REBOOT: #469 Inpatient Heart Failure

Hey listeners, you're about to hear a Curb Siders classic episode. If you heard it the first time, listen again for that space learning. But if you haven't heard it yet, then you are in for a treat. So without further ado, enjoy and don't forget to check out our Patreon at patreon.com/curbciders. If you want ad free episodes, bonus episodes and a whole bunch of other cool stuff, patreon.com/curbciders. So Moni, did you hear about the cardiologists who went to a team building exercise? No, I did not. So they're doing trust falls. And the one cardiologist said to the other cardiologist, and trust me. Trust me. When you have to explain it, that's usually not a good sign. Okay, I can use RJ's pun. He wanted us to say a heart failure is a fluid situation, but don't worry. We are here to help you stay afloat. So all the listeners picked like compare the two and let us know which one you like. This should be a poll. Yeah, we'll have, yeah, we'll have a poll, guys. The Curb Siders podcast is for entertainment education and information purposes only. And the topics discussed should not be used to lead the diet and treat cure or prevent a disease or conditions. For the more that you use the same express on this podcast or solely those of those and should not be interpreted perfect official policy opposition of any empty the cyclone possibly cash like more hospital and affiliate outreach programs. If indeed there are any fact there are not pretty much we are responsible if you see about you should always do your homework and let's know. And welcome back to Curb Siders. I'm Dr. Monia Meene and I'm joined by my effervescent co-host Dr. Meredith Rubin. How are you this evening? Doing great. Yeah. And on tonight show, we discuss inpatient heart failure management with our guest, Dr. Groucher Pundraff. And before we do get to all that, a quick shout out to the updates episode with Dr. Michelle Kudelson that came out not too long ago. The outpatient effervescent have pet episodes for 58 and for 60 respectively. Great stuff. And this episode compliments that well. So you get outpatient inpatient. It's great. And well, you'll hear just a little bit more about that here in a second. But first, Meredith, will you please remind the good people in the audience? What is we do on this show? Sure, Monia. I'd love to. We are the internal medicine podcast. We use expert interviews to bring you clinical pearls and practice changing knowledge. And tonight we have a fantastic conversation with our guest, Dr. Pundraff. He's a professor of medicine in the director of the Heart Failure Mechanical Circulatory Support Program and infiltrative Cardiomyopathy Program and the director of GW's Heart and Vascular Institute at the George Washington University School of Medicine and Health Sciences in Washington, D.C. He has an advanced heart failure and transplant cardiologist. He has a keen interest in education and developing educational programs nationally and internationally and in developing innovative solutions and clinical program building to improve equitable heart failure care. He has served as co editor of Heart Failure Self Assessment programs on editorial boards, including Jack, heart failure and directed development of heart failure curriculum for PCPs in Latin America. He has spoken widely about national and international meetings. Dr. Pundraff is governor for the Washington, D.C. chapter, past share of the Heart Failure and transplantation section of American College of Cardiology. And tonight we went through some really great tips for guideline directed medical therapy. Initiation and a lot of on the transitions of care during the hospitalization, as well as a lot of key pearls for diuretic therapy to think about. So without further ado, let's get to it. A reminder that this and most episodes will be available for CME credit for all health care professionals through VCU Health at curbsiders at vcuhealth.org. Okay, Dr. Pundraff, welcome to curbsiders are very excited to have you. We like to start by getting to know our guests a little bit past medicine. So can you start by telling us a little bit about a hobby or interest you have outside of medicine? Glad to be here. So thanks for having me and in terms of outside medicine, I actually love traveling. That's one of the things I, you know, anything I can get on a plane, a flight and or ride somewhere that's one thing I'll do. Other thing is I love cooking and cooking is not just a hobby, it's a passion. I actually in the process of writing a cookbook. And I, you know, even though I'm a heart failure, card carrying heart failure, transplant cardiologist, I also, you know, have been kind of involved a lot of food nutrition related projects over the last couple of years. So yeah, I love to cook for myself, obviously, I love to eat, but for friends, family and, you know, compile recipes and great recipes as well. Do you salt in your recipes? Well, you know, do you have to give the official answer for that or the unofficial answer? But no, I actually, I mean, I do a very controlled salt, you know, bare minimum as needed. We do have a lot of salt in the diet as it is in all the different ingredients. So I try to control that. And what's your favorite cuisine to cook? Oh, boy, that's a tough question because I actually cook almost everything. But, you know, again, yeah, I don't, I wouldn't draw favorites. Asian is more kind of close to home food and Asian would be across the board, not only Southeast Asian, the subcontinent, but even across Thai and the Malaysian food. But, you know, I just said, even French Italian, everything. So in your travels, is there somewhere you've specifically enjoyed going for the food? And that's actually a great question. I spent somewhere in France actually driving through Brignanian champagne area and it was this amazing food, but, you know, really fresh ingredients. You didn't really even need to add much. But, you know, I'd wait now is actually, I would say one of the places where I love going for food. And I mean, they're twice and I, it's just amazing food. It's healthy. It's so many different vegetarian options. I do eat meat as well, different kinds of protein, but it just fabulous the food out there. Awesome. So we'll switch gears and I guess ask one more question. What is some like meaningful advice or feedback that you received throughout your career? Well, there's a lot of advice. I have been fortunate to, you know, work with some remarkable people. Early on, I think during my early days of postdoc, he is clinical, at the clinical researcher, I had a mentor who I always wanted to look back on. And he was one of the advice he always gave me from a kind of academic perspective was, you know, don't write papers, just to write papers. You know, it's really important to write something, which is meaningful. Now quantity doesn't matter, quality matter, then I actually do kind of keep that too hard. And you know, as you go through different parts of your training, your physical life and the other thing, which, you know, is your own well-being. And I know well-being is a big word right now, but it's not in just in kind of as a, as a buzzword, but it really means something. You really have to take care of yourself, whether, and well-being can be in different ways. And it's not only burnout at work, it's also, you know, being physically fit, taking care of your health, nutrition, and doing things which you enjoy. And that's kind of what I've, you know, have been given the advice. I definitely think the first one is near and dear to Monia and me right now. Also appreciate that advice for us on a personal level. I don't know what you're talking about, but we'll leave it like that. Do you want to ask anything else? Or do you want to pick some of the week? Let's do picks of the week. Okay. So mine's pretty obvious, not having COVID. Shout out to Binax for proving that I'm negative. Like, I don't know. I, you guys may not know this, but Meredith and I actually record in the same space, which is somewhat unique, I think, for the curb. And so the amount of contingency plans I had in my mind for if I did not convert to negative really mind blowing. So anyway, so my pick of the week is the Binax. I mean, five years maybe Binax has been the pick of the week in the background. Mine is also, it's September when we're recording this. So it's now football season. And Monia and I had to actually go a full day without speaking to each other because her Michigan Wolverines were playing my Texas long horns and Texas won. And I did confer with Monia afterwards that we could still be friends. So it'll be okay. But it was a glorious day. That's amazing. That was uncalled for, but definitely I should have seen that coming. So anyway, so Meredith, that's fantastic. I'm happy for you really because we just won the national teaming trip. Please take us to cash. Like for our first case. So we will start with Miss Anita breath, a 64 year old female who presented to the emergency room with shortness of breath, bilateral lower extremities, swelling and fatigue over the past week. She's had a long standing history of poorly controlled type 2 diabetes, hypertension and tobacco use. She has noticed a gradual increase in shortness of breath that initially only occurred with exertion. Most recently, however, she's noticed she's not been able to lay flat and her shortness of breath has been worsening at rest. During this time, her feet and legs have become worse fallen. At home, Miss Breath takes met foreman 1000 milligrams twice a day, less than a pearl, 20 milligrams every day, and more than 25 milligrams twice a day. In the ER, her oxygen saturation is 91% on remayer. Blood pressure is 155 over 90 in a heart rate of 93. On physical exam, there's jugular venous dissension in an S3 gallop. The bilateral lower extremities are cool to touch, and there's three plus putting a dima to her thighs. A chest X-ray obtained in the emergency room shows fast food congestion, and her BNP is 1,100. The tripon in Sierra Cratton in electrolytes are all normal, and an EKG demonstrates normal sinus rhythm with few PVCs. So I think where we wanted to start was, does this seem like a typical patient presentation for a cute decompensated heart failure, and what other history and maybe physical exam findings you may want to know? Well, that's a great presentation, which is a very common presentation, I would say, in just going back, as you're reflecting on what you said earlier, that I'm following up on your co-pseled right after Michelle Ketessen. And I just admire and I'd honor of co-chaining with her a recent update on Heft-F. And this is something I'm sure she talked about it as well. So initially, I think when we get somebody like this, I know we're talking about heart failure here, but really you have to go back to the basics. Have to make sure, is this really heart failure? That's the first thing. And because everything which is, somebody is short of breath or has legs swelling, you really have to go through this differential, what we have learned over the years of training to this medical school as well as residency training. Because there's so many other causes in somebody with comorbid mobilities that this will be a mimic for heart failure. Not having known what the LV structure and function is. I think the clinical presentation becomes important. So starting from the point one, obviously, history, whatever risk factors that person could have. And in this particular case, you clearly have a fully controlled hypertension. She's presenting very high potential. She has legadema. She has a S-ray gallop. She has every sign or symptom suggestive of acute heart failure. Now, this is where you would start off with applying all the knowledge you have from what the definition of heart failure is. And this is where you will apply the universal definition of heart failure. I'm sure you talked about it in the past. This is the definition which was proposed by Heart Failure Society, and now has been adopted by all the guidelines for heart failure from ACCA, CHA guidelines as well. And you incorporate your signs and symptoms of heart failure so just your heart failure and then you go and look at the biomarkers. And so that's something beyond history, beyond those risk factors, beyond the acute and the chronicity of the symptoms. This is what you want to know. And that's going to help us decide if this is something else. Now, you also want to know if there's anything suggestive liver disease or any other markers of other systemic illnesses such as thyroid, are they having an arrhythmia? Anything which either could be an etiology towards heart failure or could be overlapping with a presentation of heart failure. And I think just where we are also in the course of medicine right now, I was curious to when she's presenting, do you see much role for point of care ultrasound that's being helpful? Yeah, I mean, that's the point of here. Ultrasound, the role for it has been emerging quite a bit over the years now and from multiple levels. In a lot of times, we kind of persuade on the LB injection fraction. But the point of care ultrasound can do much more than that. So this is somebody who's presenting with hypertensive disease, but you'll get an idea. If you use a point of care ultrasound, obviously, you'll know the structure, a quick look at the structure of the heart is the left ventricular hypertrophy, but more importantly, you can also look at their bina-cava. You can look at is that being a chemist standard is an intrapasic ligand gestion there. So that kind of adds on the two-year level of suspicion or whether this is going to be a acute heart failure and is the person really congestive or is there anything else which could be mimicking or presenting as low extremities swelling. Now, in this particular case, obviously, she's high-potensive, her heart rate is still high, but if this was somewhere, you were also concerned about pretty cardinal fluid around or effusions or tamponato or anything like that, that ultrasound would be helpful to. Now, there was a suggestion of any kind of acute ischemic injury that would be useful to look at wall motion or regional wall motion and mountainean students. - So would you say it like in your practice, does that point of care ultrasound? It's mostly there it sounds like to help like emphasize what you're already thinking versus really helping to decide one way or the other, is that right? - So no, so I think what I'm really meant by saying that is it's an additive information, it can be. So in this particular presentation, because what you just described, the patient is very high-potensive, as you know, as she galloped. So you're already kind of very, I have your findings, clinical findings, both symptoms as well as clinical features, physical kind of findings, which are very suggestive heart failure. But if there was a little bit of ambiguity in there, and there were other, if there was somebody, you know, had Nash or kind of Marble Beastie and then with the diabetes, they also had, you know, liver involvement or had, you know, there were more sedentary and had concern about DVTs or PE. And then the RV failure aspect comes in or, you know, with all those different comorbidities, you could have pulmonary hypertension, could be group two, pulmonary hypertension, could be, you know, so any of those differentials would start coming in. Yes, the final task aid in heart failure, but that would help you kind of decide where if this was heart failure or non-heart failure. But in this particular presentation, yes, it's more to confirm. - Got it. - Yeah, I think in this particular patient, if I recall, doesn't actually have a known diagnosis of heart failure. So I think there's a two-pronged question. So in this situation where the patient doesn't already have a diagnosis of heart failure, when is like the right time to get an echo? And then the other side of that is when, or should we get an echo for a patient that comes in and has a heart failure exacerbation, but already has a known diagnosis of it. So let's start with the not known part and we'll go from there. - Yeah, that's actually, you know, this is something which is addressed in the guidelines as well as the export consensus documents. And now, you know, when somebody comes in, has no known diagnosis, they definitely need some assessment because it's gonna tell you a couple of things. It's gonna tell you structure of the ventricle of the atrium. So it will help you go down your differential of is this really heart failure. Now, I'm assuming that you already have your biomarker levels, your, you know, anti-pro BMP, or BMP, whichever is available in your practice or in the hospital setting. And that's already given you a second level of confirmation of your, you know, or meet whether you meet the criteria for the universal definition of a heart failure. So now the echo is really helping you pinpoint and decide what kind of therapy are you gonna use? Are you gonna go for half-rept therapy, half-fept therapy? And now in these days, a lot of it's overlap is, there's a big overlap, almost, you know, out of the different medication classes, you pretty much use almost all of them in both sides, depending with some nuances, depending on the injection fraction and some of the criteria. But then it also tells you the anatomical features of what could be causing that heart failure. So as we, you know, as you look at hypertrophied ventricles or in large atria, that's gonna guide you to a different, differential within heart failure itself. So I based on my own practice and as well as the guidelines as well as the expert consensus document, is recommend that you should get an echocardiogram of anybody with a suspicion for heart failure. So now going back to your second question, one of you, which was, you know, somebody already has a diagnosis of heart failure and they're coming in for exacerbation. Now whatever the etiology may be, you know, they have arrhythmia, they may have infection, may have thyroid disease, they have, you know, you name it, but it could be, but that is a different situation. You really don't need to just repeat protein echocardiograms unless you have a question which is going to be answered and is gonna change your management. Now, if somebody is coming in and they are, let's assume they are congested and right now it's not a concern about low-alput failure, they are just congested, they're in your, if you look at your classical human dynamic classification in the quadrant of vet and one, they have a blood pressure, they are warm, they just congested, they have all the signs of increased healing pressure. In this person, the old treatment is going to be de- congested therapies. That's gonna be the main goal initially to relieve the symptoms. So getting an echo is not gonna be additive in the sense that you're not gonna really change your management. Now, at some course, if that situation changes in the sense that it is are responsive to your initial treatments or there's a clinical decompensation, they become hypotensive or you are worried about something else going on and then getting an echo would be a good thing. Same thing is for, you know, if you are treating somebody and you had an echo and is there any usefulness of repeating an echo and that's again should be driven out of the question. And I'm going to do with this knowledge, what I'm going to obtain from echo cardiogram to change my treatment. If it's just like, oh yeah, I'm just already have the information, I'm going to treat it and I'm going to send them out. That's different. But now if somebody had a lot of valula regurgitation, somebody had moderate to severe valula insufficiency whether it be mitral valve, triconspeed valve and you say this is a volume dependent state and I want to reassess it after I de-conjust them, I want to know what's the severity of that valula insufficiency? Am I going to really address this? In this particular hospital, say because now there are so many therapies out there for that or emerging therapies out there. So am I really truly assessing the severity of it and that's when the repeat echo may be useful after you initiate the therapies? No, that's helpful because I think for a long time I had this practice pattern and this is a conversation I have with residents a lot where like they come in volume overloaded and they're like, well, they haven't had one in a while. Well, maybe we need to talk to the patient a little more and get a little more history about why it isn't they might have had this exacerbation, right? And the thing that I never put together until preparing for this and then also putting together things we do for no reason talk is I don't think I ever put together that like you can get like volume status dependent valvular changes, right? And so I don't know why I didn't put that together, but I didn't. And very helpful to realize that because you don't want to go chasing something when it's like, well, this is something that actually might go away if you just give them the therapy that they require at that time. Yeah, we do see that a lot, Mone. I think, you know, when we we initially get called on on consults or just primary and the level of valence of efficiency, remarkably, is going to go down with appropriate e congestion and other, you know, application therapy. So really helpful getting that information. So I think talking a little bit about decongestion, that's actually a good segue for us. So for Miss Breath, who's clearly like volume overloaded, we want to start a diuretic like therapy for her. For her, she's obviously going to be like naive to that therapy, but wanted to kind of get a little bit of your insight on how we would start her diuretics. Yeah, that's a great question. And you know, something which we all deal on a daily basis, right? So, so I think she's diuretic naive. So that's a good thing. Knowing what her starting electrolytes are, especially kidney function is helpful, especially because as you try to gauge what kind of dosing you're going to do. So, you know, obviously the guidelines recommend that and most of us have a practice of saying if you are naive, you can just start with pure somide, for example, and usually a 40 milligram IV dose. But I just want to make a point on this particular presentation because in her case, she's also hypertensive. So while you are going to de-conjust her, a lot of it's also going to be after low reduction. And that is key. Sometimes the missed that point is we focus on the de-conjustive part of therapy in patients with hypertensive heart failure. We are not aggressive enough on the hypertensive, especially the after low reduction. So that has to be going hand in hand because otherwise people or you, like all of us will get in your trouble very quickly in the sense that we'll keep trying to get that de-conjection done and they're hypertensive and you start having kind of real injury as well. So this is where I think it has to go hand in hand and this goes back to those basic four quadrants of kind of, you know, human dynamic principles and physiology because as you reduce after low, you can have a better kind of overall output, better diuretic effect and it's going to augment you. So that's number one. Now going back to the choice of diuretics and the dosing, you know, it's just COVID. You know, if they're totally naive, they're kind of depending on what kind of how much volume overload they have, you could, you know, somebody's older, somebody's not, you know, it's mildly overloaded and mild, it's kind of subjective breakdown. Especially if somebody has a lot of kind of splanked congestion, you're not going to see that. But you know, based on their symptoms, you could do a 20 or 40 of fearsmide as a boilers fast and then see what their response is. And now you can gauge their response in two hours and see what the, how they're responding to it. If they're responding well, then you can then decide on your next dose. You can stick with the boilers. Now, if they are not responding and you're given other boilers or you increase the dose from either 40 or 80 first might or they were already so volume-related, they ended up getting 80 in the beginning and depending on response, if they're not, then you want to increase that either the dose or the frequency or sometimes both. And that becomes important because just giving the same dose over and over again is not going to work because you're going to have breaking phenomena, you're going to have, you need to really reach the threshold. I want to go back in a minute to the afterload part because I think that's actually a good point I want to talk about. But when you're thinking about increasing the diuretic and you're doing increased to frequency for bolus dosing still, is there a maximum amount that you would do that frequency at for, let's say, for osamide? Yeah, no, you can go like three, four times a day. So you can go to the question to ask is at that point, you know, is that strategy really working? And that's, you know, if you have to go so frequent, that means either you're not getting the amount of response you want or there's something else kind of interfering whether there's underlying kidney disease, there's, you know, either acute or chronic kidney disease and there's a diet of resistance, even usually not in an eye patient, but you can have breaking phenomena. It also could be, is there anything else? I mean, is there simple things like, you know, is there any obstructed uropathy? Is, you know, is the bladder full? Are they even making the urine or is that obstruction in the bladder area? So the urinary tension. So those are kind of things I would first alongside look at. There are other tricks you can do. You can also look at a spot urine sodium and, you know, after a bolus, you can check a spot urine sodium in a few hours and see if, you know, they are a proper responding to it or not. And so that's the trick. And actually, that's in the guidelines. And actually, talking about guidelines, I do want to just kind of, for the audience, refer them to a latest document, which came out this year on acute heart failure management, which is an update of a document from 2019. So I encourage, you know, your listeners to kind of take a look at it because it's a very practical advice. And this is not that, you know, a large guideline document with 1A, 1, 2, and 3s. And, you know, all of us know we sometimes, you know, after two pages, we jump to the last page and done. But it's, it's, this is bite size information, very succinct, very practical information, what to do in, in different settings. Same thing like FREF, FREF, FPEF, and now, with the acute heart failure as well. So, you know, matter of the going back to the question you mentioned about the dosing of the frequency. So the other strategy, which I personally use, is a drip, an infusion. So if I see the patients on a responding, I go to an infusion. And I'm sure you're going to ask, come back and say, oh, well, that's great. What about the dose trial? Is that something coming? Or am I taking a thunder over me? You take it. You know what I'm going to ask. Okay. This is, Michael, because if you think back in the dose trial, which was a few years back now, was comparing Bolas dosing versus, correct, or continuous infusion, and you know, it didn't show any change, different than outcomes. But the outcomes were different. When you look at the total urine output, it's a little different outcome in decongestion rather than changing mortality. My goal at this point, I'm on the bedside. I'm the one taking care of it. Right now, my goal is not what's going to happen 30 days or a month after in terms of mortality. Right now, the goal is what's the urine output when we're getting. And if you look at the dose trials, there were some issues with the inclusion criteria who were included in the population. So it's a little different. So that sometimes it doesn't apply to a lot of clinical patients we see in practice. And we know that a chronic or a continuous infusion gives us a better result. So yeah, that's my usually thing is if somebody is not responsive, if I'm giving them Bolas is one after another, I'll move on to an infusion. And that infusion can be, you know, you can go up to 20 milligrams per hour. Okay. Or a few of some I'd. Yeah. So let's say you have someone who's not naive. So you would increase their ferosomide dose, kind of max them out on dose, then increase frequency and then go to a drip or. Yeah. So if I go to 80 IV and if they're not responding, that obviously you really need to go to twice a day, it's twice a day dosing and then if they're not responding to that, you already know. If you have given somebody two doses and they have not responded the way they supposed to respond, you already know. So there's no point waiting till another day or two days, you really need to move fast on those patients. and say, "Okay, I'm going to switch over to a different strategy." And then the question is, if this was not a naive patient, this was somebody who was already exposed to loop dietics, which would be the most commonly used ones. And that's the time when you start asking why they're not responding. Is it because there's so much plankton congestion? Is it because they're not absorbing? Is it because of the CKD or the chronic kidney disease? In that case, you can use also other agents such as Bumitonide and Torsamide. And obviously, they've been trials around that too. But we all agree that I think a lot of people in the heart of the world will do that as they move over to a different loop dietic. Now if that doesn't work either, then you really need to start adding a junk dietics. And the agent dietic is really need to focus on some other aspect of the nephron. So the way to remember is all these dietics are working on some aspect of the nephron, the some are working on the loop of hand leads, and the proximal tube you. So you really want to have another junk dietic targeting another area. So adding two, so doing two loop dietics is not going to give you the result. So add a thiozide on top, whether it be Clothaladone or something else. Or a lot of people, there's a metallazone. And they have been studies on that as well without boring you with the names. They've been different, smaller studies looking at comparing Clothaladone with a metallazone. And then there's also factors of course which come in usually Clothaladone IV tends to be more expensive. What are your thoughts then when you're getting to that point where you're thinking about adjunct diuretic therapy? What are your thoughts then on adding like say an SGLT2? Great, great. This question would not have been there a few years back, right? So now we have this in our material. And actually there is data now to support this. So I can confidently say that as well as it's in your guidelines now to say early use of SGLT2 innovators because that will help you for in adjunct diuresis as well. In fact this is very important because if there was somebody you initially are going to really scale up your diuretic therapy and you're starting SGLT2 and as you start reassessing them on a daily basis of where they are, where the progress is and you have to kind of take a pause and say okay they are responding appropriately and they're coming down on their kind of volume state or filling pressures then you may even have to back off on your dietic strategy because as you say is going to as you let it to anybody that's going to state and if they're not responding obviously that's a different story. But as you let it to early on is very beneficial now and the good thing about it it doesn't have a blood pressure lowering problem. So in patients in this very patient which we talked earlier was a hypertensive but if this was saying somebody who has a ref or heart failure with reduced injection fraction and the blood pressure was low to begin with and you really don't have many other choices and as you let it to the market. And then I think the other study that came out fairly recently was also like the added effects with acetazole amide but that study came out kind of without SGLT2s and so just like in your opinion you would assume based on how the guidelines are in you would favor the SGLT2 before you go to adding acetazole amide even on the inpatient side. Oh definitely because remember age LT2 is multi multi fault right the use is multi fault because you have you know across the spectrum of heart failure doesn't matter what injection fraction now it has a supportive evidence across the whole range across the genders. So it's not gender specific it's not it has multiple benefits chronic kidney disease you know in some even liver disease now and there's a small data kind of emerging there obviously you know diabetics and cardiovascular disease. So it's a disease modulating therapy which has added benefit of being providing that a gengdarius is so it is a little mild is a pure diabetic a gengdarius. So you know to choose between those two there's a to me there's no brainer you go with SGLT2. Now on top of that if you need something yeah it is a little milder there. Okay and then I just wanted to go back to the afterload reduction part that you brought up at the beginning of this part of the conversation. So for her I'm trying to like think about how I'm favoring those things so I often I like would see her and I'm like hey she needs to be diaries since I'm favoring that but it's sounded like from the beginning that actually maybe some of the first meds I should be thinking about are her afterload reduction even before diuretic therapy. So you know she's congested so I think whether that you you're on you're right on the money you need to decongest there's no questions about that right so because you need to leave the symptoms. Now that's one because it's the total overall volume state so that's afterload is going to help alone but in this particular now if she was even more hypertensive let's say she was like you know 170s 180 now because 150s you don't know is she hypertensive at this point because she's so she has respiratory distress or discomfort that she's totally volume overloaded and that's driving the hypertension and as you relieve her that volume overload state the blood pressure may come down or is this hypertension causing that kind of a dima flash a dima as well as that. So you start off with the diuretic you know what the blood pressure is if it's still high and that's the time when you kind of start focusing on afterload so the first thing is still going to be diuretic. I think all this is very helpful going through the diuretics the thing that drives me bonkers and I think a lot of hospitals bonkers is the struggle for accurate ins and outs. So sometimes I already kind of accurately know how someone's doing so what are some kind of hacks that you have to approach that part of it because like you can't change their therapy if you don't know whether or not it's working. Yeah that's that's a that's a again a million dollar question and we can go from really a poor mind solution to really you know first world problems right so I think we have a spectrum of options in our armaturium there simple things simple obviously you know unfortunately which doesn't happen you know as frequently as we want accurate in a in a out for multi two factors but then on top of that body weight is useful but remember you just have to be a little bit of a be careful on the body weight so that's something which we have used for ages you know that's the cheap way of doing it you have a scale nothing cheaper than that every hospital has one every practice has one you can put somebody on it you can check it. Now the the only thing to be careful is when you're looking body weight interpretation in the acute setting that's useful like you know on a daily basis the delta change is useful but it's not when you start looking at long-term changes and somebody's in the hospital for a long time and they're not eating what about the nutrition or they're eating too well they were not eating well before you really have to start acting those other factors as well which sometimes we don't because we think assume that everything which is changing the weight is all fluid but again if going back to if you said the first day they came in diuretic and a couple of days you're assessing using body weight that's that's a very useful marker if especially in and outside so those are two simple things now beyond that you can do is you know if somebody has a diagnosis and this is where if they are the appropriate candidates for pulmonary artery monitors such as you know implantable pulmonary monitors in there those can be useful because if they already have it somebody who has a especially high respiratory admission a lot of practices would use that as well and if you have that already in place then you could actually assess it and see evaluate and know what your pulmonary pressures are and gets an idea whether they are responding to it they are some nuances in there because there's always a question about concordance and discordance and pressure and volume but those are little more you know rare issues yeah I think I actually had not heard about the pulmonary artery monitor as much I don't know if that's newer than how well they am in training but that's that's an interesting one one of the things and then just kind of kind of say because it's like that I've done in the past one of my interns when I was a med student actually taught me this which is if the patient seems pretty reliable and they're like on top of it it's like go in with the pen you don't mind losing and a sheet of paper and have them write down their eyes and nose and a lot of times I've noticed patients get super ink like they're very excited to be able to contribute to their care and so that's something I've used it's very patient specific but the ones that you do it on that it's it's worked for me I don't know if you've tried that or this is the first time you've ever said that so or told me that story which is mind-blowing to me but I've never done that but I do similarly ask like I try to really assess from them when they're your in output like especially the transition from the ER where that urinal put is usually not as well recorded sometimes. And so like I asked them how robust it was. So I'm like, were you filling these up quickly or not? And I use that sometimes, especially to break ties. And I also remember, if depending on your practice and your population, if you have a lot of early patient, geriatric patients, a lot of incontinence, people have diapers, people have you know, fads. So those factors come in because there's no way they're going to record that. So you know, you're really unfortunately, then you have to start like looking at how many pads that kind of change and get a rough estimate of other responding or not. And as I said, you can also use, I mean, beyond the bedside, which are obviously the easiest things to do, then you can also look at like urine sodium or the responding. That's another major. Yeah. And kind of the last little elephant in the room. And I think we've talked about the sun one of our things we do for no reason at the soads. But the sodium and fluid restricting in the hospital, I think there's something about the race activation system like this may not be the best idea. So I was just curious your thoughts on that. Yeah. So you know, that size around sodium and fluid has been kind of going back and forth, back and forth. I mean, I think as in general as Americans, we all have a very high sodium diet to begin with. So I think level of restriction in the sodium is a good thing. You know, to the fine level of what that does to rough activation, you know, in the cute setting, there's also is the same kind of principles around bolus dosing was also there. Bolus dosing of diuretic versus continues. So it doesn't really fully pan out scientifically. 100% because it's like if you look at the data and you have you have two camps on that. But I do think if somebody's totally volume overloaded, it's reasonable that there's a level. I mean, if they're drinking gallons, which, you know, that's a different story. But most of the people I feel are not bringing gallons of fluid. Now, when they already show a short of that, sodium is a different problem because sodium, unfortunately, just because of what everybody in a world where food insecurity is so prevalent and that's what you can get your hands on is usually high sodium diet. And so yeah, controlling a sodium. But on the other hand, making it so bland that they don't want to eat anymore, which in the time and nutrition is important, especially in patients who are elderly who also need a little bit of aquatic pressure, they need that album and now they're not going to eat anything because the food is like this. And so I think, you know, just common sense making sure that they don't have a bag of chips and lids around or a, you know, a nice salty burger around at the bedside. But I don't think starvation is the right thing either. But as the guidelines recommend two sort grams of sodium a day. And, you know, in my practice, I, if I am, I think a patient is reliable. And depending on the degree of volume load, I may say, you know, between 48 ounces to 64 ounces of fluid. So I guess we'll go ahead and move on with the case a little bit. So Miss Breath is admitted to the hospital. Obviously, we've been talking about that. And she begins receiving her IV for a semi and her echo reveals that her EF is 30% with signs of left ventricular hypertrophy and mild to moderate mitotic agurgitation. So given both her original symptoms as well as this new echo we got for her to diagnose her, how would you classify her heart failure? So, you know, obviously she has a heart failure based on the clinical symptoms. I think this is something important as you talk to the patient. And, you know, you're the front line, you're talking the patient, you're describing they have, he's now diagnosed with heart failure, which comes with a stigma. And I think so she has heart failure with reduced injection fraction, which is EF for 30% because anything less than 40% is reduced above 50 is preserved and between 40 to 50 is mid-range. And then you have to go into those other criteria where, you know, somebody may be improved EF or totally, you know, recovery EF. Well, we don't say recovery anymore. And I'm sure Michelle, Dr. Kittles and talked about this in her, you know, discussions with you as well. So, heart failure with reduced injection fraction, then you also classify the stage of the cardiomyopathy. So, starting from early 2000's, AHA, C-C, started classifying all these cardiomyopathy's and stage A, B, C, D. And now we updated them a little bit more. We call it, you know, address of heart failure, stage B, stage C, stage D. So, anybody who has symptoms by default is stage C. So, this is somebody I would say stage C cardiomyopathy with heart failure with reduced injection fraction. Now, in her case, you know, just based on the presentations, she's also hypertensive and she has left ventricular hypertrophy. So, the likely etiology, again, as you're working the diagnosis, is she's likely hypertensive heart disease or hypertensive cardiomyopathy. And what about her, like mild to moderate mitral regurgitation, anything to be thinking about, like finding the vascular abnormalities at the stage, or would you kind of keep going down, just worrying about the heart failure, de-conjusting her and treating the heart failure, and worrying about this new, vascular insufficiency kind of from the outpatient side? Yeah, that's great question, because remember we talked, I'll refer to it a little bit earlier. So, this is at time of diagnosis now. So, you have early, this is early finding, you know, this is the time of new diagnosis, you are going to control the blood pressure. You're going to control the afterload, you're going to de-conjust it, and then reassess it again. What is the degree of mitral regurgitation? You also, on the echocardiogram, you will want to know whether there's a prolapse of the mitral valve, of those leachlets, if there's any, there is any structural anatomical defect, or is it just functional mitral regurgitation. So, that will also, you know, you look at the echocardiogram, you look at the size of the ventricle, is it very dilated? Is it like so much stretch on the mitral apparatus, on the ring, that it's causing a functional mitral regurgitation? But anything you do is going to be first predicated on your initial treatment, because you're not going to really treat the mitral regurgitation right now. What you're treating is the cardiomyopathy, you're treating the heart failure, you're treating all the things that are shared with it, you're using your, you know, the congestion, getting them on the right therapies based on the phenotype now, and then coming back later on and reassessing the mitral, and then addressing if it's still persistent. Okay, and so knowing that she's ref, what drugs or therapies would you consider starting for her at the start? So, you know, at this current time in 2024, I think you're in 24, right? Yeah, 24. We have quadruple therapy, which is what we all say, the four pillars, and that should be your initial get, you know, a platform, which is beta blockers, SGLT2 inhibitors, Nepolisin inhibition with arbs, or, you know, entrance into septal blocker combination, and, or we, as we commonly call it, is an RNA, and the last one will be an aldosterone tagine. So, those will be the four basic pillars of treatment. Now, the sequence of it may vary a little bit, depending on the situation, the kidney function, the blood pressure, but, you know, as you alluded to earlier, SGLT2 early on now is kind of recommended, even in, even in your, uh, pencils and documents on acute heart failure, just because of the tolerability of it. As long as initially GFR is above 30. Now, in chronic heart failure, the GFR criteria will change a little bit, but initially, you know, starting off therapy, anywhere 20 to 30 and above is pretty reasonable. And then, you know, depending on the, the, the, the, the, you know, depending on the real function, blood pressure, you have arnees, beta blockers, and then, you have the aldosterone tagine. Now, what I would say is that, aldosterone then antagonist, there's not real data on inpatient initiation and management on that, but what it is very well accepted because it has such a good or marginal effect on blood pressure, but helps with the, the kind of agegendiruses on top of everything, in, in is much more tolerated at the 25 milligram dose, at the beginning dose, especially as you're also diusing people, and they have, they tend to get hypochalemic, it helps with, you know, improving the potassium level. So it's a good kind of therapeutic target to address while they're in there. And then obviously, there's now evidence to support that if you started inpatient, obviously, patients tend to stay on it out of patient as well. And then, would you say beta blocker tends to be last given like usually trying, like if you're de-conjusting and concerned for? So if you, if congestive heart failure is the initial thing, so that would be towards the last one, before prior to the charge, and then they're kind of evenly make or, you know, and you are initiating the beta blocker. But a word of caution would be to say, you know, the patient should not be starting a beta blocker on the day of the charge on the way out. On the hospital, you really want to see, give a little time period to see if they tolerated well, and then you know, at least at 24 hours and in pants before the discharge. And then I guess in this era where I think like Arnie is becoming, I feel like the goal to start that, those you would still try to start early if blood pressure could tolerate is that? So, you know, the way the trials were, so that's a good one because, you know, the way the trials, they're different trials. So they're kind of, you know, within acute heart failure, also the three different trials kind of looking at that. And in the pioneer, HF, there was, which was kind of supportive for the role of Arnie's within the in hospital state was shown to me a benefician. And then later on, there was a life study, which was more focused on class four heart failure patients. These were sicker patients. They were already at wash-outs, they had, you know, on an alperele and other agents. And then they were kind of included in trial. And if you look at the degree of high potension is much higher with Arnie's compared to ACE or ARPs. So that's just the nature of the medication, right? So that's why you have to just be careful on the blood pressure and the kidney function, the stability of it. Once they are, you know, because when you're actually die using them or, you know, decongesting them, they may be some fluctuations. So that's be careful on starting that medication, because then, you know, then the next thing happens a lot of times in practice, people get so scared with the creatinine changing and they stop everything. And then the diaries get stopped too. So I, what I would say is if you still are very congested and you're normal, tense, you first decongest the patient, use your HLT2. If you really need, you can use the ultrasound early on as well. And then as you are now shifting from, you know, whether continuous infusion to a bull, us or bull, us to a oral strategy for diuretic, and that's the time to start that Arnie. Okay, that's helpful. Yeah, I think actually they went through this similar thought process on the Dr. Kiddles and episodes, especially about the renal functions of it's almost like, I think, and they referred to Dr. Topps episode about it, who's an aphrologist and talked about how like, you almost just don't want to check certain things. That's more outpatient, but I'm very helpful to walk through again. How does this change if this is HFPEF? Like the sequence of what I start, what and do I start all of it? So yeah, how does this change with HFPEF? So HFPEF, remember, you went through with some of the kind of long term chronic management of HFPEF with Michelle. Now, there's some nuances in there based on gender and injection fraction, male versus female, especially as it relates to Arnie's. But as you'll see, two is across the board. All genders are yet. So I don't think there's much difference when it comes down to an acute heart failure, whether you have HFPEF or HFPEF, you are using the diuretic and then you can straightaway go to as you're too alongside. So that would be the side. Now, after that, then the nuances come in depending on, you know, Arnie based on gender and injection fraction for women across the whole range of injection fractions. You can use an Arnie for men, EFPEF less than 60% is where the biggest benefit has been for Arnie's, all the strength agnest, you know, clinically, even though the guidelines give the two a recommendation for more driven towards reducing re-hospitalization, we know that evidence from some of the subgroups and also a real life practice that they are very helpful to reduce re-hospitalization and achieve more diuretic, especially if somebody's hypochalemic as well to improve the potassium levels too. So that really is useful there. And then, data blocker is very different compared to HFPEF. So the role of beta blocker is there is no really a direct role of beta blocker in HFPEF unless there's another reason. So if somebody has arrhythmias, they're the atrial population or ventricle arrhythmias or PVCs or they may have, you know, coronary artery disease. So there's another primary indication for a beta blocker that would be the, then you would use that. but compared to hair prep where it's across the board on everyone. This is a very specific population. Okay. And now that we have done all that, I think the other question starts to become like trying to establish ideologies. And obviously this patient has a lot of risk factors for coronary disease. I assume she needs an eschemic evaluation. I think the question I always have more than anything is is this something that I need to do before they go home or is this something that like when we get them de-conjusted and started on these meds and then they can get that as an outpatient. So yeah. So that's the question about eschemic evaluation. That's a one which comes up all the time. So first thing it should be predicated to what are risk factors. So not everybody wants on warrants a eschemic evaluation. So it should be driven out of what your risk is pre-test probability. Now if you have a 32 year old with no other risk and now you have hair prep, but there's hypotensive or depending on where your practice is, it's familial. Not everybody really needs to run into an eschemic evaluation. And even the guideline that pre-clear on that. But if you have risk factors and then or you have symptoms suggested of angina, that's the one where you really want to do inpatient evaluation. Also sometimes from a kind of a logistical challenge perspective, it's easier to do it while they are in there to know the etiology of it. Now the question always is, what are you going to do with that information? Is there somebody are you looking at a surgical re-vascularization? If firstly if they have no symptoms because that's where that topic comes up is, if you find an etiology, if you have coronary stenosis, does it really explain the cardiomyopathy or the heart failure? And if that's the case, is that something treatable? So those are kind of different layers of questioning which come in. We are routinely at Caches at Memorials, Will do eschemic evaluation on patients who have risk factors, especially their, you know, also, because we also serve a lot of underserved patients. So from a totally logistics perspective, it's just easier for them to get it done while they are there. But it's okay that if their risk factors are not much and you know, you're not sure and there's a fluctuation going on in the renal function and you can then do it outpatient on a follow-up. Okay. Yeah, I think we think about the resource stuff too for some of our patients too. So that's helpful to know. And the eschemic evaluation, does it have to be a cardiac catheterization? No, and today is the end age, not necessarily at all. Again, you know, depending on your pre-test probability and age and everything as what else is going on. So somebody you do not expect to advance age or renal disease. So you don't think there's going to be too much calcification, you can do a CTA. Stress test is still there. You can still utilize the stress test. There's obviously, as an advanced heart failure person, I can tell you that we see some patients who come later to us in their, you know, life journey for advanced therapies and they had stress test and then we end up doing a catheterization and we find significant disease. So because remember, the false negative rate can be there, especially if there's balanced schemia. So if you're really doing a true evaluation, it should be either a CTA or cardiac catheterization. Okay, very great. So I think this is a great point for us to maybe just summarize. We've already talked about a lot, but before we kind of take the case down, it's next twisty turns. I just think that the few things that I wanted to highlight is just emphasizing when to get the echoes on which patient. So obviously, new onset suspicion for heart failure to get your echo, but for everyone else to kind of make sure that you have a reason to be checking for it. And then I think the other thing to be thinking about is, you know, the patients that are coming in to be pretty lenient, I guess, and I don't know if that's exactly the right word, but starting the guideline directed like medical therapies early, but being cognizant of their other comorbidities. And so it seems like kind of a cross-saboard reasonable to start as gel tea to early often on these patients and everyone else you're going kind of have to be considered of their other issues, heart rates, blood pressures, all of those other things that we have to think about. And I don't know if there's anything else you wanted to add, Mooney. No, SGLT2 is for everyone. I know I think it was at SHM. We were like, oh man, as gel tea to seven aparty. And I just feel like we're reiterating that on this episode. The ride continues. Yeah, the issue of the two is a statin for heart failure. Yeah. I'm going to be putting in the water soon. It's a t-shirt right there. All right. I'm going to, I'll advance the case. So on hospital day three, mis-breaths condition worsens. Her blood pressure is now 95 over 60. Her heart rate is 125 ohm and her oxygen saturation is 92% with two liters. And her urine output is significantly decline in the past 24 hours. And on exam, she's cool and her legs are slightly modeled. So I think it's fair to say this is cardiogenic shock until proven otherwise. And so So I think this is one of those things that we talk a lot about on these inpatient episodes where the diagnostics and the treatment are kind of having to happen in parallel. So anticipating that she'll be transferred to the CCU, I think we do kind of need to understand the next steps. But I think sometimes with logistical challenges, the transfer doesn't maybe happen as soon as this very scared petrified hospitalist would like. And so sometimes I'm kind of told, you know, double the diuretic dose instead of the ionotropes, which I can't start on the floor. So are there situations? So that to me, it feels a little counterintuitive as somebody that doesn't work in the CCU. So are there situations which I can expect somebody who's like kind of already fallen off the wrong side of the starling curve to actually respond in these situations to the doubling of the diuretics? So you know, I think there's all the dependent what's going on, right? There's a little more nuanced answer I'm going to give to this one. So is there a situation where somebody may get benefited from increased viruses? Is possible. It's possible in the sense that if they, it's not that they are dry, they're not dehydrated, they may still be volume overloaded but they are in low output failure. So those are two things which goes hand in hand. The filling pressures are still high. They still may be in volume overload, but now they are also in low output failure and that's why the blood pressure is low. And sometimes what happens is out of a worry that maybe, or maybe the diuretic is causing the low blood pressure, we start holding the diuretic in these patients. When the answer is, you know, supported therapy of blood pressure or whether ionotropes assessing hemodynamics and everything else. But I think before that what you can do is while you are waiting for transport, I think this is something which is just kind of bedside things, making sure that they're still not getting some of the other neurominal agents which may have been started on. So making sure that we stop those because that's kind of sometimes is because they are new therapies, they've been started on them and now they are hypertensive as well. But in this particular case, if you just based on the clinical definition of shock, you know, 30 points lower than their average mean, systolic of less than 90, obviously, mortal skin, all the stuff, suggestive of shock. So they really, really need what they really need is kind of either a pulmonary, archric editor as well as, you know, ionotropes or pressure depending on what you're going to find on them. And that's also useful because that's also going to tell you what your volume status is. Because a lot of these patients may still need an IV diuretic, but they just need an ionotropor something else alongside perinol profusion too. Okay. And how do you think through which ones to start? I know I'm getting bold as hospitalist here, but which ones to start and then is there any to avoid in the situation? Yeah. I mean, because here you're doing empiric right now because assuming that you don't have a swan, you don't have right hat cat on them. So you're doing empiric therapy is using their low output failure. So you want to depending on the blood pressure. But they are totally hypertensive. If they are, if they are like getting hypertensive, they are lactic acid doses from the hypertension, you really need to maintain their blood pressure and profusion. So which is across the board as much as we hate that you need a kind of a way suppressor. And that's going to be your first one just to maintain the blood pressure above a certain map. From an I know trope perspective, you can do, you know, if you are hypertensive, you can use dopamine, but you have to be cognizant of the heart rate because if they're tachycardic on top, that's going to make it worse. My choice usually is melanon or debit mean depending on, you know, if I am suspecting that's low output failure in a cardiopathy patient, those are the two ones. I would usually go to melanon or debit mean again, depending on blood pressure. They are already hypertensive. Melonon is not going to be tolerable or if they are very tachycardic, you're not going to, you know, tolerate these either debit mean or dopamine or even melanon well. In that case, if you just may have to first bring up the pressure. And then obviously if they're really, really kind of fast, read me out something going on, then you're talking about kind of more temporary mechanical devices and stuff, all that stuff. So that's the way I would see now. There's the other caveat is in this particular patient, you're saying hypotensives, but if this could be somebody in shock and hypertensive, goes back to where that your way, so that later story. And that's where you would use things such as nitroglyphs in the nitrite. Again, not possible on the floor because, you know, no floor will allow you to start a nitroglyphs in nitride across the, I don't think anywhere across the board. But that could be an option if somebody was in shock, the lactobacus is going up there in pulmonary deema and they still are, if you really, and they still may have hypertensive in that case, where you would use a pure, pure, visual alley. Definitely thankful we don't work in an open ICU, but there's certainly hospitals that are as possible as that do. I think the other thing that goes with it is the diagnostic part of it. So, like, thinking about one who actually needs the right heart catheterization and then the timing of one that is actually the most helpful to you as like trying to figure out what's going on in the therapies they need to be on going forward. Yeah. So this comes up across a lot. Now, you know, assuming we're still talking about this particular patient, but I'll first start with that and I'll go to a general kind of criteria. In this particular patient, she's already declared herself, right? So you really need to know, and this is the patient you're getting to the CCU, the CICU, or ICU, whatever that infrastructure is in your hospital. So now that's a patient who needs a swan right there, you know, assessment of their filling pressures, assessment of their cardiac output, all the stuff. That's number. And this is obviously more of you in the shocky state, but there's a lot of other patients who may not be in that state. Those are the ones who, you know, may be either getting hypotensive, they may not be shocky, but they're getting hypotensive. Or you have to peel back on therapy. They came on therapy. This is a cute and chronic heart failure. They're already on good medications to begin with. You're just diagnosing them doing, you know, all the things. And now, certainly, you're peeling off medications. So this is where you should really think about, okay, why am I have to cut back on medication or stop medication? Or they're not responding to your diet, the strategy, or their kidney function is getting worse. So those are kind of three, or their symptoms are not improving. I mean, those are four kind of big classes or situations where you would want a right for the cat. Okay. So let's go back to Ms. Breath. She briefly requires if she's staying in the CCU, she gets her Ionotropic support, and she's actually able to wean off of it after she's dry. She gets transferred back to the floor, and now she's on room hair. A demon has improved everything. And so now we're trying to think getting her ready for discharge a little bit. So what medications, let's start with that first. Are we focusing on at this point? So assuming this was all cardiac shock from lower foot failure, and you know, somehow she wasn't that still state where she didn't need more advanced therapies, and she's off the curve. She is back in the lower quadrant on your hemodynamic profile. And now, and now you're going to start medication. So again, the most tolerable medication would be an SGSU and then depending on your blood pressure, you could do ultrasound and antagonist. If your blood pressure is reasonable, you can add an Arnie. I would be a little cautious on introduction of beta blocker at this point. If they were in truly in shock, they were in ICU on Ionotropes, you know, introduction of beta blocker, I would delay it at this point. This is in fact, it again, all depends on, you know, how many days you're going to be in there. What else is going on? But you know, if this is very close to her discharge state to whether hospital, whether home or anywhere else, then I would actually even defer the beta blocker introduction to the first follow-up visit. Now, she is still there and she has a robust blood pressure. And you know, despite introduction of the other three classes of medication, then you could do an introduction of beta blocker at the last one again. So this is like my age old question. And I feel like this is why we're doing this episode. What should I favor? Is it better for someone to be on the lowest doses of all four pillars of medication? Or to be starting to tightrate them higher on the medications that they can tolerate? Yeah, no, this is an absolutely super important question. And it's being kind of, it's being addressed everywhere, you know, again, documents on the podiums, on everywhere because more and more evidence is that low dose of all is much superior than high dose of a few. Because you think about it, you're addressing different pathways. So you get an incremental benefit, additive benefit of different pathways of blockage or, you know, modulation. And that's what you will miss. and also patients tend to tolerate more the lower doses and higher doses of one. So more the barrier would be the principal. And so you would start off all the lowest doses of four, then if they're able to tolerate, then you would escalate them. - All right, well that answered that. Yeah, that's definitely the one. I think the reason that we heard it said this is like the whole reason we're having the episode is as I referred to in the past, I'm just a petrified hospitalist at baseline when it comes to this stuff. And so sometimes I kind of feel like I've seen some of my patients get re-admitted with like precinct be and I sent them out on all these medications and it's probably just like, probably it's not happened very often, but those are the ones you remember, right? And so I don't know, do you have any words to sort of like make me feel better about this? - Yeah, no, so I think, you know, that's an important question, but I think it happens, it will happen. And I think that's where nuances will come in, nuances like you gotta look at the patient age. You know, what else is going on? Is there something which is causing the autonomic dysfunction or they dehydrated? So what happens is it goes back to what we had initially talked about. You know, you started as a healthy two and the past we didn't have that. Now you have as a healthy two and can give a pre-putin diurosis. You started the Albusara antagonist and the past, you know, if you look at the Medicaid data, I need where between 30 to 60% of the patients are on an MRA. And so now if you are pushing it, which is the right thing to do, that's gonna help you with Diatec 2. So this is where you need to adjust the dose of your regular loop diuretic before they go out. And that's kind of the important thing. So yes, you got all the four medications and because our needs are gonna help also with the after low reduction, accentuate your diocese. So as you are getting those three tasks of medication on, you just make sure that the patient is kind of not totally dehydrated. And the same thing as I said about beta blocker that don't do it the day of discharge, because you wanna see if they were able to tolerate it for a day. And unfortunately in the current world, in the United States, we have one of the shortest hospital stay duration around the world for heart failure. And the duration of heart failure stays, one of the shortest around the world in the United States. So what happens is we are packing up so much within that duration, because we also know when patients go out without those four medications, a lot of them will never end up going on that. I'm sure you discussed the evolution HF and other large registry showing patients who were started on medication in the four classes and by the end of one year, a majority of them were either not on medication or were there was a reduction in dose. Two thousand of the patients were off beta blocker doses and MRAs and everything at the end of one year. So this is a real problem. So yes, there's a rare chance of somebody coming back with precinct copy. It's usually because we didn't address the dietic dose before they went out. And we adjusted the dose they often, they went out and now they're back again. - I think that probably is what happens because I feel like even during my relatively short career so far, I think the guidelines had changed during them. And so that's when it became recommended, I believe, to watch someone when you start their oral diuretic before they go. But I definitely don't think about it as much for the other guideline therapies. And I think because of the recent studies kind of recommending relatively quick titration in the hospital, it's definitely sometimes feels like I'm throwing it to them as they're walking out the door and then praying that nothing bad happens. - So this is where there's other things that things you can do is obviously you have to be careful with the age, the oxygenarians and you have to be careful because sometimes that may be a population where you may have to be gentle as much as I like to be aggressive but they may or may not tolerate those. So one size doesn't always fit all, even though we want that thing to happen. Other thing you can do is, you can always do autostatic vitals on these patients, especially their early patients before discharge, will kind of get you an idea because other than just clinical exam which we don't utilize autostatic vital as much because usually that's what kind of makes them fall and is that autostasis. So that will also get you a little bit more comfortable whether they are worse evolving status in there. - Yeah, I like that. - And then the other thing is like, you know, as you transition, which is the other bigger picture is the post discharge follow-on because you really need that. That's kind of how soon can they be seen and reassessed? - Yeah, I mean, I think that's the other part that often comes up is, you know, the trials all had very quick follow-ups. Like within a few days and I just don't think that that's realistic and so I think that's the other part that's the struggle when I like part of why I don't want to add everything when they're going because I don't actually know when they're going to be seen. - So, you know, at Kashlek Memorial, we actually do. And I think a lot of the centers who are now focused on quality of care around readmissions and everything, and investing in those systems, we actually have our patients seen in our discharge clinics by our care providers and, you know, extenders and WPPs within a week of the charge. So they are, unless they're somebody who doesn't come for, you know, totally different reason, but they are all, they all get an appointment within a week to look at, you know, the volume status, adjusting the dose of diuretics, the medication dose with the base and blood pressure, getting the blood work done, being sure they're not really injury or hypokinemia, I didn't know that. - I think one of the things that was that caught me off guard early when we were kind of implementing all these new guideline directed therapies was this washout period for, you know, ace and arb stuff. So I was curious your thoughts on the need for that versus not because certainly that adds to length of stay which, you know, whether or not that's an important metric, we can, that's for another episode, but specifically about the washout period. - So, you know, washout period is very important. I don't think there's any question about that, especially coming off an ace into an arney because there's an actual risk of, you know, ingedema. And so I don't think, you know, and that's why it's very clear on the labeling as well. One of the few things which is very clear. So you really want the 36 hour washout period. Now, I mean, if this is a length of stay, I'm sure, as you said, you can talk at another time. But, you know, that's a different story. You can always do an arb. You can start an arb and that can be replaced pretty easily. Or you can start an arb and then they can go out and get into an arney. - Okay. And I think one of the things that was, they actually covered this at length in the outpatient episodes, but just as have said it here, the cost of the arney has become kind of prohibitive for a lot of patients, I think. And so just kind of keeping that in mind is important. Obviously we have other options that aren't as good, but obviously it's better than not having anything at all. - Yeah. And that's actually what the, even the guideline writers acknowledged that, that, you know, because of different, either with a side effects or costs, could be a factor in some patients. Yeah, if that's withstanding those two factors, everybody should preferably an arney as a class one. But if that's a factor, now remember a lot of the patients on federal insurances cannot get other assistance. At the current time, the out-of-pocket expenses are getting limited now and by next year based on the current negotiations between the cost of medication as well as out-of-pocket expenses for seniors, that's going to be limited to a certain amount which is going to be for all medications. So that's going to be really cutting down that out-of-pocket costs for patients after that. So that's definitely there. And, but that is still a problem which can be for some people that much amount as well and that case making sure they are on an armbits that. But they are assistance programs, you know, I think, and this is kind of key is, you know, working with the case managers that the court transition coordinators or outpatient clinics to make sure you can tap into those assistance programs because there's a better from the vendor itself, whether from, you know, if somebody cannot really afford to cover the cost of it, we actually, we try to get them all those other assistance. - Great. And we've talked a little bit about appointment timing within the first two weeks after discharge. I think the other part that I tried to stress with my team is sort of the patient education piece, especially in someone like this patient who's a new diagnosis, who's sort of managing their diuretics and things like that. So could you maybe walk us through how you like to think through that and explain that to patients? - Yeah. So, you know, patient education is so important and this should start right, the journey should start right in the hospital itself because you have a captive audience at that time. Now, remember, a lot of the retention, the rate of retention is gonna be low because there's so much going on at that time. So it's not just once and done kind of deal. This is an ongoing journey and ongoing. and this is where that team effort comes in between patient and our patient teams. And if obviously they spread around. Inpatient, you know, starting from, you know, the medical teams, walking through the diagnosis, explaining them what that means, what that kind of, the medications mean, what each medications perceived side effect could be. Because that's where a lot of the discontouration is because the patients were not aware of the perceived side effect. So when that side effect happens, what happens is they stop it because they were not aware about it. But if I find very commonly, when you talk through and you explain the patient what that side effect is. And when they feel it, if it's not something which is major, they say, "Okay, I know about it." This was expected. Even things like orthostatic, you know, disiness sometimes and fencing in your hominal blockers. If they are aware that panic level goes away. Then talking about the disease state, things such as diet, lifestyle, exercise, you know, sodium fluid, all those things. Awareness of how to be, you know, aware about when they're decompensating again or, you know, what to do, what to, how to titrate some of the medications, diuretics, if they're reliable on their own. And then the diagnosis per se, what that diagnosis really means and what that kind of diagnosis now. I do tend not to talk about numbers right up front about mortality and this and that because that does make people very upset and panicky. Because already hearing, heart failure is a kind of a, you know, a scary thing to kind of start with. But then also utilizing your pharmacist, depending on, again, each system, they may be pharmacist, they may be care coordinator, they may be, you know, social workers, bedside nursing, all of them. So having different layers of education is important because one person, just, you know, the cardiologist, the hospitalist is not enough. Because that just, you know, you're going in, you're talking, it needs recurrent reinforcement of the diagnosis, the change in life style, all those kind of things. Every time they get a medication administration, they need to talk. And then that journey continues as they come to a follow-up appointment. Obviously, if depending on the system, there will be things such as community navigators, we have community health workers, we should go to the house, right after this charge. You know, look at the kind of home environment, help them at home again, educating them about the diagnosis, what they need to do, keeping the appointments, all the stuff. And then in a, on the outpatient ambulatory follow-up that journey of education should continue. Awesome. I think that's a good place where we could do take-home points. So what are like maybe your three take-home points for the listeners from, you know, what you want to make sure they take away from this episode. Yeah, I think one of the things is, you know, I would say, we can just do therapy. You know, you're going to be, you're going to go aggressive. You know, somebody's all over loaded, just don't, you know, I say, don't massage the same thing till that. You know, escalate therapy quickly. If not responsive, go to the next level, whether it's bulls, then increase the frequency if continues, but do something different. You know, institute some of those medication classes we talked about early on, especially at GILT 2 as we talk about. They are, you know, you can really strategize based on blood pressure, you know, whether MR is not like one or none kind of phenomena. There's a gray area in there. So is, if you cannot tolerate Arnie's or bear blockers, you still can do as you do an MR. The last thing I would say is education is key and making sure that transition of care is important because that's the key focus in overall outcome. That's what's going to, you know, decide what's going to happen in 30 days, 90 days and long term that transition of the day, making sure patients have the right medications that those are, if somebody was already on before and now they really know what they're going home on. They really have those, if there's a possibility, have those medicines on the bedside, if they don't have it, making sure when the pharmacy you're sending it, they have those medications. A lot of times we send patients home and they get, we send them to the pharmacy, a lot of times we may not even have the medication. Or they need a priori-traxiation and so patient shows up to the after this challenge and there's no medication from them. And then you know what that results in. So that's kind of what I would say. Awesome. This has been another episode of The Curb Ciders bringing you a little knowledge food for your brain hole. Yummy! Still hungry for more? Yep. 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