Dr. Ajay V. Srivastava discusses appropriate triaging for patients presenting with signs of cardiogenic shock, heart failure or ventricular failure as well as related treatment strategies.
Back to Symposium Page » So for our next speaker, Um, I have the pleasure of introducing Dr Sevastova. Dr. Sevastova joined us about five years ago or six years ago. Now. Hey, Comes came from training both at Yale and Stanford. Uh, he is superb, clinician. Ah, wonderful colleague. And ah, really, uh, bright star in our cardiology program. Hey, has more ideas than time, and he's always working very hard. Thio try to improve the quality of care that we give our patients. So I'm very anxious to hear his talk, So a J take it away. Make sure your microphones on. Thank you. So the topic. I'll be speaking about this morning for about 30 minutes. So so related Thio triaging the acute heart failure patient on by this, I mean, when a patient comes in to the emergency room or your clinic with shortness of breath, signs and symptoms suggesting decompensating heart failure, how do we triage? Who needs what? Um, just gonna go back once. Like your That's my disclosure slide. So why do we want to focus on talk about heart failure and cure us? Um, striking numbers. So worldwide, we have more than 25 million patients admitted for acute heart failure each year in Europe, it's about greater than a million admissions or presentations for heart failure each year in the U. S. Is greater than a million patients each year. And these are numbers from about 10 years ago statistics, so we can be quite sure that we've exceeded these numbers in the past decade. What is also striking is the number off acute heart failure admissions that happened in the United States. A little more than a million equals the number off admissions for acute myocardial infarction in the U. S. Almost pretty close somewhere between 1 to 1.5 million. The mortality rates once the patient leaves the hospital with an acute and my is about 3 to 4%. But within that year, we're looking at a T least a 10% mortality in somebody who presented to the hospital with acute heart failure so we can see that you know the number. The number of admissions is similar to acute and my mortality is much higher. This is a disease. Once you get the diagnosis, it pretty much stays for life, depending the spectrum varies, But the patient always has heart failure. But the emphasis placed on this is not even close to what it is for acute myocardial infarction, the mortality is dramatically higher compatible, cute and my because we have not had advances and diagnosis or treatment on gets not one proponent or an e k G that we can pinpoint Thio to make a clear diagnosis. So this is some of the reasons why we thought we should have a talk on just acute heart failure because we all see it, no matter what are special. Algae is this is not something just coming into a heart failure specialty. It could be the emergency room physician, the intensive care physician, Thea the cardiac electro physiologist, A nurse practitioner or physician assistant taking care off. You know, even a general medicine clinic. Everyone sees and touches heart failure patients. So what do I want to know first, when I see a patient, you never have difficulty breathing or has low blood pressure or not feeling well. I have a few questions in my mind. Is this patient at an imminent risk off death? First, is this heart failure? And if it's heart failure, is it just heart failure or is it cardiogenic shock. Is it LV failure? RV failure or the bi ventricular failure? How are the kidneys doing? And then what is my plan? Um, immediate plan on long term roadmap or exit strategy plan, So I quickly wanted to touch upon the first topic is especially at imminent risk for death on Is this cardiogenic shock? Is this heart failure? And I would like to you quickly go over this document that came out towards the end off last year from the society off cardiovascular angiography and interventions. The focus of this document was they understand that there are various different specialties touching these patients. And can we come to some sort of consensus to say who has shock separate those patients from just heart failure on Can we come up with a simple diagnosis that people can use irrespective off what field there in So the traditional definition off cardiogenic shock, low systolic blood pressure that does not respond to your immediate early intervention. If somebody comes in on their hypertensive, you don't think it's heart failure. You give them a fluid bullets, they don't improve or, you know, if you think that overmedicated and you cut a medicine back in their blood pressure does not improve. So systolic blood pressure less than 90 based on an echocardiogram, usually a bedside ultrasound or a history of heart failure. You know that the slow blood pressure is related to the underlying heart failure. And if you have a cardiac cat, I'm alright. Form games, catheter. And you know that cardiac output cardiac index on your confident that their index is less than 2.2 and they're filling pressures are adequate meeting about a wedge about 15 to 17. That's usually what's been used as a definition off cardiogenic shock. What? They proposed this. Okay, so that is the textbook definition off shock. But when we see patients in acute heart failure or D compensated states more often than not, we don't have a right artistic realization to start with. Who needs a swan Ganz catheter on? Yet we have to treat this patient while we're trying to figure out is if somebody who needs a swan so we should start Mawr upstream than the textbook definition off cardiogenic shock. And they came up with this pretty simple, easy to remember backside tool going from A to e. So he is a patient who is an extremist, meaning this is somebody where there needs to get on California's support, like ECMO right away. Or that patients going to pass this. It could be somebody who went into V fib, VT. Arrest. And you need immediate restoration off circulation D s, some on then you work your way down the casket all the way. At eight is somebody who comes in with heart failure, not looking like they're in shock based on their blood pressure. They're still making urine. Liver function may be a bit up. Kidney function may be a bit up, but still but still intact. But you're worried that this patient could ever go into shock over time or showing early manifestations of stock. So that's your actress patient. Then you get a little sicker. You get into be sort of the beginning stages of shock. This is just slightly low blood pressure, maybe a little increased heart rate. That's the beginning stage. Then you get into it more your classic shock that that's someone who's now hypertensive and you have to start a small dose of the beauty mean or mildred known or legal fed a presser or in a group D is okay, you've done that. They're not getting better. And this, and now you're thinking about is this. Somebody needs a balloon bomb. And in Pella, some mechanical support. So that's the and then e f quote is a patient who is profoundly sick, usually the e you know, with somebody who's present in cardiac arrest. So they came over this easy bedside tool to use. Um, okay, And then So if you get into the details off that stage or impending shock where the patient is not in shock, it could be a steamy could be an acute heart failure presentation on the right. They came up with some clues and basically the way you triage patient in general for heart failure or shock. Look at the physical ed time, some biochemical markers. And then, if you have any more dynamics beyond just the blood pressure used them. In many cases, all we have is just a systolic blood pressure. So this patient who is at risk, they had an event, whether it's newly diagnosed, cut him out with the heart failure or a non stem me or a stand me they still intact? They're still confusing. Well, they're filling. Pressures may be up, and you're gonna use the two by two. Table to triage. Okay. Where is their heart? Failure on the systolic. Blood pressure is still okay. Then you get to the beginning stage where now they're sort of getting a little sicker. And the key difference? You see, between the last stage and this stage, there's still confusing. And the way we assess confused assess profusion in acute heart failure. Off course, you can feel their extremities and see if they call the warm. It gives you a sense of the vascular resistance, but the gold standard and what's easy to get is elected. You can get an arterial or venous selected bedside off a blood gas on def. You don't have a Catholic or in it does not have to be from you know the problem. P a port. You could just get a prayerful Venus selected or an arterial acted use that it's a lacked It is less than two. You could be reasonably confident that at that time the patient is still able to maintain and organ perfusion. But what you're looking for here is that low blood pressure, systolic blood pressure, less than 90 or a map that under 60 and getting a bit tacky. Colic. So that's your stage. Be patient, then you get to the next stage. So now you're beginning to see markers off and organ perfusion on um, or decompensating patient. What is most useful for profusion, like I just said, is you lacked it on your blood greater than two, and now you start seeing your kidneys bump up a little bit. LFTs bump up a bit. Your G, B and B will be elevated more often than not a normal NT BNP or reduced NDP MP in the setting off what otherwise looks like cardiogenic shock strongly suggests that the underlying ideology is probably not a metrical or problem. And there's other reasons probably for shock, maybe based military shock or something. Uh, so the negative predictive value of N. T. B and B is useful If it's normal or low, it's very unlikely to be shocked our cardiac related shock. So in this stage you have your classic shop. You have a market off end organ hypo profusion. You have a systolic blood pressure that slow If they had a sworn you're going to see low cardiac output, Low cardiac index, you get to the next stage. So now you put the patient on China tropes. You put the patient on pressers, you're trying to improve them. And despite what you're doing, you're not seeing these lab parameters or their blood pressure or the Swan Ganz catheter readings change. Usually, once you've started a basic in a trope or oppressor, hoping to resuscitate the patient and within 12 to 24 hours. If you're not seeing any change in your bedside vitals or the lack did, that is a time to now call a heart failure concert or if this is being managed by the I C U service, get a cardiology council that the first step. If there's no heart failure team president over there because you're not thinking about escalation, and more often than not, you absolutely will need a swan Ganz catheter in that patient to help guide for their decision making. Three. Extremist patient This is a patient comes into cardiac arrest. Usually, the lack data is profoundly elevated, and what's most useful beyond just lacked in this patient is also looking at this year and bicarb levels. In fact, there's a good amount of data showing that a reduced bicarb early on is in fact a better predictor more than lacked it because lactic takes time to go up. But your bike up drops very quickly and they get a Sadat IQ. So having a reduced by car early on should really get everyone going in terms of what do I need to do to resisted the patient calling? You know whether it's needing ECMO, whether it's needing other forms of mechanical circulatory support on what the society also did. They came up with the website cheat sheet. You can go to the website on just Google Sky Shock and you'll be able to find this. And for those a few sort of getting into this space in terms off acute heart failure, shock management or even if you're using this to get your nurses on board, think of it in some ways, like an early stroke screen. You print this and you just have it, and you could have, you know, if you have a patient who they're they're on DRIPs whatnot, you could have the nurse fill it out. You could do with daily or a couple of times a day, and you can see which way the patients going and use that as a marker. So while you're busy doing take care of other patients, if they see a trend towards worsening, they alert you so you can act with before the patient, um, goes into a court blue state. So that's sort of the shock classifications or the shock pyramid in terms off, using the traditional to buy two table that we use for bedside assessment. You know the patient warm is a patient. Cold is a patient. Dry is a patient wet that still stands. I still use this. We find this extremely useful bedside. When I see a patient, you know you get a feel for their prayerful temperature by their feet as well as their hands on. Is it cold? Is it warm? It gives you something to work with, and then looking at the JVP gives you a sense which group they fall under. You can certainly supplement this bedside, but if you have a little pocket ultrasound that we use on grounds to get to confirm, you know what, does it really function grossly look like What is the IBC look like? Is it collapsing? And then that objectifies your exam a bit mawr and give you more confidence in your bedside diagnosis, and you can see how you know if they're warm and dry. Then that patient, usually evasive, dilated on they're not in a reduced cardiac output state. More often than not, what they need is just diary sis on. This is important because the majority of patients who present to the hospital with acute heart failure I said more than 11.5 million patients every year in the United States. It has to do with volume. You look at all the acute heart failure trials published thus far. Our even from the registry, the dopamine trials, majority of patients who come into the hospital with acute heart failure symptoms. It has to do with volume. It is not as much as we think it is not the reduced cardiac output that brings these patients, and it's almost 60 to 70% is because of volume, which is why outpatient volume management is crucial toe reduce presentations to the hospital with acute heart failure. So this question comes up a fair bit. Who needs a swan? Who does not need a swan? Ganz catheter? Um, when the Swan Ganz catheter was discovered in the eighties, there was rampant use. People were using it for any patient coming in with any heart failure, signs and symptoms. Any shortness of breath. Some. It was clear it was heart failure. Some. It wasn't clear, so it was sort of a cluster, all comers. Everyone was getting a small on. Data started coming out that do we really need sworn Ganz catheter in every patient? And then, in the late nineties, there was an editorial that came out that suggested that youth off sworn Ganz catheter actually increased mortality in I. C. U patients. And this then led to a dramatic drop in the use of Swan Ganz catheter. Because everyone associate ID sworn gangs with mortality on bond, it fell away. So then, more recently, with advances and more often emphasis on him oh dynamics, acute heart failure, cardiogenic shock people started going back and looking at these trials that looked at P A catheters and acute heart failure. That's fascinating. That majority off these trials that were done looking at Swan Ganz catheter in heart failure. Left out, the patients will probably benefit the most from its one Ganz catheter, namely the impending cardiogenic shock patients, the patients in cardiogenic shock where it truly would be useful. I think we all agree that, you know, if somebody comes in with just sort of that a or B stage of heart failure where it looks like there's some volume, their blood pressure is 100. Blood pressure is 1 20 or elevated at 1 50. We don't need a Swan Ganz catheter. We can use our physical exam lads echocardiogram to guide how we manage that patient. It's most useful in these patients who are going into shock, showing early signs of shock or encourage any shock, which the prior evidence did not look at. But more recently, given the emphasis there multiple papers every year, there are a few papers coming out that showing use of Swan Ganz catheter. In this shock Patients is extremely useful and not just useful in terms of triaging, but has a direct correlate very effect on outcome that how these patients do so with that, you know, sworn guns has been again, now is back in vogue and is being used and triaging. Who needs it? Who doesn't need it? We do a fair number of swans. In fact, any patient was transferred to us in acute heart failure or shock. More often than not, ends up getting a Swan Ganz catheter to supplement what we get from the echocardiogram to see in which boxes patient falls. It helps an immediate management as well as road mapping. Where this patient goes from here. Are we thinking about l've Odd Heart Transplant Valley, a shin bi ventricular failure, So it offers a lot of information beyond just cardiac output and volume. On this is the shock spiral made famous by Juliette Hawkman, The shock trial years ago where what they showed is, even if it starts with an L V problem, the cardiac output drops and then the end organs start. Getting affected ultimately leads to the sewers like response, and why this is important is, you know, the vascular resistance early on might be the textbook definition off a high SPR clampdown state, like our chronic heart failure patient who's not on guideline directed medical therapy, but in this patient, once they're going into this profound acidosis. Kidneys are involved. They're going to a certain response. You may or may not see this high SVR that were used thio. So often times you can get a patient with reduced cardiac output, but in SPR that looks okay or even reduced because this patient has now reduced cardiac output. And it sounds like respond. So don't just use the s s. We are in isolation. Just take it into clinical context is useful to give you an idea where in the spiral this patient is, and then it helps you decide. How do I break the spiral? So that's the classifications again. Um, so this is the paper that now looked at okay, this is great, this classifications, but does it actually work in practice? So this was a shock working group. About eight centers spread across the U. S, East Coast, Midwest, the West Coast, and said, Okay, let's take this classification applied to our acute heart failure shock patients, about 1400 patients and let's see if it stands and it stood well, so great is all comers Green s patients with myocardial infarction and blue is heart failure. And you can see as they applied the staging as the staging increased, their mortality increased. So this sort of validated what we expected. And this is fascinating, right? So if you look what these graphs show is congestion on mortality, oftentimes we think reduce TF. Reduced cardiac output is why these patients are in shock or why they actually die. But the case is really, ah, high mortality is such a bad prognostic feature and way more than ejection fraction or cardiac output that decides what their mortality is. So it's crucial again volume management in these patients, whether it's chronic state, whether it's an acute state in sepsis, we keep their filling pressures high. But in heart failure Ah, high filling pressure such as that. Either you unload that ventricle, get that volume off. They need renal replacement therapy. Diaries is but generally congestion is a bad sign. So now that we have that Okay, so this is sort of a practical worksheet on how we work with our shock heart failure patient. You know, systolic blood pressure is low. Um, I seeing any evidence of end organ hyper profusion. There'll acted this up. Okay, Now I'm gonna start sort of activating people do get care to this patient. This might involve heart failure of the I. C u team. Get an echocardiogram and you have an e k g. And then you decided that somebody goes to the cath lab or is this somebody we can put a bedside swamp? Figure out what's going on? You have some him. Oh, dynamic parameters. And then you go from there. There are a host of devices available, you know, if the left ventricle the right ventricle in terms of mechanical circulatory support, some offer some cardiac support, Some offer a lot more cardiac support. Some offer lung pulmonary as well as cardiac support. And this is what we do. Once we get a swan Ganz catheter information, we then decide. Okay, What best one device is best suited for this given patient and when and what should trigger mechanical circulatory support. So 1st, 1st, 1st is timing right. We wanted if you do it too late, the best device is still not gonna offer is good outcomes. So timing is crucial picking the right support device and management off this patient after to achieve the best outcomes. So this is sort of I worked through in terms, love. Okay, what do I want to know with this patient? Um, that all pertains to shock Now if we talked about Okay, now let's think about the patient in heart failure doesn't look like they're in shock. You've established they're not in shock. Generally, the presentations are Okay, so one of the blood pressure and you use that to triage where they fall. And then more often than not, Like I said, it's from me oedema. But you can also have other presentations, like right heart failure, acute coronary syndromes, post cardiac surgery. Heart failure is not uncommon because you know usually are right out on the surgical service that managed for the focus on the chest and surgery, not playing emphasis as much toe volume. And these patients, One of the Communist reasons for readmissions relates to volume again. You sort of uses two by two table, just like you do in shock. I mean, the same two by two table. And your triage. Is this patient in shock or heart failure? Um, going to go back One slide. Sorry about that. Why keep skipping eso once you've done this Onda treatment generally for patients acute heart failure. You want to relieve their symptoms If their high poxy make you want to fix their oxygen and usually by diaries thing them, their oxygen levels usually improve. So those three go together usually symptoms oxygenation, volume, status. Then you try to find the reason why they're in heart failure. Is this an acute event? De Novo Heart failure, like my apologies, cardiomyopathy, myocardial infarction? Or is this acute on chronic heart failure? We certainly want to optimize the chronic therapy. We just had a talk from Dr Heywood. This is an opportunity. If they're not in shock and they still have volume, it's a good opportunity. Good time to consider drugs like, uh, Cuba. Drill about certain, um, to unload the ventricle and then identify who needs device therapy. I mean, oftentimes we see patients come in with a favor. Rapid ventricular response, Some Miss CRT opportunity. So there's clearly a role, um, toe, then sort of quarterback and figure out immediately. And what I need to do for this patient and then ultimately, is follow up. You know, you've done what you have to do. You get this patient plugged in with a good program or system to take care of these patients. Most common reasons why heart failure patients get admitted to the hospital that early treatment you have done their symptoms have not really improved on or you have chemo dynamic evidence. You know, whether it's worsening arrhythmia, coronary syndromes, kidneys that these patients get admitted for. And we heard about this earlier from Dr Heywood. The It's been a fantastic time in a chronic heart failure. The advances you know, some people about certain of aboriginal, which is called in, or for reducing heart rates. SGL t two inhibitors probably artery sensor monitoring. Um, l've adds new frontiers in cardiac transplantation, but really not seen that much in acute heart failure. Sadly, this was one trialing looking at several accent, which is a hormone produced in pregnancy. It has basil dilatory effects. The thought was, Is it like BNP? Can be caused? Some basic basal dilation could be caused natural uteruses and get people to feel better. Pretty impressive. Large trial 6500 patients, Um, but it was disappointing in that did not show any improvement and outcomes. There's some data now being presented on a couple of different drugs at the age a Dubuque. Attractive, witty, but not necessarily in the acute heart failure patients. So really, we don't have a whole lot new in terms off treatment for these acute heart failure patients. But what we can do is certainly improve how we make our diagnosis, how we improve care to reduce acute heart failure presentations in this go hold. This is the paper that actually came out this year in circulation saying, can we do better with patients who come into the emergency room or clinics with acute heart failure? This particular paper looked at emergency department presentations. Now, this is a busy slide. But what they did is if any patient came in with acute heart failure had symptoms suggestive of heart failure. Not everybody got an ultrasound it with a clinical diagnosis, but they made a wrap. The protocol was, when we're gonna make a rapid diagnosis, give them a good dose of ivy diabetics upfront, and then they and then they looked at mortality. And then they looked at readmissions and they looked at re presentations on. It was really impressive what they found. So they called it the code heart failure. So if patients came in, they made a rapid diagnosis. They follow the code heart failure protocol and they were able to show, reduce study their readmissions, improved outcomes both immediate Long term reduced E g length of stay on, even reduced immediate in patient hospital admissions. By being aggressive upfront with an early good dose of diuretics. We actually did something similar in our population as well. This started We were doing this last year as well. When we said we're gonna have a process we're gonna look at to emergency rooms across our system. And we presented this at the hopefully Society of America last year on. Basically, we took a few 100 patients about almost 500 patients on applied this court heart failure and what we were able to show very quickly. Within a few months, we reduced the length off state. We reduced hospital length off state and we reduce the number of patients admitted to the hospital on. We were beginning to see more use of bedside ultrasound as well as an increase diuretic dose. This was early days, and this is just pretty cove. It s O with covert. Obviously, we had to hold but restarted this and looking to implement this across the system to improve early, uh, diagnostic accuracy and care of these patients. So this is my last slide. Pretending to take home points use elected usual, acted freely To make this diagnosis is the just heart failure. Is it? Shock after you elected is preferable. But both worked quite well. Low serum bicarb early on is extremely useful. A low BNP level argues against in being cardiogenic shock, it could still be shocked or basic military have extremely low threshold to use the permanent artery catheter in somebody with hypertension on underlying history of heart failure especially. Don't wait too long to transfer these patients. If you think they're not doing well, they're doing okay for now, but we don't know which way they're going to go. It's better to get this patient at a shock center where we can provide this level of care. Be aware of the mixed shock where if you do a swan, gangs patients can have a normal SPR would still be in cardiogenic shock s O. This is a big team here. We You know, this obviously can't be. This is one of the reasons I tell my friends or my refereeing physicians The reason you want to transfer is not because you can't manage just the takes, a village and the bandwidth to take care of these patients between interventionist vascular surgeon CD surgeons, intensive ists, us how staff advanced practice clinicians on by sea level of care. That's my cell phone. If anyone wants a text, reach out anytime to talk about a patient. We do have a 24 7 number as well. 858626 L bad. If there is a patient you wanna consider transfer for acute heart failure, I'll stop there. Thank you very much.