Hello, my name is Dr. Saras Chandra Vallabha Josula, and I'm an interventional and critical care cardiologist at Wake Forest University School of Medicine. I'm here to discuss our topic, heart pumps, which one, when, how, and why, which is a part of the session, mechanical circulatory support for cardiogenic shock, a SWOT analysis. These are my disclosures. None of these are relevant to today's conversation. So cardiogenic shock, as you know, is a primary cardiac problem that results in decreased limb perfusion, decreased perfusion to the systemic circulation and resulting in clinical and biochemical manifestation. So despite this being a central hemodynamic insult, really the definition of shock, like every other shock, is inadequate tissue perfusion. Cardiogenic shock is largely classified as wet and cold. This is a phenotypical shock, which is essentially a clinical judgment that we make when we evaluate a patient. Are they cold or warm in their extremities and are they wet or, you know, do they have a high volume filling pressures or are they dry? And so wet and cold is still two-thirds of cardiogenic shock, but the remaining one-third are these two blue boxes where it's dry and cold or warm and wet. If it's dry and warm, it's rarely cardiogenic shock. These patients are often vasodilatory due to whatever reason, septic, spinal shock, anaphylaxis, acute pancreatitis, et cetera. Cardiogenic shock has been defined differently in different trials, and importantly, as you can see in this slide, they've largely been defined by central macrovascular hemodynamics. Despite these being microvascular abnormalities, as you can see, blood pressure is often used, associated with use of cardiac index and pulmonary capillary wedge pressure, which are obtained on a right heart cath, and some studies have used end-organ hypoperfusion in the form of urine output, altered mental status, or extremities, or lactate, which is an all-comer end-organ damage. So this, it all depends on which criteria are used, so somewhat to standardize this, the Society of Cardiovascular Angiography and Intervention came up with the SCI stages. This is a very intuitive stage classification where A is very beginning and E is extreme where patients are receiving CPR in the setting of cardiac arrest and cardiogenic shock, but they also came up with these very neat physical exam biochemical parameters and hemodynamic parameters to define these stages of shock. This is something we do very intuitively, but it's nice to know, especially when you're transacting with other physicians or other teams, trying to communicate the acuity of illness of a given patient in front of you. This is the pathophysiology of cardiogenic shock. And this is largely a central insult, and this is specific to acute MI, but as you may imagine it's pretty true for all other etiologies, too. It's largely a central insult resulting in two real manifestations. One is increased filling pressures in the heart causing back pressure into the lungs, pulmonary edema, cardiogenic pulmonary edema, respiratory failure. And there is the other, which is decreased perfusion causing organ failure, organ injury, and potentially a SIRS-like response where you have a vasodilatory state despite being low cardiac output. These are some data from our group where we looked at the epidemiology of cardiogenic shock across the various types of etiologies. As you can see, this is all-comer cardiogenic shock with post-cardiotomy as the etiology. This has steadily been going up. This, again, is all cardiogenic shock of multiple etiologies pre-transplantation or pre-LVAD implantation. So as you can see, the overall message what I hear is that there has been a steady increase in the prevalence of cardiogenic shock. This is post-STEMI. This is post-non-STEMI. The scales are different. STEMI is much more common than non-STEMI, but regardless, there has been a steady increase. So that essentially leads me to my next issue, which is I briefly want to emphasize this before we went on to discuss the different mechanical circulatory support devices, is that it's never the device, it's never any particular intervention that saves lives. It's a process of care. It's a system of care. So if you have strong cardiogenic shock centers analogous to trauma care where we have level one, two, and three levels of care, I think that goes a long way in improving outcomes in this patient. These are a couple of review articles and opinion pieces from colleagues at Inova Fairfax in Virginia where they looked at clinical hemodynamic criteria, shock teams, how these patients are transported, how do they go to the lab, how do they involve multidisciplinary input from interventional cardiology, critical care, cardiology, cardiac surgery, advanced heart failure to provide the optimal care for these patients. These are a couple of opinion pieces we wrote about multidisciplinary care. In this, as you can see, depending on where the cardiogenic shock patient is along their clinical course, whether they're in the ED, they come to the lab, they go to the CCU, they're on the floor. There are multiple needs and patient issues that come up that requires multidisciplinary team input at every level. The relative involvement of each team member depends on where along the course of this trajectory the patient population is, but regardless, we need a lot of these specialists. Similarly, there's another review article we wrote on acute cardiovascular care, and as you can see, cardiogenic shock is bang in the center of interventional critical care and heart failure cardiology. So essentially, multiple subspecialties of cardiology in addition to non-clinical or non-physician subspecialties like respiratory therapists and nurses and rehab specialists, et cetera. So this led to the evolution, natural evolution of cardiogenic shock teams. These are protocols from three different sites across North America, but largely, as you can see, it often involves multidisciplinary input from interventional cardiology, critical care, cardiology, advanced heart failure, and cardiac surgery. And depending on how they organize it, these four specialties are almost always involved in the care of these patients. This is an opinion, this is a systematic review of these protocols that essentially shows that there has been an improvement in outcomes and survival for the implementation of these process of care. Now, please note, so far, we have not even discussed mechanical circulatory support devices. So that's important to know that mechanical circulatory support devices don't independently save lives. They have to be tied into a strong systems of care and a protocol. So this is a broad overview of how we manage cardiogenic shock with percutaneous techniques, surgical techniques, supportive care. I'm not going to belabor the point, but I just wanted to give you a big 10,000-foot view before we zoned in into circulatory support, which is the need for today's discussion. This is a nice summary slide that I like to put up before I start my talks on MCS, primarily because it tells us all the biggest considerations that we have in mind when we care for these patients. First and foremost, most importantly, is what ventricle do we want to support? Is it the right? Is it the left? Or is it both? Second, how quickly do we want to implement a given mechanical circulatory support? That determines a lot of what we implant, and how quick, how much cardiac output do we need? What are the flows from these devices that we can expect? And importantly, what is the peripheral vasculature? Like sometimes some of these patients have severe peripheral vascular disease. You can't send up equipment, large board equipment, keep it in for too long because the limb's done ischemic or whatnot. So it's important to understand all of these various considerations before you zone in on an X device as your device of choice for caring for these patients. This is, I'm sorry, it's a reference to Dr. Tirani, but this is kind of just something I made up on the side. But essentially, this is a slide that I put up that I say, what are my indications for MCS? I mean, there are many standardized indications. But for me, simplistically, as a bedside clinician, the one thing that I really care about is if I'm thinking about it, there is something to be said about, you know, your intuition that's come from years of training, it's probably the right time. Of course, objective parameters, rising lactate, worsening hemodynamics, more than one inotrope in vasopressin, which is a majority of our shock patients, so the threshold is not really very high. Poor hemodynamics, again, I understand there's a subjective parameter. Before organ failure, this is an important point, and we can talk a little bit more about it as we go. But the point is, there's no point putting an MCS in patients who already have renal failure, respiratory failure, hepatic failure, on dialysis. At that point, the ship is sailed. We are not supporting the circulation for anything meaningful, because all the end-organ damage that has to happen has already happened. So before this, it's probably best utilized. Before high-risk intervention, now suppose you have a shock patient, you're going in there, you've got to send their LAD, prox LAD, or left main, and their entire anterior wall is down. It's probably a good idea to discuss circulatory support before you do that PCI. And again, as a bridge to recovery or advanced therapy. So this is an important slide on PV loops. I'm not going to belabor this point. It's more of a heart failure slide. But the reason this is important is because depending on what you pick as your MCS device, your LV hemodynamics behave differently. And so it's important to understand intuitively these PV loops before you commit patients down to a given device of choice. These are data from our group where we looked at the epidemiology of MCS use across the nation in different phenotypes. This one is in patients pre-LVAD, multi-etiology, cardiogenic shock. This is in patients with post-cardiotomy cardiogenic shock. This is STEMI. This is non-STEMI. The majority of these studies essentially show that MCS devices are either stable or coming down. And the decline is largely because IBPs have stopped being in favor after the IBP shock 2 trial, which we'll talk about. There has been an exponential increase in the use of impellers and ECMO devices, especially in the post-surgical population, ECMO devices are very common because surgeons are very comfortable cannulating. In the medical heart failure side, impeller devices are getting very common. So as you can see, this is a kind of broad overview of how these devices are used in current practice. These are, again, data from our group specifically looking at ECMO. As you can see, there's been an exponential increase in ECMO, especially after 2008-2009 when there was a flu pandemic and people got really comfortable using VV-ECMO in the ICU. So what is essentially an operating room technology with some niche ICU indications or pediatric indications started creeping into the adult population and they've become ubiquitous. VV-ECMO is largely for pulmonary bypass, but as you can see, our discussion largely in this talk is going to revolve around VA-ECMO, which is the cardiopulmonary bypass. These are data from the ELSO registry. As you can see, there is again, 2008-2009 is kind of that inflection point beyond which ECMO use is just magnified across the country. This is a very nice paper from Naveen Kapoor and his group from Tufts, where they essentially looked at a conceptual model of hemometabolic shock, where they said that shock is essentially hemodynamic insult initially in the systemic circulation that progresses if untreated to a metabolic problem, because there's hyperperfusion of all your end organs, hepatic, renal, respiratory, hematological, different systems, and then gradual shutdown, and then it becomes a metabolic problem. They develop a search-like picture. So conceptually, our practice should try to intervene along the spectrum before this hemodynamic insult becomes a metabolic insult. And these are data from our group where we looked at organ failure in patients with cardiogenic shock, and essentially, it's an intuitive concept that multi-organ failure patients have much worse outcomes compared to single-organ failure compared to no-organ failure. So it's indirect evidence of this hemometabolic concept that was discussed by the other group. These are a couple of device algorithms that I find very useful, but I want, again, want you to go back to the original. I'm not going to go into each of them in detail, but I want you to go back to our original discussion where we said, essentially, how many ventricles do we want to support? How much support do we want in terms of liters of support of cardiac output? How does the peripheral vasculature look, and therefore, what should our strategy be? So this is kind of a quick and dirty slide. I want to say, if you want to know how much flow you want, which ventricle you want to support, whether or not you want to unload your LV, how quickly should you implant these devices, speed, and then what catheter sizes they are based on peripheral vasculature, and if not, you want to go transeptal, and this, again, is a diagrammatic depiction of the same concept. This is the intra-aortic balloon pump. There are very standardized indications, contraindications. Two indications that I found intra-aortic balloon pumps very useful are mechanical complications of acute MI where they have severe papillary muscle dysfunction and mitral regurgitation. That's a great indication, and patients with ventricular septal defect due to acute MI where you really can unload the left ventricle very well and really help these patients. The balloon length depends—the balloon volume dictates what the length is, which, again, you can measure to a patient's height, and then typically the two balloons we use in practice are the 40 or the 50cc balloons. The others are more pediatric. This is how it looks. All of you have seen this. I'm not going to belabor this in great detail. This is the Impeller. Again, it comes in various configurations. These ones here, Impeller 5.5 and above, are almost always surgically implanted. These are large bore, 21 and 19 French. The 14 French Impeller CP is smart assist. The 2.5, which we don't use anymore, are all percutaneous. We do them in the cath lab. This requires an axillary cut down. This is how it looks. It's just a depiction. I'm sure you guys have all seen this in your clinical practice, but this is an axillary Impeller, as you can tell. This is how an ECMO circuit looks. Largely, it is a large bore venous cannula in the central vein, which is usually IVC or SVC, large bore arterial cannula somewhere in the aorta, either proximal ascending aorta or thoracic or descending aorta, and it's a venous and arterial cannula with an external oxygenator and external rotatory pump. And this slide has the various different configurations of ECMO and whatever other shape and form they come, but I just wanted to put it up there. This is a nice meta-analysis that compares the Impeller to the IABP. The take-home point is Impeller gives you better hemodynamic support, but also causes higher complications of limb ischemia, bleeding, and neutral on mortality. This is the IABP SHOCK 2 trial that we briefly discussed. This showed that IABP did no better than no IABP in patients with acute MI and shock, which was published in 2012, and kind of that's when IABP started falling out of favor. Its signal was relatively neutral across all subgroup analysis. This is the Impeller, impressed trial that looked at Impeller versus IABP, and it was comparable outcomes. Like I said, mortality was comparable, but it had more improved hemodynamic support, but also at the risk of higher complications, so this started getting more and more popular. This is a meta-analysis of ECMO versus other mechanisms of mechanical circulatory support. Again, it's a little, obviously, biased because of how you measure these patients. These are data from our group where we looked at complications in MCS. As you can see, MCS comes with a lot of complications. The large-bore peripheral cannulas, these are rotatory circuits with an Impeller circuit in the LV for the Impeller or an external pump in the setting of an ECMO. Large circuit in the case of ECMO tools, we have point-of-vascular access with large-bore cannulae. You're bound to have complications. I want to highlight the hematological complications because that's what, as ICU physicians, we see most in our practice. Lastly, I want to highlight that ECMO is used – it's not supposed to say ECPR up here. This is supposed to say Impeller versus ECMO complications comparison. I apologize for the slide, but essentially, this was a really nice propensity-matched study. Last sample size, I forget which data set. I think either this is Medicare or Optum, but essentially, they looked at IVP to Impeller. As you can see in this retrospective match study, Impeller had a higher signal to mortality and complications. There are ongoing prospective studies that are going to confirm this, but this may change how we perceive the risk of using an Impeller. This is some of the things that I want to tell you. This is a patient of mine who came in with cardiogenic shock. As you can see, we have a 14-french Impeller sheet with a 9-french Impeller catheter through the right common femoral. This is a swan-gans catheter on the other femoral vein, and as you can see, to make sure that this patient doesn't have limb ischemia, we did distal limb perfusion. We stuck in a 6-french sheet on the common femoral artery on this side, pulled it through to a bypass loop, pushed it back down through an antigrade stick, essentially a needle stick to cannulate the leg in the SFA, so not the CFA, but the SFA towards the toes. So we are essentially pulling blood out of the left limb, putting it through the circuit and perfusing the right limb distal to where the ECMO cannula is. The other thing is this north-south mixing syndrome or Harlequin syndrome, which essentially is because the LV is receiving blood, which is deoxygenated blood that comes in through the lungs that are not particularly ventilating, and then the ECMO is shooting arterial blood from down here, and so the mixing cloud meets somewhere here, depending on how powerful your LV ejection is, and the way to approach this is to measure arterial saturations in the right radial artery, left radial artery, and in the femoral arteries, which kind of helps you localize where this transition point is. I'm not going to go too much into this, but all ECMO comes at the risk of LV distension because the ECMO is essentially high pressure, five liters of cardiac output going retrograde in the aorta against a weak left ventricle, so the LV does not eject and gets distended. There are many ways to unload the LV, as you can see. I'm not going to go through each of them. This is a meta-analysis of all forms of LV unloading in patients with all etiologies of cardiogenic shock, and as you can see, there's some benefit to this. These are data from our group looking at combination MCF, so specifically looking at the IBP as an LV unloading tool in patients with VA ECMO, and here looking at the impella, the impella signal was neutral, whereas the IBP signal was neutral, too, but showed a mortality benefit in patients with acute MI, which essentially are patients that tolerate these filling pressures much more poorly than other patients. These are data from our group and others that have looked at PA catheters. I just wanted to highlight this to you. As you already know, PA catheters are very, very important in understanding mechanical circulatory support, so if you're taking the time to put in a 14 French or a 17 French RT or cannula release, you can also put in seven or eight French PA catheters on the venous side because it gives you tremendous amounts of information for caring for these patients, and this is a study from the cardiogenic shock working group where they showed that PA catheter use and using these parameters to understand and make decisions leads to a mortality benefit, so there might be a resurgence of PA catheter use in this specific population. There are data and studies going out on this, so stay tuned. Lastly, ECPR, this is the arrest trial published in Lancet. As you can see, 15 patients in each group, but the protocol care where ECMO is incorporated into cardiopulmonary resuscitation, taking the patient to the cath lab while on mechanical cardiopulmonary resuscitation and performing revascularization, if appropriate, for acute MI has shown significant mortality benefit from the use of this protocol. Again, this is not a device-specific study. It is a protocol-specific study, and I'll keep harping that point because it's important for every institute to have a protocol while caring for these patients. This is a brief illustration. Many of you have cared for such ICU patients. They have lines and tubes everywhere, conceivable, and essentially it's multidisciplinary care, and what I want to highlight is how many specialists are required to provide this resource-intensive care required for this one patient. This is a quick and dirty ECMO weaning protocol slide. Nothing that you may have not already read about, but essentially how do you monitor these patients? How do you assess these patients? How do you wean the ECMO? Every institute has a different protocol. This is a protocol that I found in a very nice review article in circulation, but I wanted to make sure that you had access to this. Lastly, I want to highlight this very nice perspective piece that was published in CCI looking at randomized trials, and unlike many things in cardiology, which have tens and thousands of patients in trials, the sample sizes for many of these randomized trials in cardiogenic shock is very limited. It's a tough space. It's very tough for patient recruitment. Despite this, this is a study from our group where we looked at MCS-assisted PCI, so use of MCS to support percutaneous coronary intervention in patients with acute myocardiogenic shock, and there's been an explosion of devices. More and more patients are getting these, and this is despite the fact that there is limited data. So this is the most important need of the hour is to get better data for these patients, so I'm hoping that some of you on today's talk and many others are working nationally to help develop good quality science in this field. This is a fertile field for high-quality data. With that, I'll thank you for your time, and I'll be happy to take questions. Thank you, and have a good rest of your day.

heart pumps

cardiogenic shock

intra-aortic balloon pump

impella

ECMO

mechanical circulatory support