's a different way of putting the same thought.
Speaker: Excellent.
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?
Speaker: Right.
Speaker: So I'm going to give you one of my favorite quotes.
Speaker: And that quote is,
Speaker: Good judgment comes from experience and experience comes from bad judgment.
Speaker: So what that means to me is that really, really to get good at practicing medicine, the part is practicing.
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.
Speaker: You have to get yourself into trouble and then you have to get yourself out of trouble, hopefully.
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.
Speaker: And it's a real patient in front of you.
Speaker: And looking at them and talking to them provides insights that you just can't get any other way.
Speaker: And I think that's a great place to stop.
Speaker: Steve, thank you so much for your time and for sharing your expertise and thoughts with us.
Speaker: And I look forward to having you back on Critical Matters soon.
Speaker: It's been a genuine pleasure.
Speaker: Thank you for having me.
Speaker: Thank you for listening to Critical Matters, a sound critical care podcast.
Speaker: Make sure to subscribe to Critical Matters on Apple or Google Podcasts and share with your network.
Speaker: Sound Critical Care is transforming the way critical care is provided in hospitals across the country.
Speaker: To learn more, visit www.soundphysicians.com.
