Okay, I think we'll get started. Welcome everybody. Thanks to all of you who are joining us tonight for a very exciting webinar focused on important topics that are related to cardiogenic shock. And we're featuring three diverse and outstanding speakers. I'm Ashley Harden. I'm one of the advanced heart failure and transplant cardiologists at UT Southwestern Medical Center in Dallas, Texas. And I'm going to introduce next three of my colleagues that are here with me tonight. First we have, let me go back one slide, Katie Ginder, one of our awesome nurse practitioners here at UT Southwestern who specializes in the management of patients who have advanced heart failure, LVAD, and transplants. And then we've got Dr. DeWade who is joining us from the University of Rochester, also an advanced heart failure transplant specialist. And then Ben Wong, one of our PharmDs who is at Stanford, who is a specialist in all things cardiology, advanced heart failure, and pulmonary hypertension. So welcome guys. We look forward to your talks. Just to review our learning objectives today and tonight, to review the clinical trial data and current use of medical therapy and the management of cardiogenic shock, evaluate the role of acute mechanical support in the management of patients with cardiogenic shock, and to be able to discuss at the end of this webinar the importance of the cardiogenic shock team and strategies to optimize patient outcomes. We'll review here next our agenda. So I'll finish our welcoming remarks here in just a second. Our first talk will be given by Katie, and she'll review the definition, epidemiology, and phenotypes of cardiogenic shock. And this will be followed by a talk really with an overview of medical therapy, vasopressor support, and inotropes by Ben Wang, and then followed by a discussion of the mechanical circulatory support options and the role of the shock team, importantly, with Dr. Jowade. And we will have hopefully plenty of time for a nice panel discussion at the end. And just a reminder, continuing education credit information. To claim your credit, we're required to complete a course evaluation. And this is available in the HFSA Learning Center and is also available at the conclusion of this event. Thank you, and enjoy the webinar. We're going to start, actually, with a case. Perfect. We're going to go on to the case here. Mr. Beattie. So we'll actually be using a case to take us through the three lectures and follow up with the outcome at the very end. So this is Mr. Beattie. He's a 50-year-old man who had chest pain that woke him up at 5 a.m. And it's now 6 p.m. in the evening. He has a medical history of hypertension, hyperlipidemia, diabetes that's decently well-controlled, well-controlled, with a hemoglobin A1c of 6.7%. He is taking no medications. His blood pressure on arrival to the emergency room this evening is 88 over 70 with a heart rate of 94. And on exam, you notice that he looks like he's uncomfortable. He's in acute distress. He has an elevated jugular venous pressure, no obvious murmurs on exam, and his legs feel cool to the touch. You do a bedside echocardiogram that's revealing for a left ventricular ejection fraction that's severely depressed at 20% and some mild mitral regurgitation. His labs return notable for a lactate of 3 1⁄2 and a creatinine of 2, which is higher than his baseline, which is normal. You notice that his EKG shows antireceptal ST elevations, but he's also developed Q waves here, and the antireceptal and lateral pericordial leads. So management decisions, what to do. At this point, some of the pertinent questions, some questions you may be asking yourself is, number one, does he qualify for a definition? What is the definition of cardiogenic shock? Is he clearly in cardiogenic shock? And what should we do about this? Should we take him to the cath lab now or later? Should we try medical stabilization first or not? So next, I'm going to turn it over to Katie Gender to review the definition, epidemiology, and phenotypes of cardiogenic shock. Thanks, Katie. Hi, everyone. Again, thank you, Ashley, for that great introduction. Again, my name is Katie Gender, and I am a nurse practitioner here at UT Southwestern in Dallas, Texas. I predominantly work with the advanced heart failure, VAD, and transplant team, but with also the cardiology service. I have no disclosures. So the objectives for my portion of the talk are to define cardiogenic shock, identify the ideologies of cardiogenic shock, recognize the different phenotypes, and understand the utility of prognostic models and risk scores. I do have some pre-presentation questions. There will be a poll. What physical exam findings and clinical lab values are most consistent with cardiogenic shock? A, cool extremities, elevated JVP, blood pressure of 99 over 58, creatinine 1.02, and a lactate of 1.5. B, cool extremities, elevated JVP with a blood pressure of 86 over 51, creatinine of 2.5, lactate of 3. C, warm extremities, no JVP, blood pressure 115 over 65 with a creatinine of 3 and a lactate of 2.5. D, warm extremities, elevated JVP, blood pressure of 98 over 76, creatinine 1.9, and a lactate of 1.5. My second question is, a patient presents in cardiogenic shock with chest pain that started greater than 12 hours ago, and EKG is notable for anterior ST elevations. What is the next most appropriate step? Most appropriate step? A, diagnostic left heart cath only, no intervention of lesion. B, nitrates and right heart cath with leave-in PA catheter plus minus inotropes, if indicated. C, nitrates, monitor chest pain, and admit to the CICU. Or D, left heart cath with immediate PCI, if indicated. So I'll take some time for the poll questions. So after that, let's start with the definition of cardiogenic shock. First and foremost, it's a clinical syndrome of mixed ideologies, phenotypes, and presentations that is associated with high morbidity and mortality. It's a cardiac disorder that results in both clinical and biochemical evidence of tissue hypoperfusion. So here are some operational and guideline definitions that have historically been used to define cardiogenic shock. As you can see for the clinical criteria, there are some common themes. And one of those is having a systolic blood pressure of less than 90. Other biochemical evidence of hypoperfusion would indicate either a urine output of less than 30, elevated creatinine, or elevated lactate. Other clinical findings could be altered mental status, narrow pulse pressure, confusion, dizziness. Here is some data from the US National Inpatient Sample Database ranging from 2004 to 2018. And while this data is a little bit older, you can see that there continues to be a rise for cardiogenic shock hospitalizations. And while there is a rise, the good news is that inpatient or in-hospital mortality has ultimately decreased over the years, beginning in 2004 to 2018. However, if you follow the trend downwards, it still remains relatively high, with in-hospital mortality being close to 35% to 40% based on this inpatient sample database. So what are the ideologies of cardiogenic shock? Kind of classified these into three areas, cardiomyopathic, which could be myocardial infarction, severe right ventricular infarction, acute myocardial infarction, acute ventricular infarction, acute decompensated heart failure from a non-ischemic cardiomyopathy or dilated cardiomyopathy, advanced septic shock or myocarditis. Then you can have tachy or bradyarrhythmias that contribute to cardiogenic shock. And lastly, mechanical issues such as severe valvular insufficiency stenosis, acute or severe septal wall defects, and or cardiac tamponade. So what are the risks for cardiogenic shock? As we kind of alluded to, Mr. BT looking at the comorbidities that he has, some risks that are identified in the literature are older age, a history of anterior myocardial infarction, hypertension, diabetes, past multivessel CAD, and a prior diagnosis of heart failure. And while this picture on the left doesn't necessarily define the risk for cardiogenic shock, I think looking at Mr. BT and his clinical picture, we can follow the pathophysiology to understand what happens in acute MI cardiogenic shock. So first there's the insult, and you can see that there can be decreased cardiac output, hypotension, decrease in coronary perfusion pressure leading to tissue hypoperfusion, and ultimately ischemia, leading to progressive myocardial dysfunction and death. However, if you look at the second yellow box down, in someone who has an acute MI, revascularization can be key to relieve the ischemia and ultimately have a good outcome and possibly a good quality of life. So acute coronary syndrome remains the leading cause of cardiogenic shock, and I did want to take time to provide you with some quick statistics to kind of emphasize that point. Acute MI accounts for 81% of patients in cardiogenic shock. Cardiogenic shock complicates 5% to 10% of cases of acute MI and is the leading cause of death after MI. While inpatient mortality has improved, the 6 to 12 month mortality has remained unchanged at approximately 50%. And lastly, survivors of MI associated with cardiogenic shock have an 18% chance of 30-day re-admission after discharge, which is a slightly lower risk for those with STEMI versus in STEMI. So talking about this, I wanted to start with the shock trial. And the primary endpoint for the shock trial was all-cause mortality at 30 days. The secondary outcome was all-cause mortality at 6 and 12 months. So what this shock trial looked at So what this shock trial looked at was ACS within 36 hours. The patients were randomized within the first 12 hours of diagnosis, and treatment was given within six hours of randomization. In the intervention group, there was emergency revascularization. If PCI was feasible, they would proceed with that. But if it was not, then they would proceed with CABG. In the control group, they received initial medical stabilization and could undergo revascularization at a minimum of 54 hours. It's important to note what the initial medical stabilization was, and that included intraaortic balloon pump and thrombolytic therapy. So looking at the outcomes here, we can see at 30 days, six months, and one year, revascularization improved overall survival. In the 30-day group, while it was not statistically significant, there was a 9.3% absolute reduction. There were long, short-term, and long-term benefits at six months and one year. Next, I wanted to look at the culprit trial. This included acute MI. Two-thirds of those patients had a semi-cardiogenic shock, multivessel CAD. And these patients were randomized either to early revascularization with a culprit lesion-only PCI or early revascularization with a multivessel PCI. This trial demonstrated a 9.5% absolute risk reduction of the composite primary endpoint, which was all-cause mortality or renal replacement therapy. So from these two trials and others that have been completed and done, it's important to look at the guidelines and how they guide us in our treatment for these patients. So this is based off the 2021 ACC AHA Sky Coronary Artery Revascularization Guidelines. And if we look at our patient within the case study, we can say a patient has a STEMI with ischemic symptoms. Symptom onset is a symptom onset with ischemic symptoms. Symptom onset is greater than 12 hours. If the patient has cardiogenic shock or heart failure and PCI is feasible, it is a class 1 indication for primary PCI. Or in STEMI, if a patient has cardiogenic shock, immediate invasive strategy is also a class 1 indication. Again, just reiterating, immediate revascularization or in STEMI when cardiogenic shock is indicated. The guidelines also say that culprit-only PCI in STEMI and cardiogenic shock is warranted. And there may not be an advantage for stable-appearing non-culprit arteries if a patient is truly in cardiogenic shock and may actually cause harm. Next, I wanted to move on to the hemodynamic phenotypes because I feel that using the hemodynamic profiles can help guide our pharmacologic and mechanical circulatory support treatment, which Ben and Anas will get to. to in a few minutes. So the first one is the classic cardiogenic shock, also similar to Stevenson profile C for those of you that know that, cold and wet. So you're going to have an increase in your pulmonary wedge pressure and a decrease in your cardiac output or cardiac index. Next, you can see in the top second right column, cold and dry, this is considered uvolemic cardiogenic shock in which your wedge pressure may be normal, but you will have a low cardiac output. These presentations or patients presenting like this may be more likely to have a previous MI or CKD. The warm and wet profile or vasodilatory cardiogenic shock, or as we often say, mixed shock, can have an increased wedge, low normal SVR, and low cardiac output. This can be related to a SIRS reaction in conjunction with an MI and is associated with an increased incidence of sepsis and mortality. Here are some other phenotypes to kind of understand cardiogenic shock and our treatment strategies. I thought this was interesting to identify pre-shock patients and identify them early in case they continue to slide. So here they have classified normotensive hypoperfusion as a systolic artery pressure of greater than 90, a cardiac index of less than 2.2 with an elevated SVR of greater than 1600. The hypotensive normal perfusion population would be a systolic arterial pressure of less than 90 with a cardiac index that's actually greater than 2.2 and a normal SVR state. When thinking about our treatment strategies, it's important to use our hemodynamics that we may have with leave-in PA catheters or if a patient goes for a right heart cath. And so this is looking at LV dominant shock, RV dominant shock, and biventricular shock. As you can see with the LV dominant shock, you're going to have a low central venous pressure or RA pressure, an elevated left-sided filling pressure or wedge with a high PAPI. In the RV dominant shock, you're actually going to have the opposite. So your CBP is going to be high with a low pulmonary wedge pressure and a lower PAPI score. In biventricular shock, you may have an elevated CBP, a variable wedge pressure, but it may also be high and a low PAPI. From this, it's important to note to define cardiogenic shock and these phenotypes and variables, all of them still have a systolic blood pressure of less than 90 and a cardiac output of less than, sorry, cardiac index of less than 2.2. Looking at the risk scores, I identified two that I thought that I would share today. The first one is intraaortic balloon pump shock two score. This is looking at acute myocardial infarction, cardiogenic shock mortality within 30 days. I know this image is a little blurry, but I'll go over the variables with you. So the first one is age greater than 73, history of stroke, hyperglycemia, elevated creatinine, elevated arterial lactate, and TIMI flow grade less than three after PCI. From this graph, you can see that the higher the score, the increase mortality. There is an increase in mortality. From the card shock store score, this is a risk predictor for in-hospital mortality of cardiogenic shock. It has very similar variables and criteria compared to the IABP shock two score, but just a little bit different. So age greater than 75, altered mental status, previous MI or ACS, low ejection fraction of less than 40%. It has different levels to kind of quantify the blood lactate as well as the GFR. Again, for this, the higher your risk score, the higher your risk for in-hospital mortality due to cardiogenic shock. Lastly, I wanted to talk about the staging and classification of cardiogenic shock. And the SKY stages have been used more recently. So as you can see at the bottom, the SKY stage A is a patient with risk factors who may be stable, but not currently in cardiogenic shock. And as you work your way up to E, E would be extremists requiring multiple interventions who may be experiencing mechanical circulatory support with multiple pharmacologic agents to help stabilize the patient. C is the classic presentation of hypoperfusion and hypotension. As you can see, as you move up towards SKY E, in-hospital mortality and long-term mortality increases with each stage. And while we still use Intermax profiles, I think this has been more used recently as far as classifying our acute decompensated heart failure patients as they move towards durable mechanical circulatory support. But it's a similar classification that uses the NYHA classes as well as functionality of the patients. On the left, these are just the brief Intermax profiles with a graphic that I think is helpful to understand a patient's functionality. So if you look at Intermax 3, that is dependent stability in someone who is on continuous intravenous inotrope that may be stable, but they can rapidly decline as they move from Intermax 2 to 1, with 1 being critical cardiogenic shock. At that time, they will have life-threatening hypotension despite rapidly escalating inotropic therapy, and we would need to consider temporary mechanical circulatory support or other advanced therapy options. So for the pre and post questions, you can go ahead to select your answers. What physical exam findings in clinical lab values are most consistent with cardiogenic shock? Okay, 100%. Good job, guys. So yes, cool extremities is a clinical symptom or physical exam finding that's consistent with hypoperfusion. Elevated JBP is indicative of elevated filling pressures. Again, you have your blood pressure criteria of a systolic blood pressure of less than 90. And then serum creatinine, elevated serum creatinine and elevated serum lactate are also lab values consistent with hypoperfusion. One moment. I'm just having difficulty moving the slide. Oh, there's the answer. Okay, the second poll question. A patient presents in cardiogenic shock with chest pain that started greater than 12 hours ago. An EKG is notable for anterior ST elevations. What is the next most appropriate step? Great, another 100% left heart cath with immediate PCI as indicated. So as we saw in the shock trial for STEMI, early revascularization is key, so you definitely want to intervene sooner rather than later. Now I will turn it over to Ben, or Ashley. And here are my references. Awesome, thank you, Katie. I think you raised so many important points. You know, part of, you know, with the first step, honestly, is the ability to recognize cardiogenic shock and understand what definitions we've used in the trials that we have to study cardiogenic shock and understanding when to escalate care if your patient's not doing well. So here we have Mr. BT after, you know, we all heard Katie's lecture, everybody knew. We identified cardiogenic shock. We sent him for revascularization. Importantly, even after he presented, late for an anterior STEMI. So nice job there. We were following guideline recommendations. And despite this, poor Mr. BT remains hypotensive with an elevated lactate and still poor urine output. So you're worried about him. You get another echocardiogram, shows about the same. His EF is still 20%. He's got some anteroceptal and lateral wall akinesis, not unexpected, mild mitral regurgitation, and importantly, no ventricular septal defect. You think he needs to go on vasoactive medications because revascularization enough was not able to get him out of DODGE. And so importantly, how do we know which vasoactive medication to choose and what evidence do we have to support the use of these medications? So on that note, I am gonna turn the screen over to Ben here. Sorry for the delay. Hi, all. Thank you. Thanks so much for that wonderful presentation, Katie. I'm Ben. I'm the CTU pulmonary hypertension clinical pharmacist over at Stanford HealthCare. And it's my pleasure to be discussing inotropes and vasopressors, encouraging and shock with you. I do not have any disclosures. And for our first pre-presentation question, we have two of them. In the Optima-CC trial, patients with acute myocardial infarction related cardiogenic shock that were treated with high dose epinephrine compared to equivalent dose norepinephrine experienced a significantly higher A, cardiac index at 72 hours, B, arrhythmia, C, incidence of refractory shock, and D, mortality. So in the Optima-CC trial, patients with acute myocardial infarction I'll give you a moment there to answer it. Okay, thank you for your answer. Question two. In patients receiving inotropic therapy for cardiogenic shock, complete lactate clearance at 24 hours is associated with A, higher doses of dopamine, B, lower in-hospital mortality, C, higher hospital mortality, and D, lower doses of epinephrine. Thank you for your responses. Cardiogenic shock often characteristically manifests with end-organ hypoperfusion and dysfunction, and they often involve some of our most vital organs, namely the lungs, the liver, and the kidneys with mechanical ventilation actually required recently in a paper that was published in JHLT this year at 54-76 percent of patients with cardiogenic shock. Furthermore, renal failure requiring CRRT was actually up to 13-25 percent of cases. In response to this and all of our clinical experience, in the 2022 ACC, AHA, HFSA guidelines for the management of heart failure, they do speak with a class 1 recommendation about patients with cardiogenic shock, suggesting that intravenous inotropic support be given to them to maintain systemic perfusion and preserve end-organ performance. More specifically though, what is actually the preferred vasoactive strategy? Lucky for us, we do have some evidence which I'll review later. But in general, I would say that this is, and purport that this is really an art in addition to the science because cardiogenic shock is so hemodynamically diverse, especially with regards to etiologies and which ventricle involved, that it can be really difficult to actually cluster phenotypes and do those evidence generation studies where you can really get a sense of what is the best vasoactive strategy to start out with and how to adjust accordingly. Because there is such sparse evidence available for the optimal vasoactive inotropic strategy, then we actually have drug selection guided by ultimately the underlying pathophysiology like in our case, we had the acute myocardial infarction-related cardiogenic shock, where early revascularization was paramount to success, and also really the hemodynamic profile that Katie went over. When we look at these patients and assess whether or not they are either vasoconstricted or vasodilated or poorly perfused, we favor the use of vasodilators for those who are vasoconstricted, and vasoconstrictors for those who are vasodilated, and inotropes for those who are poorly perfused. Which ventricle is involved, either biventricular failure or just RV dominant or LV dominant shock is also a consideration. What I'm hoping to come out of this presentation with is really an overview of the vasoactive agent pharmacology, so that you can have the tools needed to customize your patient's response to therapy as well as to their specific hemodynamic parameters that you're seeing. The pharmacology of vasoactive therapy, I've made a little schematic here for you to see and simply outline the receptor profile agonism of the adrenergic agonist and catecholamines. You can see here on the left side, it's mostly adrenergic agents like the isoproteinol, multibutamine, epinephrine, dopa, norepinephrine, and funnelephrine. On the right side, you'll actually see drugs that are non-adrenergic in mechanism and not relying on adrenergic receptors. Their position is largely based off of what I believe to be analogous pharmacodynamic effects. Another way of thinking about these drugs is also the colloquial inodilators versus inopressors versus vasopressors, which really describes their action on the body. As a summary or an overview of what's going on with this slide, the middle figures show Alpha-1 in that red triangle, adrenergic activity, and then you can see Beta-1 and Beta-2. They're laid out based off their relative receptor profile agonism. What I've tried to do here is to show that, for example, if you look at dobutamine, it has some mild Alpha-1 activity, but then you'll have more Beta-1 activity and Beta-2. That speaks to, again, Alpha-1 is a restricting effect. Beta-1 is more chronotropic and inotropic in nature, and then Beta-2 is more chronotropic with some peripheral vasodilation. As you balance out those effects of these adrenergic receptors, you'll see some comparisons drawn here between the drugs. Of note, norepinephrine, I did place down there in the vasopressor arm. Of course, it does have some Beta-1 activity and some inotropy as well, so don't hate me on that. Ultimately, it does have less Beta-1 activity, obviously, than a drug like dobutamine or epinephrine, and has a more predominant Alpha-1 effect. One thing I want to draw attention to is the milrinone. On the right side, the very top, is an inodilator, and that it furthermore has a different kinetic characteristics than the other drugs. You'll see I didn't list anything kinetically for the other drugs, but that's because those drugs generally have a half-life on the order of minutes, and often undergo COMT or monamine oxidase clearance. Whereas milrinone is standalone special in the sense that it is renally cleared, unchanged. It actually has an elimination half-life on the scale of hours, like two-and-a-half hours in normal patients, and in those who have renal failure or on dialysis, it actually prolongs even further. In extreme cases, like in patients with CVVH, it's been noted that the milrinone half-life can extend all the way up to 20 hours. But what is also special about this drug in comparison to the others is that it is also able to serve as a pulmonary dilator. On the note of that, when we think about patients with cardiogenic shock, especially in those with significant RV or by the involvement, it is notable to think about pulmonary vascular resistance and to consider the effect of these agents that we use on pulmonary vascular resistance. There are pretty limited in vivo human studies, and the majority of the data is from animal studies. But ultimately, drugs that have alpha-1 adrenergic activity have a pretty dose-dependent pulmonary artery vasoconstriction, which doesn't mean that it wouldn't serve the RV well necessarily, but as doses escalate, it can certainly increase pulmonary vascular resistance and RV afterload. Now, if this is a drug that has inotropic activity though, then that may ultimately counterbalance and improve RV performance overall. Again, it's based off of patient response. Vasopressin is nicely a drug that doesn't have an associated pulmonary vasoconstriction, and milrinone is actually a pulmonary vasodilator, so it would actually have beneficial effects there. The caveat, of course, is that systemic perfusion is important for RV performance ultimately. Systemic hypotension would actually be bad for RV ischemia, RV perfusion. The use of milrinone gets limited by that often. I wish I could say all the benefits of these therapies in addressing hypoperfusion and hemodynamic derangements is all that there is to the story, but there really is unfortunately some risks that are associated with these vasoelectric therapies. Medications that augment both phreatic output and enhance SVR can also increase the risk of increased myoperative oxygen demand and endothemia, and of course, perfluorethemia as well, and lastly, the risk of arrhythmias. In our case, somebody who has myoperial infarction-related cytogenic shock, especially if there's no revascularization as a bridging to that intervention, escalating doses of vasoactive therapy can actually worsen ischemia and work towards ultimately what Katie talked about earlier, which was this kind of spiral of ischemia inflammation and vasodilation, which worsens ischemia inflammation and vasodilation. And unfortunately, because of the increased utilization of vasopressor therapies kind of spirals further until the ultimate pathology is stressed. The other comment I want to make is that in cases of refractory cardiogenic shock, not just those who have acute myoperial infarction, as cardiogenic shock progresses, it can also be associated with an inflammatory and vasodilatory phenomenon. And then without saying, there's also the mixed shock picture that she discussed, where vasodilation is also a big hemodynamic feature. So, you know, of the landmark kind of randomized controlled trials in cardiogenic shock, we don't have a lot. These are pretty easy slides to make in the sense that, you know, we have kind of a sentinel paper, the SOAP2 trial in 2010, that evaluated shock of all origins with septic shock being the predominant form of shock they looked at. And they compared dopamine versus norepinephrine as vasopressors. And so the doses that were used of dopamine, for example, all the way up to 20 mics per case per minute, and norepinephrine, you know, also up to higher doses as well. And when used as a vasopressor, they really didn't see any difference in mortality at 28 days in all comers. Now they did see a significant increase in arrhythmic events though, with dopamine usage instead of norepinephrine. And they did a subgroup analysis of those who are coming in with cardiogenic shock with kind of mixed etiologies, this is again all comers, that showed dopamine did have increased mortality at 28 days. And I think it's postulated that this is related to arrhythmic events as well. One thing I do want to note is that in this trial, there was open label usage of dobutamine actually in both arms. And so it's a little bit hard to exactly compare the dopamine versus the norepinephrine because dopamine was really used both arms open label. I think what I've kind of taken away from this trial ultimately is that the use of dopamine as a pressure, vasopressor at high doses can be problematic. And, you know, it's used solely to augment blood pressure is probably, you know, not superior in any way to norepinephrine. Then we have something a little bit more specific to the Optima-CC trial, which was done in 2018. It was a multi-study double-blind RCT of patients who had acute myofascial and partially related cardiogenic shock, like our case, that was after a revascularization. And it was a pretty small trial of 27 versus 30 patients comparing epinephrine versus norepinephrine. The primary outcome was actually change or evolution of cardiac index where they found no difference there. And what they did find, however, was that epinephrine was associated with an increased incidence of refractory shock. Within that definition, of course, is lactic acidosis. And there's some knowledge about kind of type B lactic acidosis with associated with epinephrine. And some things that I picked out and I wanted to share with you all is that as you look at the study and look at the supplemental, the high doses that were being used in this trial. So ultimately six hours after randomization, patients were using doses as high as 0.9 mcg per minute and 0.8 mcg per minute in both arms. So this typically exceeds at least our institutional max at Stanford. And then the other thing I wanna note is that open-label dobutamine again was used here in about two-thirds of patients on both arms. Furthermore, dobutamine was actually overlapped with norepinephrine for about 90 hours. So I guess more than three days, you know, as compared to the people who were using epinephrine. And then finally, you know, as kind of acute myocardial infarction related cardiogenic shock continues to improve its outcome, heart failure related cardiogenic shock continues to escalate in prevalence and severity. And so there's a trial here, the Do-Re-Mi trial that was conducted in 2021 is a single-sided double-blind randomized controlled trial. They looked at cardiogenic shock in the CICU and majority of which were SCI-CHC, about 80%. And they looked at dobutamine versus norepinephrine, about a hundred patients in both sides. What they looked at was a composite outcome of in-hospital all-cause mortality, stroke, and also cardiovascular slash renal events. And what they found was across all of those events, they were unable to find a difference between the two drugs. Furthermore, I would say that just, you know, kind of understanding a little bit about the baseline inclusion criteria, that CKD was defined in about 40% of patients on both sides and that very few patients came in on carvetolol. And this is just a little caveat because carvetolol has been noted, at least in some small studies in humans, that it can blunt actually the hemodynamic effects of dobutamine. So I'm really grateful for Do-Re-Mi because I know everyone says, well, you know, we didn't really learn that much. They're kind of the same, you know, norepinephrine and dobutamine. But the reality is that there was, I mean, first of all, you know, we really did think of these drugs as very different. And so this trial actually did demonstrate that probably in the global sense, these drugs are not that different in the way that they behave and perform in cardiogenic shock. And then there was quite a host of secondary analyses that came out of this trial that helps us learn a little bit more about these drugs. And one I wanna highlight is a secondary analysis that the study investigators actually did looking at milrinone versus dobutamine in patients in this trial that did not have a baseline acute kidney injury. And, you know, what we found from here was that in those without a baseline AKI, we actually saw milrinone had a lower risk of the primary outcome of death, primary outcome, which was the composite outcome, sorry, and also death, which to me is kind of impressive to see. And, you know, if you're looking at a subgroup, we're looking at 27 versus 41 patients. It's actually not that much smaller of an analysis than the Optima CC trial that was done for conduct previously in 2018. And so when you see this, it kind of speaks to the fact that, you know, probably milrinone is a stronger inodilator and probably without the accumulation in the setting of renal failure, it's a drug that inodilates. And in those who are probably in the earlier stage of cardiogenic shock, it might actually be just the right drug for this specific type of cardiogenic shock. But again, as we said, you know, the further cardiogenic shock deteriorates and is associated with vasodilation and inflammation and ischemia, probably drugs like milrinone, especially in those with poor renal function is unlikely to be any more beneficial for dobutamine. Oh, sorry. My takeaway from the trials ultimately is that milrinone and dobutamine have comparable short-term clinical outcomes in survival and that, you know, norepinephrine compared to all these other drugs has been really favored as a first-line vasopressor when it's needed. And in cardiogenic shock though, I will caveat and say that, you know, it appears rarely to be a monotherapy, even in the clinical trials that evaluated these and came out with the outcomes that norepinephrine comes on top. And then from the SOAP-2 trial, we also learned that dopamine, when it's used at vasopressor doses over like 10 mikes per kick per minute, probably, you know, when compared to norepinephrine associated with increased mortality and arrhythmic events. And then lastly, high-dose epinephrine compared to equivalent doses of norepinephrine in AMI-associated cardiogenic shock was associated with a much higher incidence of the refractory shock. If you remember, that was your pre-presentation question. So in terms of monitoring for clinical response, you know, what I will say is that there's still gonna be different things to pull together to get a hemodynamic assessment. These are the things that are suggested to have cardiac telemetry for arrhythmias, ART lines for blood pressure, transmitting CPP, not for the aspirin value, but for the trends, doing a pulmonary artery catheterization to kind of be able to get indications of RV performance as well as be able to calculate cardiac output. And then, you know, general markers of tissue perfusion and performance, such as like LFTs, BMP, looking at urine output and lactate clearance. So in a nice review of cardiogenic shock, the management of cardiogenic shock that was again published this year, they looked at suggested perfusion and decongestion goals, and these were the ones that were suggested. So of course, blood pressure with a restoration of systolic blood pressure over 90 millimeters of mercury, making sure that there's adequate urine output and not oliguria, that patients cleared lactate within 24 hours, and that cardiac power output was increased as well as PAPI or pulmonary artery fertility index was increased. And then lastly, some markers of decongestion, which is that the left side or wedge pressure was less than 15, or the right atrial pressures were less than 15 as well for the right side. Again, a secondary analysis from the DO-RE-MI trial, I just want to point out here, they looked at the response to inotropic therapy, looking at pulse pressure improvement of over 30% at 24 hours, as well as complete lactate clearance at 24 hours. And what they found was that lactate clearance at 24 hours was the strongest independent predictor of survival in patients. And so I do think that being simple, lactate clearance is an important marker of success when we are treating patients with vasoactive precartogenic shock, and that we should consider early escalation of therapy, or even considering acute mechanical circulatory support for those who have a poor response within 24 hours. And then, so in conclusion, for sky stage C shock, we probably should consider dobutamine versus milrinone as your initial inotropic therapy selection. If you need a vasopressor, it's often norepinephrine, and sometimes it can be a good starter in those with just mild, low blood pressure, but it really shouldn't replace inotropic therapy when it's indicated. And then lastly, I would say that progressive escalation of pharmacologic support or lack of clinical response really does kind of warrant a high-frequency reevaluation, and sometimes, and in many cases, for those really severe cases, escalation to temporary mechanical circulatory support. Okay, so for the post-presentation question, let's take a stab at it again. Actually, there was quite a spread from the pre-presentation, so let's see if I didn't bore you to sleep. In the OPTIMA-CC trial, patients with acute myocardial infarction related cardiogenic shock treated with high-dose epinephrine compared to equivalent dose norepinephrine experienced significantly higher, A, cardiac index at 72 hours, B, arrhythmia, C, incidence of refractory shock, or D, mortality. Emphasis on significantly higher. All right, so the majority of you answered correctly. The answer was the C, incidence of refractory shock. This is essentially what they found, significantly higher incidence of refractory shock. They did find a higher incidence of arrhythmias and mortality, but it was only numerically elevated, not significantly elevated in this case. OK, question number two. In patients receiving inotropic therapy for cardiogenic shock, complete lactate clearance at 24 hours is associated with A, higher doses of dopamine, B, lower in-hospital mortality, C, higher in-hospital mortality, and D, lower doses of epideptics. Wow, okay, look at that. Okay, 97% answered B, lower in-hospital mortality. So again, getting that lactate clearance to 24 hours is practically, in my eyes, kind of a performance measure for cardiogenic shock. All righty. That's it for me. Those are my references. Thank you so much for your time and attention. I'll hand it back to Ashley now. Okay, awesome. Thank you so much, Ben. I think really interesting data to really show to the audience that, you know, it's these management decisions oftentimes which kind of inodilators, vasopressors, vasoconstrictors, and things of that sort sometimes are institutional dependent, how you were trained. It's nice to know mechanisms of action. And we actually have some really interesting questions that we'll answer during the Q&A. That we'll answer during the panel discussion that came up about starting Milrinone in particular with an AKI and how we manage patients in that setting. Do we avoid it? What dose might we start at? So really interesting data. Again, hard to study cardiogenic shock in general with large randomized controlled trials and a lot of data to support the management decisions behind what we do. So lots of interesting things to discuss. So we'll move on to Mr. Beattie. Back to Mr. Beattie. So he underwent early revascularization after Katie's lecture. And we initiated inotropic support after Ben's lecture because he wasn't doing well and needed some additional help. His urine output was poor and his lactate was still elevated. But despite doing these things, and I think we started him on Milrinone, he remained hypotensive with poor urine output and his lactate continued to climb. A repeat echo again at this time showed a severely depressed left ventricular ejection fraction. And now he has a large LV apical thrombus. And you think he needs more than you can support him with with inotropes to treat his cardiogenic shock. So this raises the question of what is the shock team and what's the role of the shock team for this patient or patients like Mr. Beattie? And what are our options at this point for temporary mechanical support? Is there a device that we should or should not use, especially in light of his LV apical thrombus? So I'll turn it over to Anas. Hi, good evening, everyone, or good afternoon, depending on where you are. Thank you so much, Ashley. Thank you for the HFSA. And thank you for everyone who has been able to join us for this. What I'll be talking about today is the mechanical circulatory support options and the role of the shock team. I have no relevant financial disclosures and, you know, it's such fantastic presentations to follow, so I have a hard act here, but what I hope at least I can convey to you with our time together is first to review the importance of an interdisciplinary shock team to optimize management of the cardiogenic shock patient, talk about the different mechanical circulatory support platforms available for use, but also touch upon the fact that these are not benign devices and acknowledge that there are common complications associated with them. And we'll touch briefly upon monitoring and de-escalation strategies as well. And before I get started, I'd like to pose a question to you, and my first question is use of a shock team has been associated with all of the following except increased overall use of MCS, increased use of advanced MCS such as ECMO, Tendon, Howard, or Impella, misuse of invasive hemodynamics, or reduced CICU mortality. And the second question that I'd like to pose to you before I continue is when should insertion of an impeller device in cardiogenic shock not be pursued? Is it if someone has mild aortic stenosis, mild aortic regurgitation, bioprosthetic aortic valve, or the presence of an LV thrombus? I'll be curious to see what the results are at the end. Before we start talking about cardiogenic shock and the shock team and support options, I just want to touch upon the concept of defining cardiogenic shock. It's my slides, move forward here. What's really important is this can be a very confusing overall concept. One thing that's really evolved in the cardiogenic shock space, especially over the last few years, is the development of a universal language that allows clinicians, providers with multidisciplinary backgrounds to efficiently and effectively communicate the clinical situation to define themselves in. I think that's really what the power is of the SCI and the SCI cardiogenic shock working group shock stages. Because what it really does is leverage two important parameters that both Ben and Katie have touched on, of perfusion and hypertension markers that are readily available at any stage, and it really allows to phenotype where a patient is in their cardiogenic shock trajectory. As we start thinking about the concept of mechanical circulatory support when medical therapy is not quite enough, consider defining and expeditiously communicating these stages after which you might have to at least start thinking about whether that's where you're headed. As we consider how we approach the cardiogenic shock patient, especially as it pertains to consideration of mechanical circulatory support, I thought it was wise to maybe establish a roadmap that conceptually might allow us to hone our thought processes. We'll start off by talking about the shock team, which is a concept that is, in my opinion, incredibly powerful, both in concept and clinical practice. Really what the shock team concept emphasizes is you want to find the right patient, you want to find them at the right time, not too early, not too late. You want to make sure that they're in the right setting, and you want to make sure that if you're going to pursue a mechanical circulatory support option that you choose the right device. There is a large team collaborative involved in the shock team. It may involve providers from multiple backgrounds. For instance, at my institution, a shock team call involves my critical care colleagues, interventional cardiology colleagues, surgical colleagues, myself as advanced heart failure and transplant, as well as palliative care. Really what it allows us to do is perform a rapid multidisciplinary review. It can inform us of additional necessary diagnostic testing that I might not have thought of, but my colleagues did, and really optimize selection of the correct therapeutic intervention. We know that the shock team approach works. There are a number of analyses out there in the literature that prove this over and over again. One such representative study that I wanted to post to the group, I think, features several of the key themes that we find in the literature. This particular analysis was from the Critical Care Cardiology Trials Network, which included 24 participating centers of whom 10 had a formalized shock team. One of the strengths in this analysis is an equal distribution of not just patients with acute myocardial infarction-related cardiogenic shock, but as discussed earlier, it's a cousin, sometimes less recognized, but heart failure-related cardiogenic shock. What this analysis did was looked at about 1,200 patients who were admitted with shock between 2017 and 2019 to a CICU, and compared outcomes and management strategies among centers who had shock teams and those that did not. What's notable here, well, first of all, I'll point out that if you take a look at the ICU mortality in both groups, quite high, almost a quarter of the population and higher, which, again, sort of emphasizes the patient population that we're helping care for, but centers that had shock teams tended to use pulmonary artery catheters more to define hemodynamics. Interestingly, tended to use advanced MCS more, but overall, MCS was less in those who had a shock team. And again, advanced MCS, by that I'm referring to, as the authors did, to things like via ECMO, an impella device or tandem heart, suggesting perhaps that nuanced and deliberate considerations to pick the right device for the right patient was perhaps more efficiently done in centers with shock teams. Now, as we think about the next steps, then, well, what are some considerations that we have? And I like to think about this as making sure that there is an exit strategy once I commit someone to mechanical circulatory support. And again, these devices, as we will get to, do come with complications. So what might some exit strategies be? Well, hopefully I can try to recover native heart function. Perhaps I won't be able to, and I need to figure out if there are going to be candidates for advanced therapies such as heart transplants or durable ventricular assist devices. It can be a bridge once candidacy is approved to such advanced therapies such as transplant and LVADs. But there are also some factors that really make me question whether a temporary mechanical circulatory support platform is the right next step. So for instance, if there is evidence of hypoxic brain injury, if there is uncontrolled bleeding, if vascular access is prohibitive, if there's a consensus of futility that I will not benefit the patient or that we will not benefit the patient, or if ultimately we feel that there is ineligibility for advanced therapies, those are some factors that should provide pause about whether going to an MCS platform is the correct next step. And again, discussing with a shock team allows for those determinations. Now, one point that I think it's important to discuss is there really isn't much randomized controlled trial data until very recently that tells us a routine use of temporary mechanical circulatory support should be pursued. Now, this is actually quite a good time to be talking about this subject because just earlier this year, we effectively had the first positive randomized controlled trial, the Danger Shock trial, which improved survival with the use of an Impella CP in the context of acute myocardial infarction and cardiogenic shock. But, you know, still some considerations even with a positive trial. For instance, it took a long time to recruit and the support was only in for two to five days and not significantly longer. But what it does represent, I think the fact that this is, you know, one of the only positive, if not the only positive trial in this space is how difficult it is to really study this in a randomized controlled trial setting. And as I mentioned, you know, the majority of trials that have been performed so far really do not provide evidence that support the routine use of MCS with the exception of Danger Shock. And I list several registry studies and trials in this slide, not for the purpose of going through them individually, but just to point out that this is a question that's been asked for many, many years. And only now, you know, are we getting some positive reproducible data. So moving on then, I've considered a temporary MCS and what I intend to do and what are some things that may make us say, this is not the right next step and say, you know, where do we go next? And in my opinion, the next step is really phenotyping the shock that we're dealing with. And again, this brings to the concept that we want to be choosing the right device for the right patient. This was touched upon earlier by Katie and Ben as well. But one possible way to think about this is, well, you know, I'm heading towards an MCS platform. What am I dealing with? Am I dealing with a left ventricular dominant pathophysiology? In which case I might choose something that provides more left ventricular unloading and support. Instead, do I have right ventricular dominant pathophysiology or do I actually have biventricular failure? And the figures on the right hand side of this slide are not necessarily intended to provide an exhaustive list, but as you can, but to sort of highlight the concept that there are many different configurations. There are many different options, which most of the time are very dependent on institutional practices and operator experiences. And again, that's where getting many heads in a room and talking about what the next best step is, is a very appropriate step. So then let's talk about what our MCS options actually are. And here again, is not an exhaustive list that contains all configurations, but some of the options that are available to us. If you divide this by right ventricular support or left ventricular support, and this is why I find this diagram particularly helpful, going from the left to the right, you might consider an impella device for right ventricular support. Maybe you would pursue a tandem part. If you need left ventricular support, perhaps a balloon pump or an impella device, or you need bigger guns, such as a tandem heart, or you might need to go to via ECMO. Now, all of these platforms provide differential levels of support, but what's important to consider is, what exactly are you targeting? Are you targeting just left ventricular unloading? If that's the case, then perhaps an impella devices might be the right next step. Are you targeting RV unloading, in which case an impella RP, or a tandem heart in a right atrium to pulmonary artery configuration might be the next step. Are you dealing with problems with coronary perfusion? For instance, an ischemic patient who's in shock, but awaiting bypass surgery. In that case, you might consider a balloon pump instead. The key is to realize that all of these devices provide differential amounts of support. They are dependent on the patient comorbidities and what the patient in front of you needs. All of them will have considerations regarding vascular access. So for instance, large arterial sheets for peripheral via ECMO versus relatively smaller arterial access for a balloon pump. And this is all dependent on, again, the patient that is in front of you. So what are some contraindications and complications that you might consider with some of these individual device platforms? Well, if we consider the balloon pump, one of the benefits is it's widely available relative to other MCS platforms. You may expect lower rates of vascular complications. However, the risk of vascular complications exists as does limb ischemia. There are other complications that involve air or plaque emboli. Some contraindications to consider would be severe peripheral arterial disease or the presence of severe aortic regurgitation, which would be made worse by the contrapenalization mechanism of the balloon pump. How about an Impella device then with a representative figure there on the left? But the benefits are you can get more flows than a balloon pump, whether it's placed in the groin, for instance, in the Impella CP or whether it's surgically placed with the Impella 5-5 platform. There are complications associated with this as well. Hemolysis tends to be more common with the Impella CP rather than the surgically placed Impella 5-5. The pump can migrate. It can be malpositioned and require repositioning, whether at bedside or under fluoroscopy. And again, limb injury could be a complication. Contraindications to consider, well, the presence of a mechanical aortic valve or the presence of a left ventricle thrombus. As you can imagine, this is a pump with a rotor that's literally unloading the left ventricle. And if there's a big clot in there, that can cause a pump malfunction and a poor clinical outcome. Moving next to then a tandem heart. Well, it can be useful in certain situations, such as for instance, if you do not have an aortic valve, or if you cannot cross the aortic valve for whatever reason, can be also useful if you have a small left ventricular cavity or the presence of an LV thrombus, like we just spoke about. And because of the way this pump is placed, which is essentially involves drainage from the left atrium, and that requires a puncture through the interatrial septum, you are creating an iatrogenic interatrial shunt. And that over time or down the line can be a possible complication. The cannula can migrate again because you're creating an intraatrial shunt and the cannula can fall back, for instance. So cannula migration can be problematic. And because the pump is essentially drawing blood from the left atrium, and then returning blood into the aorta, severe aortic regurgitation could be made worse with a tandem heart, and that is considered a contraindication. And then finally, peripheral via ECMO. Benefits are it can provide full cardiac support, and with the addition of an oxygenator that can be added to the circuit, can also provide pulmonary support as well. Over time and with more experience, cannulation is possible at bedside. So that's an advantage as well, especially in the context of someone who was critically ill and possibly even arresting in front of you. Some complications would include thrombus because of differential oxygenation. If you have native heart recovery, you could potentially have hypoxia, and that's commonly seen in the North-South syndrome, particularly if your lungs are also not oxygenating well. So differential hypoxia is a complication of via ECMO. And then limb injury. I mentioned that vascular complications are common with all of these devices. And certainly that is no different for via ECMO, which frequently requires large bore arterial axis. Again, aortic regurgitation, you have to be careful with. And so hopefully, I've given you at least a broad overview. There are certainly nuances to mechanical circulatory support platforms, which we can discuss as a panel. But I present to you now my post-presentation questions. And the first question is, use of a shock team has been associated with all of the following except. It's still a little bit more of a spread, and the data that I presented to you from the CCTN registry suggested that increased use of advanced MCS was lessened in centers with shock teams. Question two, when should insertion of an impella be avoided in cardiogenic shock? Thank you so much, and I'll turn it over again to Ashley. Awesome. Thank you, Anas. That was fantastic. A nice overview of how to appropriately use the shock team, the benefits of the shock team, and then the different types of temporary mechanical support devices that we have, depending on the phenotype of shock, and whether we're RV or LV predominant, or have biventricular dysfunction, and helping us to dictate which temporary device we might use. I want to circle back before we open things up for a panel discussion. We have a few really exceptional questions that I think everybody can give their input on. Mr. Beatty, given your expertise in the diagnosis, and early recognition, and management of cardiogenic shock, he was revascularized early. He was started on inotropic support with very close monitoring in the ICU, and you recognize that he was not improving very short-term with the above interventions of revascularization and vasoactive medications, and you escalated ultimately to VA ECMO after activating or discussing with a multidisciplinary shock team. He had otherwise been an excellent candidate for heart transplantation and underwent an expedited evaluation for advanced therapies, and he is now several months post-orthotopic heart transplantation and doing remarkably well. I think our last slide here is probably one that says, thank you. Thanks for joining us. Thank you so much. I'm going to open up our panel discussion. If you have questions, please feel free to type them either in the chat box or the Q&A box. Our panelists will ask everybody to turn on their cameras, so we can discuss some of these questions, and I will help lead us through them. We have a couple of answers that have been addressed in the Q&A box, but I want to come back because I think this is an important question that comes up frequently when deciding which inotrope in particular to use, and maybe we can have Ben discuss his thought process and his choices out loud about Milrinone in particular, and if there's a specific serum creatinine level, in particular patients who are on HD or PD, what are your contraindications to starting Milrinone? Then what dose do you start at if you're going to use it in someone with an AKI or let's say someone who's on intermittent hemodialysis? It's a great question. Yeah, super great question. Also, I just want to say I have no financial conflict of interest. I'm not trying to push Milrinone on everybody, but with that said, I think that it all comes down to the trials, at least from the literature, it just doesn't seem to demonstrate that Milrinone is particularly harmful in this population, but there's a risk for accumulation of these drugs. In my eyes, when you're using Milrinone of 0.25, it's probably closer to 0.5 or 0.6 over time. So that means that in patients who you do want to use it because the physiology asked for it, then you maybe start with a little bit lower dose, you can see how they respond. The other big aspect is really maybe not so much the credit cut-off or what level of renal failure you're dealing with, it's more that can you tolerate the accumulation of something that has these dilating properties? If that's the case, somebody who is hypotensive and can't clear this drug, that's when I tend to avoid Milrinone because I'm afraid that once I've committed, I can't take it back. Yeah, I think those are great points. For me personally, I often avoid it if someone's in-stage renal on PD or hemodialysis. That being said, we have some patients who have certainly been on outpatient on peritoneal dialysis and are still on the hypertensive side. Those are always interesting patients to manage. Certainly, if you're on Milrinone for an inotropy and you're so hypotensive that you're having to use a pure vasopressor or vasoconstrictor, those are times that I switch to dobutamine. This raises the point to the follow-up question to that was starting inotropes with concomitant use of beta blockers for arrhythmia purposes, either prevention of arrhythmias that can all be stimulated or triggered by our inotropic medications or for treatment of concomitant arrhythmias. Ben, if you want to comment on the concomitant use of beta blockers with inotropes and then maybe we'll turn it to Anas and see what his thoughts on that are as well. Because it's obviously a very common complication of all the inotropes we use. We see all atrial and ventricular arrhythmias. Sure. I'll jump on the screen. It's one of those really controversial topics, ultimately, that I think people differ in their perspective on this. From my perspective and just out of my training and background, it's not a very common practice for us, but there is some pretty provocative literature talking about patients who are out there on ambulatory inotropes using beta blockers. Some of the theory might make sense in those who can tolerate milrinone, for example, if you're using a non-adrenergic agent, that is working underneath the adrenergic receptor and you give a drug that antagonizes the adrenergic receptor, you probably could engage in some level of remodeling there, and that might actually be worth something. However, I think it just comes down to the fact that we don't measure the amount of catecholamines that are endogenously available and the person is using to compensate for their heart failure. If we use a beta blocker in that moment and we lose the endogenous catecholamine effect on your adrenergic receptors, and you deepen the shock, then it seems like conflicting pharmacology in my eyes. At this point, I'm probably looking for more data to convince me otherwise. Yeah, that's a great answer. Anas, what do you think? Yeah, I think it's, thankfully, Ben put that one first. I do agree exactly what Ben said. I mean, that's the clinical setting in which I will use it. For instance, someone's on inotropes, but they're showing me evidence of recovery, and I feel like that they can tolerate it with objective, whether it's invasive or end-organ data. In the acute setting, my practice is also to generally avoid beta blockade, especially if someone's in shock. That's a situation in which I generally tend to avoid concomitant cues. Although I do agree, Ben, this is a question that's come up in my mind a lot, and the literature actually is quite provocative about this to use your word. Then Katie, what has your experience been? Do you have any input? Thank you for letting me go last. No, I agree. I tend to agree with Anas a little bit. I think if looking at the patient and their overall clinical picture, if it is someone that is in acute cardiogenic shock, and we know that they're low output to treat arrhythmias, I think historically here we have not used beta blockers necessarily in that space or capacity. But I think if we're trying to bridge someone to recovery after they've stabilized, and we see that their end-organ perfusion has improved, they don't have a lactate, their renal function is stable, that is someone that I would feel comfortable trialing a low-dose beta blocker, either for bridge recovery or using for arrhythmias. I feel that we tend to use amiodarone a little bit more. Here, if someone is having sustained atrial or ventricular arrhythmias, if they're truly in cardiogenic shock, requiring inotropic support and temporary mechanical circulatory support. Yeah. I agree with everybody. We've used it. If somebody needs an inotrope because they're low output heart failure, but not fluoride cardiogenic shock, and they've been on chronic beta blockers, we may reduce that to a low-dose and start milrinone. Of course, we don't want to compete with the beta receptors and use dobutamine in that context, or if somebody's stable, we're sending home on inotropes as a bridge to recovery. This segues, we tend to use quite a bit of amiodarone if we need to, and acknowledging that there is a negative inotropic effect, a beta blocker effect of that medication as well. Then lastly, if patients are having so many arrhythmias and they really cannot tolerate inotrope support, even with an antiarrhythmic drug on board, that may be a reason to go earlier to a temporary mechanical support device, if you're just really unable to get away with any inotropes. That segues nicely into another question. What do we do with patients in terms of using inotropic drugs if the patient is in AFib or especially if they're having AFib with RVR? We certainly, I think, have all seen these patients coming in, crashing and burning in AFib or AFlutter and RVR. Maybe, Anas, we'll start with you on this one. How do you handle those patients? Yeah. I think, obviously, trying to figure out what am I going to use to potentially cause the least amount of hemodynamic damage to the patient. In general, if I have someone in inotropes, if they go into arrhythmias, like Katie said earlier, amiodarone generally tends to be my first choice. But at all times, I'm assessing hemodynamics, making sure that I don't need to escalate whether I also have concomitant ventricular tachycardias or not. But in general, amiodarone tends to be my favorite drug in that strategy. Katie, how would you handle this? Consoled EP. No, I'm just kidding. I'm joking. I'm joking. Yeah, I think I agree. I think, especially if the question was like AFib with RVR, right? So I think that was the question, right? So it's like our EP colleagues always say the chicken or the egg. So if they're volume up and they're decompensated, you obviously want to try to diurese them. I think I would use markers of inorgan perfusion to guide my decision whether or not I felt like they could tolerate a beta blocker. But if I had concerns again about cardiogenic shock based on my exam or how the patient is looking to me, I think I would lean towards amiodarone, especially if they were stable. But I think that comes back to whether or not in that strategy for your patient, you're really trying to stabilize them, rate control versus cardio over it. But I think I would lean towards amiodarone. Ben, what do you think? I actually thought Katie did such a good job of describing this problem as the chicken or the egg, because it's like ultimately, you know, if this is a new presentation of cardiogenic shock from new onset AFib, like who knows, maybe AFib caused this whole problem to begin with. And we might just have to like aggressively rhythm control this first then. But with that said, you know, if somebody develops AFib, which is a complication of decompensated heart failure, it may be helpful to compensate their heart failure. And so it's really hard to know what the right answer is. And that's why we use so much amiodarone, just by the toxicity. Yeah, I think all really great points. I would say if someone's coming in really like cardiogenic shock, they are unstable, you know, in this circumstance, we cardiovert them early and try and get them out of that, you know, arrhythmia that's presumably contributing to their shock or taking that out of the equation and either stabilizing them with an antiarrhythmic drug. I think once we get them out of that, if they really, if we need to try a low dose of an inotrope, we've done that in those situations before. And once they're stable, think about early ablation in those patients in particular. Perfect. Let's see, I think we've addressed most of the questions. If anyone has any other questions, we have a few minutes left. Feel free to ask them. You can either put them in the chat box or Q&A. Any last burning questions? I think similarly, you know, VT comes up a lot, and I think we manage those patients in a similar fashion where, you know, if really we can't get away with, you know, inotropes, thinking about maybe an earlier mechanical support, depends on how hemodynamically driven we think ventricular tachycardia might be. Is it all dilated, dysfunctional, volume overload, wall stretch, or is it scar-mediated VT? And that also helps us manage those patients in particular. Okay. Any other comments from Katie, Ben, or Anas? Any important points you want to bring up from the talks just as some take-home points or questions to address you think that are common or popular? No, I don't think so. I just want to thank everybody for joining. I want to thank Ashley and HFSA for allowing me the opportunity to present and discuss this. I think for everyone here, I hope you learned something, and I know that I learned something even working on this presentation, and I hope that you're able to take this information and apply it to wherever you work within the field of cardiology, medicine, anywhere. Thanks, Katie. I think just to summarize, defining cardiogenic shock, what one of the more common presentations of cardiogenic shock is in the context of acute coronary syndrome. That's where we have most of our higher quality data, but certainly we see a ton of patients who have non-acute MI-related cardiogenic shock, and the heterogeneity of that population makes it hard to study, really, in randomized controlled trials just for the differences in phenotypes and predominant ventricular dysfunction and things of that sort. But early identification, escalation to inotropic support, trying to preserve end-organ function, and then an early, really, discussion with a shock team, even if the discussion ends up saying, we're not going to do mechanical support right now, but we're going to monitor closely in the CICU critical care setting with serial lactates, and we're going to constantly update and evaluate their SKY score and SKY staging, and then using a universal language to communicate with everybody in terms of intermax profile and or SKY stage in our patient population, and then differentiating which temporary mechanical support to use in the context of exit strategies, either reversibility or eligibility for advanced therapies. So thank you so much, everybody, for joining. Happy to take any last-minute questions. We'll hang around for a minute or so. Appreciate it.

cardiogenic shock

multidisciplinary shock teams

clinical trial data

management strategies

acute myocardial infarction

early identification

vasoactive medications

mechanical circulatory support

inotropes and vasopressors

revascularization

impella devices

heart transplant