SCCM Resource Library-Extracorporeal Membrane Oxygenation: Mechanical Circulatory Support for Cardiogenic Shock: Past, Present and Future

Video Transcription

Hello, my name is Dr. Saras Chandra Vallabha Josula, and I'm an interventional and critical care cardiologist at the Wake Forest University School of Medicine.  I'm here to discuss our first topic here, extracorporeal membrane oxygenation. This is a part of the session titled, Mechanical circulatory support for the cardiogenic shock,  past, present, and future. These are my disclosures. None of these are relevant to today's discussion.  So cardiogenic shock is defined as a state of ineffective cardiac output that is primarily  due to a cardiac disorder, but essentially, like every other shock state, results in clinical and biochemical manifestations that cause impact tissue perfusion.  This is a classical learning of shock classification, where we look at if a patient is warm or cold based on a clinical examination, and if they're wet or dry.  Usually this phenotype of cold and wet is the most common cause of cardiogenic shock. Whereas if they're warm and dry, they're often due to vasodilatory shock due to some other  reason, either sepsis or anaphylaxis or acute pancreatitis and such. But these special phenotypes of dry, cold and dry, and warm and wet also exist when they're mixed shock.  So it's important to understand that not everybody is cold and wet. Recently the Society of Cardiovascular and Geography and Intervention came up with the  SCI stages of shock, which I find very useful to transact when you talk to other physicians.  As you can see from this pyramid, it's a gradual progression from stage A to stage E, wherein  stage E is somebody in cardiac arrest actively receiving this cardiopulmonary resuscitation.  And these are the various physical exam biochemical markers and hemodynamics that are associated with these stages.  I'm not going to belabor this slide, but I wanted to put this up here as a useful reference. This is a classical pathophysiology of cardiogenic shock.  Atheromy, which remains one of the most common etiologies of cardiogenic shock, essentially  first results in central macrovascular hemodynamic disturbances, as you can see from this circled area. And these macrovascular hemodynamic disturbances reflect pressure two ways.  One is they cause hypoperfusion of the systemic circulation, resulting in decreased perfusion  to the renal hepatic and other systems, causing an inflammatory state, but also reflect backwards to the lungs, causing elevated LVDP and pulmonary edema.  These are data from our group where we looked at the epidemiology of cardiogenic shock across multiple spectrums. I'll put these slides up.  The general message, as you can see, in contemporary era, there has been a persistent increase in cardiogenic shock across the national landscape.  These are patients with post-cardiotomy cardiogenic shock. These are patients with multiple etiologies of cardiogenic shock pre-LVAD.  This is in patients with STEMI, and this is in patients with non-STEMI. So across the board, there has been an increase in cardiogenic shock due to increased acuity,  increased comorbidities, sicker older populations as we progress in our medical care. This is just—I know the talk is about ECMO, but I'm briefly going to touch upon a summary  of the various MCM devices. I'm not going to go into each of them in detail, but I put this up here with a useful reference,  something that we can always go back to every time there are questions about how these circuits work.  But depending on which ventricle you want to assist, how much the requirement of cardiac output is, if there's need for respiratory support, what kind of caliber there, peripheral  vasculature is, whether or not it can accommodate these various devices. All these are considerations that go into putting in these devices.  Again, from the same study, set of studies that I showed you earlier, this is a slide deck showing the use of mechanical circulatory support across the national landscape for  cardiogenic shock. Again, this is in patients in post-cardiotomy. This is—so this is in patients pre-LVAD, this is patients post-cardiotomy.  These are in STEMI and non-STEMI patients. As you can see, the general consensus is that MCM devices have either held stable or come down in the recent past.  That's primarily because of the decrease in the use of IABP after seminal IABP shock trials, but a concomitant increase in Impella and ECMO across the board, which is becoming—which  are quickly becoming the devices of choice for advanced cardiogenic shock. So how about the timing of MCM?  This is a very nice slide from Naveen Kapoor and his group in Boston, where they essentially looked at a sort of theoretical model where they say the initial shock is essentially  a hemometabolic shock, where initially it's a hemodynamic insult and gradually becomes a metabolic insult.  And our role as physicians caring for these sort of patients is to arrest it before it becomes a metabolic problem.  These are data from our group that we published a couple of years ago now that showed that depending on how many organ systems you have involved in cardiogenic shock, your mortality  is significantly worse, which kind of lends indirect evidence to this hemometabolic cascade.  So there are multiple algorithms, like I briefly summarized earlier, depending on which ventricle  you want to support, how much cardiac output you want, whether the pedestal osculature can accommodate the device, whether the patient needs lung support or not.  There are various devices that are—various device selection algorithms that have been published.  Again, not something I want to discuss in great detail, but I wanted to make sure you have the resources you need should you go back to look at this talk. So ECMO.  ECMO is one of the most common devices. It really took off in the flu pandemic in 2008-2009 winter when VV ECMOs were largely used for respiratory bypass.  And from then on, the comfort of physicians caring for these patients, implanting these devices has resulted in increasing use of even renal arterial ECMO.  Today's talk is largely going to be renal arterial ECMO because that's where cardiogenic shock patients mostly gravitate towards.  So the most common cannulation style is peripheral where you put in a large venous cannula into  the IVC through the femoral vein and a large arterial cannula into the descending aorta through the femoral artery, either same side or opposite sides.  This is a separate central cannulation strategy where it's the right atrium for the venous cannula and ascending aorta for the arterial cannula.  This is a dual lumen cannula on the same side, but it's upper extremity. So the venous is in the SVC, the axillary or the subclavian arteries have the arterial and cannula.  There are multiple iterations or multiple variations of this configuration, the VAV cannulation, the VVA cannulation, and again, like we talked about, both on the same side  in the groin and opposite side in the neck. So there are multiple ways. The whole purpose is to get a venous cannula that's draining either from the central veins  or directly from the right atrium and an arterial cannula that's either draining into the central  arteries or into the ascending aorta, essentially bypassing the entire cardiorespiratory system. So these are data from our group where we looked at the epidemiology of ECMO use.  As you can see, this is in patients with acute myocardial infarction. And as you can see, these numbers have taken off.  These are absolute numbers across the nation in a national stratified sample. And VA ECMO use has really, really taken off. These are data from the ELSO registry.  The numbers have really taken off, kind of tapered or held stable in the 2,000-something range. So this is becoming more and more common.  I'm sure many of us are already seeing it in our practice way more ubiquitously than we did initially.  So some of the considerations when it comes to VA ECMO are, like we briefly alluded to, how are you going to cannulate? Where are their access sites?  What is the caliber of the vessels? How can we cannulate? So that's the most important consideration.  As an interventional cardiologist, I'm often dealing with these questions, often consulting with colleagues in the unit or elsewhere in the ED or such, discussing how we cannulate  these patients. This is the next important issue, is distension and venting. We'll touch upon this in great detail in subsequent slides. I'm not going to talk much here.  And the last issue is distal limb perfusion. This is a very critical issue because, as you can imagine, these are large cannulae.  There are usually 22 to 24 French on the venous side, 15 to 17 French on the arterial side.  And many people who have coronary disease or cardiogenic shock also end up having peripheral vascular disease.  So their vasculatures are not as compliant and accommodative for these large cannulas. So how do we perfuse the distal limb, especially on the arterial side, beyond the insertion  of the VA ECMO catheter? So these are important considerations.  This is a table that I got from a really nice couple of review articles. But I found this very... This is something we all discuss intuitively.  This is something we all have noted in our practice, but it's just nice to put up a list of indications and contraindications.  One of the most important things that I will tell you is the most important consideration is when we are putting a patient on VA ECMO, we have to be absolutely sure that we know  or at least have a direction as to what their exit strategy is going to be.  Are they a bridge to recovery, as in you're waiting for the ventricle to recover? Are they a bridge to transplant or a bridge to LVAD or are they a bridge to nothing?  And that's when we get into trouble, is when we don't have a good, well-defined understanding  of the exit strategy, a full-fledged conversation about it before we implant, and then we have this patient on ECMO without a good exit strategy.  So that's probably, in my opinion, that's one of the most important considerations when we look at these patients. This is a very heart failure cardiology slide.  I just wanted to put this up here because these are PV loops that we measure routinely in translational research where we look at how the heart behaves for pressure and volume  depending on what state it is in and what the loading conditions are. I'm not going to belabor the point, but I just want to put this up here just for somebody to see.  And it's important that in VA ECMO, as the speeds go up, it gets narrower and narrower and the pressures, the interventricular pressures go up.  And even though the pressure, absolute pressure goes up, the ejection decreases. So the native ejection, which is defined as thickness of these boxes, decreases.  So the ventricle is doing less and less with higher and higher pressures as the flow in the ECMO goes up, which is where the whole distension and unloading discussion comes about.  So that's a direct segue into this slide is how do we unload the LV?  There are many ways to unload the LV. As you can see here, you can do an interatrial septostomy where you just create a mechanical puncture between the left and the right atrium.  And because of the higher pressure on the left side, it vents directly to the right side. Or you can put in a trans aorta cap like a pigtail or something into the LV and put it  to passive suction. Or more recently, we've been putting in impellers or balloon pumps. Balloon pumps are obviously further down in the aorta where the impellers are directly  in the LV sucking blood out of the distended LV. Or you can put a catheter in the left superior pulmonary vein, draining from the left atrium.  There are many ways to drain the left-sided system. These are data from our group where we looked at ECMO use with concomitant MCS, and as you  can see, nearly 30% of patients with ECMO received either IBP or impeller on the same day, which is an indirect way of measuring LV unloading. So why is LV unloading important?  So the issue is, as the ECMO flow goes up, or there's more and more reliance on the ECMO, which essentially is injecting blood into the arterial tree in a retrograde fashion,  be it in the axillary or subclavian, be it in the femorals, or be it even direct ascending aorta, your blood is going against the natural flow.  So essentially, there is blood going backwards at very high pressures that's pressurized by the membrane oxygenator and centrifugal pump that sends blood back.  And therefore, the aortic valve has to open against this very high-pressure circuit. So that is a problem, one.  Two, the native LV ejection, which has to, the LV has to pump into the systemic circulation against this very high-resistance circuit.  And remember, this is already a diseased left ventricle. That's why you have them on ECMO.  Especially in the setting of an acute myocardial infarction, these patients have, you know,  huge inotropic metabolic requirements, and you're trying to pump against this high-pressure circuit.  And so after a while, the LV just gives up and starts distending and does not eject. The aortic valve doesn't open with every beat.  And then that's when the pressures inside the LV go up and they reflect backwards, high  left atrial pressures, high pulmonary pressures, pulmonary edema, cardiogenic, worsening cardiogenic pulmonary edema, mitral regurgitation. So you need to be careful with that.  So that's why LV unloading is crucial in these patients. This is a systematic review published in JAC a few years ago, where they essentially  look at all studies across all spectrums of cardiogenic shock with any kind of LV unloading. And they showed a positive effect.  This is a more nuanced study published from the German group, who is very active in this space, where they looked at LV unloading in the setting of VA ECMO compared to VA ECMELA,  which is VA ECMO plus EMPELA. And this actually showed a mortality benefit from early LV unloading within the first couple of hours.  These are data from our group, a couple of studies. This is looking at use of IABP in ECMO unloading. As you can see, overall, the signal was neutral.  But when you split these patients by etiology, there was a benefit for IABP in patients with acute MI, but not as much for post-cardiotomy shock or everything else.  And the theory is that the heart failure ventricles have had more time to adapt to the high pressures.  Whereas an acute MI is an acute insult, the LV is supposedly in good health before the acute MI happens, and therefore it can't deal with even modestly elevated filling pressures.  And so that's why unloading probably has the biggest role in these patients. These are data from our group looking at EMPELA, which is EMPELA and IABP.  The signal itself was neutral for mortality. But as you can see, there is a much higher risk of complications, which is kind of intuitive  when you're using too large-bore arterial access. This is a perspective piece we wrote the other day, but I wanted to kind of show this because  the LV unloading is still a work in progress. It is not a perfect science. There are many areas that we think we know well.  There are many, many more areas that we think we know, but don't know what to do with it. And there are some zones that are completely naive for our field and are potential threats  to outcomes in our patients.  This is again work from our group looking at complications. As you know, ECMO is a large arterial circuit, and so it's a centrifugal pump.  You have shearing forces that go in as the blood comes and goes through the circuit. Blood tends to stick at various parts of the circuit.  You have to have these patients on anticoagulation, so there's a lot of potential complications that can happen.  This is another study looking at LVAD to EMPELA, which is percutaneous LVAD is largely EMPELA and compared to IABP. And as you can see, these have their own set of complications.  I've highlighted the hematological complications to you because that's where I think we get into a lot of issues when they have prolonged MCS in the ICU.  So this is a patient we did many months or years ago. This is not exactly for an ECMO, it is an EMPELA.  As you can see, we have a 14-inch EMPELA sheet and the EMPELA catheter through here. But what we did is, I want to highlight, is we did distal limb perfusion.  So we stuck, so this is a common femoral going up, there's a swan in the femoral vein on the other side. But what we did is, we stuck the groin on the other side.  So this is a six-front sheath in the common femoral artery, which we used to essentially create a bypass circuit and send it back down this way through an anti-grade stick.  So this is sticking towards the toes. And so we are perfusing the limb distal to the stick from the EMPELA sheet. So trying to achieve adequate limb perfusion distally.  This is another issue that we often creep into in the ICU is, as the LV starts recovering,  the LV is much more functional, the LV is pumping blood. But this blood, which is coming through the pulmonary veins after going through lungs  that are not particularly oxygenating, is actually deoxygenated blood. So you actually have deoxygenated blood in the LV coming forward, whereas the ECMO circuit  is sending retrograde oxygenated blood. And they meet in between somewhere here. And where this level is depends on how far, how well the LV is ejecting.  So if it's here, that means the LV is not doing a whole lot. If it comes further down, that means the LV is doing a lot of this work.  This is called Harlequin syndrome or North-South syndrome. But essentially, the way to measure this is actually to get an arterial sample in the  radial on the right, and an arterial sample in the radial on the left, and an arterial sample on the femoral artery.  And then measuring the PaO2s will tell you where this transition point is, which can then help you dictate strategy of how you treat them.  So the ECMO device is a complicated device. It has multiple issues that need to be measured. This is obviously continuous EEG monitoring, especially if it's put in the setting of a  cardiac arrest. They have multi-oxygen failure. They have PA catheters. They have Arclin. They have these ECMO circuits.  So it's very resource-intensive, very laborious, requires specialized bedside nursing and bedside technical staff who are good with these circuits.  And this is just a practical flow sheet that I got that shows how you should evaluate these  patients on a daily basis, what are the parameters you look at, when should you consider weaning, what are the wean protocols.  And most institutions have institute-specific protocols, but I just wanted to put this simple chart up here. Lastly, I want to briefly touch about infections.  ECMO circuits are a lot of hardware for one patient, so they always run the risk of infections. We have dual vascular access, large boards, always run the risk of infections.  So I just wanted to put up these two review articles that I published. They're largely bloodstream infections, some have respiratory urinary tract.  Obviously, over time, these shock patients also turn septic on us. They have hydrogenic sepsis for whatever reason, and then have mixed shock, and that's when  all these issues start coming up. These are data from the ISHLT registry, where it looked at mortality with the ECMO, depending on the etiology.  As you can see, depending on what the etiology is, it's at least 40% mortality and as high as 80%. So this is not a trivial device, nor is it a trivial disease state.  These are data from our group where we look at acute myocardial infarction specifically, and what I wanted to highlight is despite getting LVAD and transplant, a third never  leave the hospital alive, and if you don't get it, two-thirds never leave the hospital alive. So this is a very high-risk condition, and so we need to treat it with as much respect  and detail as possible. Again, lastly, two important points from our group looking at palliative care use in patients with acute MI and cardiogenic shock.  As you can see, these are patients with ECMO who are on, older patients compared to younger patients with ECMO.  So as you can see, less than 5% or 10% get meaningful, you know, exit strategies of transplant and LVAD.  Really, this is the most important point, is 60% to 70% of these patients die in the hospital, so it's important to understand that, sorry, and so therefore, but here in  acute MI shock, as you can see, palliative care referrals have been very minimal, less than 20% in the contemporary era.  So I think that's where the biggest opportunity for our practice is as we go into the future  when we care for these patients. With this, I'd like to thank you for your time, and I'll be happy to take any questions virtually on Twitter or send me an email.  Thank you, and I hope you have a good rest of your day. Bye-bye.

Video Summary

Dr. Saras Chandra Vallabha Josula, an interventional and critical care cardiologist at Wake Forest University School of Medicine, discusses extracorporeal membrane oxygenation (ECMO) in the context of cardiogenic shock. Cardiogenic shock is a state of ineffective cardiac output primarily due to a cardiac disorder, resulting in poor tissue perfusion. Dr. Josula discusses the different phenotypes of cardiogenic shock and the stages of shock classification developed by the Society of Cardiovascular and Geography and Intervention. He highlights the increasing prevalence of cardiogenic shock and the use of mechanical circulatory support devices such as ECMO, Impella, and balloon pumps. He emphasizes the importance of LV unloading in ECMO patients and the potential complications associated with ECMO use. Dr. Josula also emphasizes the need for a clear exit strategy when using ECMO and the importance of considering palliative care in patients with acute myocardial infarction and cardiogenic shock.

Asset Subtitle

Cardiovascular, Procedures, 2022

Asset Caption

Cardiogenic shock after acute myocardial infarction requires immediate resuscitative therapy to prevent irreversible organ damage. Mortality, although decreased significantly, remains high. Intensivists more frequently encounter patients with cardiogenic shock. The key to a good outcome is an organized approach, with rapid recognition and prompt initiation of therapy to improve hemodynamics, tissue perfusion, ventilatory support, and reversal of the underlying cause. The concept of establishing ventricular support before revascularization stresses the notion that unloading the left ventricle is key to its recovery. Different percutaneous devices for mechanical support have different effects on left ventricular afterload and myocardial oxygen demand. An understanding of the advantages and disadvantages of these devices helps the clinician select the right device in the right setting.

Meta Tag

Content Type Presentation

Knowledge Area Cardiovascular

Knowledge Area Procedures

Knowledge Level Advanced

Learning Pathway Cardiothoracic Critical Care

Membership Level Select

Tag Shock

Tag Extracorporeal Membrane Oxygenation ECMO

Tag Cardiothoracic Critical Care

Year 2022

Keywords

ECMO

cardiogenic shock

LV unloading

mechanical circulatory support

complications

palliative care

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