REBOOT: #469 Inpatient Heart Failure

Hey listeners, you're about to hear a Curbsiders 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 slash curbsiders. If you want ad-free episodes, bonus episodes, and a whole bunch of other cool stuff, patreon.com slash curbsiders. So Moni, did you hear about the cardiologist who went to a team building? exercise? No, I did not. So they're doing truss falls. And the one cardiologist said to the other cardiologist, entrust-o 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 heart failure is a fluid situation, but don't worry. We are here to help you stay afloat. So all the listeners could 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 Curbsiders podcast is for entertainment, education and information purposes only. And the topics discussed should not be used solely to diagnose, treat, cure or prevent any diseases or conditions. Furthermore, the views and statements expressed on this podcast are solely those of the host and should not be interpreted to reflect the official policy or position of any entity aside from possibly cash-like moral hospital and affiliate outreach programs. If indeed there are any, in fact, there are none. Pretty much, we are responsible if you screw up, You should always do your own homework and let us know. And welcome back to Curbsiders. I'm Dr. Moni Amin, and I'm joined by my effervescent co-host, Dr. Meredith Rupit. How are you this evening? Doing great. Yeah, and on tonight's show, we discuss inpatient heart failure management with our guest, Dr. Grusher Pundrath. And before we do get to all that, a quick shout out to the updates episode with Dr. Michelle Kiddelson that came out not too long ago. The Outpatient, HefRef, and FF episodes, 458 and 460, respectively. Great stuff. And this episode complements 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 it is we do on this show? Sure, Moni. 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. Pandra. He's a professor of medicine and the director of the Heart Failure and 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 is 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 in 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 JACT, Heart Failure, and Directed Development of Heart Failure curriculum for PCPs in Latin America. He has spoken widely at both national and international meetings. Dr. Pandrath is governor for the Washington, D.C. chapter, past chair 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 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 healthcare professionals through VCU Health at curbsiders.vcuhealth.org. Okay, Dr. Pandrath, welcome to Curbsiders. We're 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, you know, in terms of outside medicine, I actually love traveling. That's one of the things I, you know, anytime I can get on a plane, a flight or drive 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, because I love to eat. But for friends, family and, you know, compile recipes and create recipes as well. Do you use salt in your recipes? Well, you know, do I have to give the official answer for that or the unofficial answer? But no, I actually, I mean, I do 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. It's 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 as well as Malaysian food. But, you know, as I said, even French, Italian, everything. So in your travels, is there somewhere you've specifically enjoyed going for the food? That's actually a great question. I spent summer in France actually driving through Burgundy and the Champagne area. And it was just amazing food. But, you know, really fresh ingredients. You didn't really even need to add much. But, you know, Vietnam is actually, I would say, one of the places where I love going for food. And I've been there twice. And 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's just fabulous food out there. Awesome. So we'll switch gears and I guess ask one more question. What is some meaningful advice or feedback that you've received throughout your career? Oh, there's a lot of advice. I've been fortunate to work with some remarkable people. And early on, I think during my early days of postdoc years as a clinical researcher, I had a mentor who I always finally look back on. And 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. So now quantity doesn't matter, quality matters. And I actually do kind of keep that to heart. And, you know, as you go through different parts of your training, your phases of 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 just kind of as a buzzword, but it really means something. You really have to take care of yourself. And well-being can be in different ways. And it's not only burnout at work. It's also being physically fit, taking care of your health and nutrition and doing things which you enjoy. And that's kind of what I have been given the advice. I definitely think the first one is near and dear to Moni and me right now. So appreciate that advice for us on a personal level. I don't know what you're talking about, Meredith. But we'll leave it like that. Do you want to ask anything else or do you want to do Picks of the Week? Let's do Picks of the Week. Okay. so mine's pretty obvious not having covid um shout out to binax for proving that i'm negative like i don't know um i you guys may not know this but meredith and i actually record in the same space which is um 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 um mine is also um it's september when we're recording this so it's now football season um and monie and i had to actually go a full day without speaking to each other because her michigan wolverines were playing my texas longhorns and texas won um and i did confer with 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 championship. Please take us to Cash Talk 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 extremity 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 more swollen. At home, missed breath takes metformin, 1,000 milligrams twice a day, lisinopril 20 milligrams every day, and metoprol 25 milligrams twice a day. In the ER, her oxygen saturation is 91% on room air, blood pressure is 155 over 90, and a heart rate of 93. On physical exam, there's jugular venous descension and an S3 gallop. The bilateral lower extremities are cool to touch, and there's three plus pitting edema to her thighs. A chest x-ray obtained in the emergency room shows vascular congestion and her BNP is 1,100. The troponin, serum creatinine, electrolytes are all normal and an EKG demonstrates normal sinus rhythm with few PVCs. So I think where we kind of wanted to start was, does this seem like a typical patient presentation for acute decompensated heart failure and what other history and maybe physical exam findings you may want to know? Well, you know, that's a great presentation, which is a very common presentation, I would say. And just going back to reflecting on what you said earlier, that I'm following up on your co-positors right after Michelle Ketterson. And I just admire her and I had the honor of coaching with her a recent update on Heftep. 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. You have to make sure, you know, is this really heart failure? That's the first thing. And because everything which is, you know, somebody is short of breath or has leg swelling, you really have to go through those differentials, what we have learned over the years of training, you know, through this medical school as well as residency training because there's so many other causes in somebody with comorbidities that this could be a mimicker for her 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, what are the risk factors that a person could have? And in this particular case, You clearly have a fully controlled hypertension. She's presenting very hypertensive. She has leg edema. She has S3 gallop. She has, you know, 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, you know, 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 ACCHA guidelines as well. And, you know, 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, you know, beyond history, beyond those risk factors, beyond the acuity 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 of 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 too, when she's presenting, do you see much role for like point of care ultrasound as being helpful? Yeah, I mean, that's, you know, the point of care ultrasound, the role for it has been emerging quite a bit over the years now and from multiple levels. You know, a lot of times we kind of persuade on the LV ejection fraction, but the point of care ultrasound can do much more than that. So this is somebody who's presenting with a 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 there a ventricular hypertrophy? But more importantly, you can also look at their vina cava. You can look at, is that vina cava distended? Is there intravascular congestion there? So that kind of adds on to your level of suspicion or whether this is going to be acute heart failure. And is the person really congested or is there anything else which could be mimicking or presenting as low extremity swelling? Now, in this particular case, obviously, she's hypertensive. Her heart rate is still high. But if this was somewhere you were also concerned about precardial fluid around or effusions or tamponade or anything like that, that ultrasound would be helpful too. So now there was a suggestion of any kind of acute ischemic injury that would be useful to look at wall motion, original wall motion. So would you say like in your practice, does that point of care ultrasound, it's mostly there, it sounds like, to help 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 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 hypertensive, has S3 gallop. So you're already kind of very, you have findings, clinical findings, both symptoms as well as clinical features, physical kind of findings, which are very suggestive of 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 had kind of morbid obesity and with the diabetes, they also had, you know, liver involvement or had, you know, they were more sedentary and had concern about DVTs or PE. and then the RV failure aspect comes in or with all those different comorbidities, you could have pulmonary hypertension, could be group two pulmonary hypertension, could be, so any of those differentials will start coming in. Yes, the final task is in heart failure, but that would help you kind of decide if this was heart failure or non-heart failure. But in this particular presentation, yes, it's more to confirm. Got it. This episode is brought to you by MD Progress. Are you juggling articles, guidelines, and CME reporting? It shouldn't be this hard. MD Progress is built by physicians for physicians to help you keep on top of the never-ending changes in medicine. Precision, evidence adapted for your clinical practice, information presented as clinical vignettes that make sense and not just technical abstracts. It takes only minutes. It's accessible anywhere. You can try the daily quiz right now from your inbox or upload an image from work and have the system build a personalized education session just for you or get with a guideline when you work through a clinical case in minutes. And guess what? Your CME credits are logged automatically. Also, great news. If you're a resident, it's free. I personally have loved using MD Progress. It was super cool. So I wanted to give it something hard to do. I typed in natokinase. I wanted to learn about that for cardiovascular risk reduction. It came up with a bunch of articles. I could look at the abstract. I could link to the PDF. I could test myself on what I've learned from the article, and it's logging my CME credit. I would highly recommend that you try this out. It's learning made effortless. For our listeners, enjoy your first month free at mdprogress.ca forward slash promo forward slash curbsiders. That's mdprogress.ca forward slash promo forward slash curbsiders. This episode is brought to you by Quince. A well-built wardrobe is about pieces that work together and hold up over time. That's what Quince does best. Premium materials, thoughtful design, and everyday staples that feel easy to wear and easy to rely on, even as the weather shifts. Quince has everyday essentials you will love with quality that lasts. Organic cotton sweaters, polos for every occasion, lighter jackets that keep you warm in the changing seasons, the list goes on. Quince works directly with top factories and cuts out the middlemen so you're not paying for brand markup, just quality clothing. Everything is built to hold up to daily wear and still look good season after season. Plus, they only partner with factories that meet rigorous standards for craftsmanship and ethical production. I have mentioned it before, and I just like saying yak wool sweater, but I have this yak wool sweater from Quince that I adore. It looks great. It is so toasty, especially since it's been so bitterly cold outside, and it has held up for a couple of years now at this point, so really high quality. So refresh your wardrobe with Quince. Go to quince.com slash curb for free shipping on your order and 365 day returns. Now available in Canada too. That's Q-U-I-N-C-E dot com slash curb. Free shipping and 365-day returns. Quince.com slash curb. 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-prong 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 then we'll go from there. Yeah, that's actually, you know, this is something which is addressed in the guidelines as well as the expert consensus documents. And now, you know, when somebody comes in, has no known diagnosis, they definitely need some assessment. because it's going to tell you a couple of things. It's going to 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, antipro BNP or BNP, 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 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 going to use. Are you going to go for half-rev therapy, half-pef therapy? And now in these days, a lot of its 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 ejection fraction and some other criteria. But then it also tells you the anatomical features of what could be causing that heart failure. So as you look at hypertrophic ventricles or enlarged atria, that's going to guide you to a different differential within heart failure itself. So based on my own practice and as well as the guidelines, as well as the expert consensus documents, it's recommended that you should get an echocardiogram of anybody with a suspicion for heart failure. So now going back to your second question, Moni, 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, maybe, 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 routine echocardiograms unless you have a question which is going to be answered and is going to 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 output failure, they're just congested. They're in your, if you look at your classical hemodynamic classification, they're in the quadrant of wet and warm. They have a blood pressure, they are warm, they're just congestive. They have all the signs of increased spilling pressure. In this person, your treatment is going to be decongestive therapies. That's going to be the main goal initially to relieve the symptoms. So getting an echo is not going to be additive in the sense that you're not going to really change your management Now at some course if that situation changes in the sense that they are not responsive to your initial treatments or there 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, again, should be driven out of the question, what am I going to do with this knowledge? What am I going to obtain from echocardiogram to change my treatment? If it's just like, oh yeah, I 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 valvular regurgitation, somebody had moderate to severe valvular insufficiency, whether it be mitral valve, tricuspid valve, and you say this is a volume dependent state and I want to reassess it after I decongest them I want to know what's the severity of that valvular insufficiency. Am I going to really address this in this particular hospital say, because now there's 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 is that they might've had this exacerbation. Right. And the thing that I never put together until preparing for this, and then also putting together a things we do for no reason talk is I don't think I'd 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, Moni. I think when we initially get called on consults or just primary, and the level of valid insufficiency remark can go down with appropriate e-congestion and other, you know, application of 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 Ms. 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, Meredith, that's a great question and, you know, something which we all deal on a daily basis, right? So I think she's dietic 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 furosemide, 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 decongest her, a lot of it's also going to be after low reduction. And that is key. Sometimes they miss that point as we focus on the decongestive 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 into trouble pretty quickly in the sense that we'll keep trying to get that decongestion done and they're hypertensive and you start having kind of renal 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 hemodynamic principles and physiology because as you reduce afterload you're going to 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, if somebody's older, somebody's not, you know, it's mildly overloaded and mild is such a kind of subjective vague term. And especially if somebody has a lot of kind of splancting congestion, you're not going to see that. But, you know, based on their symptoms, you could do a 20 or 40 of furosmide as a bolus first and then see what their response is. And now you can gauge the response in two hours and see 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 bolus. Now, if they are not responding and you gave another bolus or you increase the dose from either 40 or 80 furosmide or they were already so volume-related, they ended up getting 80 in the beginning and depending on the response if they're not then you want to increase the either the dose or the frequency or sometimes both and that becomes important because just giving the same dose over and 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 um but when you're thinking about increasing the diuretic and you're doing increase to frequency for bolus dosing still, is there a maximum amount that you would do that frequency at for, let's say, furosemide? Yeah, no, you can go like three, four times a day. So you can go that. 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 either acute or chronic kidney disease, and there's dieting resistance, even usually not in a naive 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 obstructive uropathy? Is, you know, is the bladder full? Are they even making the urine or is that obstruction in the bladder area? So, urinary tension. So, those are kind of things I would first alongside look at. There are other tricks you can do. You can also always look at a spot urine sodium. And, you know, after Ebola, you can check spot urine sodium in a few hours. and see if they are properly 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 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 all of us know we sometimes, after two pages, we jump to the last page and done. But this is bite-sized information, very succinct, very practical information, what to do in different settings. Same thing like FREF, FPEP, and now with acute heart failure as well. So, Meredith, 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 are not responding, I go to an infusion. And I'm sure you're going to come back and say, oh, well, that's great. What about the dose trial? Is that something coming or am I taking your thunder away? You take it. You know what I'm going to ask. Okay. So this is, Michael, because if you think back in the dose trial, which was a few years back now, was comparing bolus dosing versus continuous infusion. And, you know, it didn't show any difference in 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. Or you're 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 what 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 our clinical patients we see in practice. And we know that a chronic or a continued infusion gives us a better result. So yeah, that's my usually thing is, if somebody is not responsive, if I'm giving them boluses one after another, I'll move over to an infusion. And that infusion can be, you know, you can go up to 20 milligrams per hour. Okay. Or furosemide. Yeah. So let's say you have someone who's not naive. So you would increase their furosemide 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, then obviously you really need to go to a twice a day, 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're 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, you know, if this was not a naive patient, this was somebody who was already, you know, exposed to loop diuretics, 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 splancting congestion? Is it because they're not absorbing? Is it because of CKD or the chronic kidney disease? In that case, you can use also other agents such as abumetanide and torsumide. And obviously, there have been trials around that too. but we all agree or I think a lot of people in the heart failure world will do that as they move over to a different loop diaretic. Now, if that doesn't work either then you really need to start adding adjunct diaretics and the agenda is really need to focus on some other aspect of the nephron. So the way to remember is all these diaretics are working on some aspect of the nephron, right? Some are working on the loop of N leads somewhere on the proximal tubule. So you really want to have another adjunct diuretic targeting another area. So adding two, so like doing two loop diuretics is not going to give you the result. So add a thiazide on top, whether it be clothaladone or, you know, something else. Or, you know, a lot of people with zumetallazone. And there have been studies on that as well, you know, without boring you with the names. There have been, you know, different smaller studies looking at comparing clothalidone versus methylazone. And then there's also factors, of course, which come in. Usually clothalidone 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. So now we have this in our armatorium. 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 HGLT2 innovators, because that will help you for a junk diaruses as well. In fact, this is very important, because if there was somebody you initially are going to really scale up your dietic therapy and you're starting SGLT2. And as you start reassessing them on a daily basis of where they are, where their progress is, and you have to kind of take a pause and say, okay, they're 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 SGLT2 inhibitor is going to stay. and if they're not responding, obviously that's a different story. But SGLT2 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 particular patient which we talked earlier was a hypertensive, but if this was, say, somebody who is half-ref or heart failure with reduced ejection fraction and their blood pressure was low to begin with, And you really don't have many other choices. And SGLT is remarkable. And then I think the other study that came out fairly recently was also like the added effects with acetazolamide. But that study came out kind of without SGLT2s. And so just like in your opinion, I assume based on how the guidelines are written, you would favor the SGLT2 before you go to adding acetazolamide even on the inpatient side? Oh, definitely. because remember HLT2 is multifold, right? The use is multifold because you have, you know, across the spectrum of heart failure, doesn't matter what ejection fraction, now it has 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 an added benefit of providing that junk diarosis. So it is a lamide is a pure diarotic, a junk diarotic. So, you know, to choose between those two, to me, it is a no-brainer. You go with SGLT2. Now, on top of that, if you need something, yeah, it is a lamide is there. Okay. and then i just wanted to go back to the afterload reduction part that you brought up at the beginning of this uh 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 diurese and so i'm favoring that but it 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 that you're right on the money. You need to decongest. There's no questions about that, right? So because you need to relieve the symptoms. Now, that's the one because it's the total overall volume state. So that's afterloads going to help alone, but in this particular case. Now, if she was even more hypertensive, let's say she was like 170s, 180s. Now, because 150s, you don't know if she's hypertensive at this point because 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 edema, flash edema, 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 the 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 it's sometimes hard to 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 you can't change their therapy if you don't know whether or not it's working. Yeah, that's, again, a million-dollar question, and we can go from really a poor man's solution to really, you know, first-world problems, right? So I think we have a spectrum of options in our armatorium there. Simple thing, simple. Obviously, you know, unfortunately, which doesn't happen, you know, as frequently as we want, accurate in and out for multitude of 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 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 is 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 factoring those other factors as well, which sometimes we don't because we assume that everything which is changing the weight is all fluid. But again, going back to if you said the first day they came in diabetic and a couple of days you're assessing using body weight, that's a very useful marker, especially in and out. 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 artery monitors in there, And those can be useful because if they already have it, somebody who has especially high risk for readmission, 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 get you an idea of whether they are responding to it. There are some nuances in there because there's always a question about concordance and discordance in pressure and volume, but those are a little more, you know, rarer 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 old I am in training, but that's an interesting one. This episode is brought to you by the Sanford Guide. Infectious diseases cases can get complex quickly. Sanford Guide was born as an antimicrobial therapy grand rounds handout over 50 years ago to make ID treatment easy to understand. Millions of health professionals have used the guide, and it continues to grow as an essential tool that individuals, work groups, and even entire hospital systems purchase. Occasional users who find the book intimidating love the app. This isn't an encyclopedic reference to scroll endlessly, and it's not an AI-generated summary. Everything is intentionally written in a brief, high-yield format from the start. Sanford Guide experts stay on top of all the evidence and distill it into guidance that's easy to understand. Search for Sanford Guide in the app stores. And Curbsiders listeners can get 20% off the already very moderately priced yearly subscriptions directly at sanfordguide.com. Go to sanfordguide.com and use the code CURB at checkout. This episode is brought to you by Babbel. Why do most of us want to learn a new language? It's probably not about memorizing grammar tables or topping a leaderboard. It's because we want to speak it out in the real world with real people. Babbel gets you there fast. Learning a language with Babbel is all about small steps, big wins, and progress you can actually track and feel. Their bite-sized lessons fit easily into your daily routine and are also easy to remember. Just 10 minutes a day is enough to start seeing real results. Babbel recognizes that real-world connections are at the heart of language learning. Their courses are designed by over 200 language experts, real human beings, to teach you relevant words and phrases you'll actually use, so you can start speaking with confidence in as little as three weeks. Babbel lets you practice real-life conversations step-by-step without the stress. You'll build the confidence to speak up when it matters, from ordering a coffee to chatting with new friends abroad. And Babbel is more than just lessons. They even offer a large collection of podcasts where Babbel experts reveal language secrets and offer an inside look at local cultures. I just recently completed my first international trip. It was a blast, and now I've kind of got the bug. So I'm looking forward to using Babbel to maybe learn Spanish or Japanese. I haven't decided yet, but when the time comes, this is where I'll look. So however you learn best by listening, speaking, reading, or writing, Babbel adapts to your style and keeps you motivated with personalized learning plans, real-time feedback, and progress tracking. Make fast, lasting progress with Babbel, the science-backed language learning app that actually works. Babbel has over 25 million subscriptions sold worldwide and with 14 languages to choose from, every course comes with a 20-day money-back guarantee. Here's a special limited-time deal for our listeners. Right now, get up to 55% off your Babbel subscription at babbel.com forward slash curb. Get up to 55% off at babbel.com forward slash curb, spelled B-A-B-B-E-L.com forward slash curb. Rolls and restrictions may apply. one of the things and i'm just going to kind of say it because it's something that i've done in the past um 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 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 their urine output like especially the transition from the ER where that urine output is usually not as well recorded sometimes And so like I asked them how robust it was So I like were you filling these up quickly or not And I use that sometimes, especially to break ties. And I also remember, depending on your practice and your population, if you have a lot of LLE patients, geriatric patients, a lot of incontinence, people have diapers, people have pads. So those factors come in because there's no way they're going to record that. So, you know, you really, unfortunately, then you have to start like looking at how many paths that kind of change and get a rough estimate of are they 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, are they responding? that's another measure yeah and um kind of the last little elephant in the room and i think we've talked about this on one of our things we do for no reason episodes but um the sodium and fluid restriction in the hospital um i think there's something about the ras activation system like this may not be the best idea so i was just curious your thoughts on that yeah so you know that science around sodium and fluid has been kind of uh going back and forth back and forth So, I mean, I think in general, as Americans, we all have a very high sodium diet to begin with. So I think a level of restriction in the sodium is a good thing, you know, to the fine level of what that does to RATH activation. You know, in the acute setting, there's also the same kind of principles around bolus dosing was also there, bolus dosing of diuretic versus continuous. So it doesn't really fully pan out scientifically 100% because it's like if you look at the data and you have two camps on that. But I do think if somebody is 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 when they are already short of that. And 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 oncotic pressure. They need their albumin. And now they're not going to eat anything because the food is like this. So I think, you know, just common sense, making sure that they don't have a bag of chips and Lay's around or, 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 grams of sodium a day. And, you know, in my practice, if I am seeing a patient reliable, and depending on the degree of volume or 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 misbreath is admitted to the hospital. Obviously, we've been talking about that. She begins receiving her IV furosemide, and her echo reveals that her EF is 30% with signs of left ventricular hypertrophy and mild to moderate mitral regurgitation. 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. So I think this is something important as you talk to the patient and, you know, you're the front line, you're talking to 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 ejection fraction, which is EF of 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 maybe improved EF or totally, you know, recovered EF. Well, we don't say recover anymore. And I'm sure Michelle, Dr. Kittleson, talked about this in her discussions with you as well. So that's number one. So heart failure with reduced restriction fraction. Then you also classify the stage of the cardiomyopathy. So starting from early 2000s, AHACC started classifying all these cardiomyopathies in stage A, B, C, D. And now we updated them a little bit more. We call it, you know, at risk 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 reduction fraction. Now, in her case, you know, just based on the presentation, she's also hypertensive and she has left ventricular hypertrophy. So there's likely etiology, again, as you're working diagnosis, 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 valvular abnormalities at this stage? Or would you kind of keep going down just worrying about the heart failure, decongesting her and treating the heart failure and worrying about this new valvular insufficiency kind of from the outpatient side? Yeah, that was a great question because remember, we talked, referred 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 decongest 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 leaflets. if there's any structural or anatomical defect, or is it just functional mitral regurgitation? So that would also, 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 associated with it. You're using, you know, decongestion, 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 this point? 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, kind of platform, which is beta blockers, SGLT2 inhibitors, neprolysin inhibition with ARBs, or, you know, angiotensin-receptor blocker combination, and our V, as we commonly call There's ARNI, and the last one will be an aldosterone antagonist. 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 your consistent 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 pulmonary edema, depending on the renal function, blood pressure, you have ARNIs, beta blockers, and then you have the ultrasound antagonist. Now, what I would say is the aldocenidin 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 kind of agent diarosis on top of everything. And it's much more tolerated at the 25 milligram dose at the beginning dose. And especially as you're also dilusing people and they tend to get hypokalemic, it helps with 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, outpatient as well. And then would you say beta blocker tends to be last given, like, usually trying, like, if you're decongesting and concerned for? So if congestive heart failure is the initial thing, so that would be towards the last one before prior to discharge and when they're kind of uvolemic 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 discharge on the way out of the hospital. You really want to see, give a little time period to see if they tolerate it well. And then, you know, at least 24 hours in advance before the discharge. And then I guess in this era where I think like ARNIA is becoming, I feel like, the goal to start that, those you would still try to start early if blood pressure could tolerate? 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 there's kind of, you know, within acute heart failure, also there are three different trials kind of looking at that. And in the Pioneer HF, there was, which was kind of supportive for the role of ARNIs within. The in-hospital state was shown to be a beneficent. 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 washouts. They had, you know, on Enalpiril and other agents. And then they were kind of included in trial. And if you look at the degree of hypotension is much higher with ARNIs 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 in you, because when you're actively diarusing them or, you know, decongesting them, there may be some fluctuations. So just be careful on starting that medication because then the next thing happens a lot of times in practice is people get so scared with the creatinine changing and they stop everything. And then the diabetics get stopped too. So what I would say is if you still are very congested and you're normal tensive, you first decongest the patient, use your SGLT2. If you really need, you can use aldosterone early on as well. And then as you are now shifting from, you know, whether continuous infusion to a bolus or bolus to oral strategy for diuretic, that's the time to start that ARNI. Okay. That's helpful. Yeah. I think actually they went through this similar thought process on the Dr. Kittleson episodes, especially about the renal function stuff. It's almost like, I think, and they referred to Dr. Top's episode about it, who's a nephrologist, and talked about how, like, you almost just don't want to check certain things. And that's more outpatient, but very helpful to walk through again. How does this change if this is HFPEF? Like, the sequence of what I start, 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 are some nuances in there based on gender and injection fraction, male versus female, especially as it relates to ARNIs. But SGLT2 is across the board. All genders are EF. So I don't think there's much difference when it comes down to an acute heart failure, whether you have HF-REP or HF-REP, you're using the diuretic, and then you can straightaway go to SGLT2 alongside. So that would be the strategy. Now, after that, then the nuances come in, depending on, you know, ARNI based on gender and injection fraction. For women, across the whole range of injection fractions, you can use an ARNI. For men, EF of less than 60% is where the biggest benefit has been for ARNIs. Allosterone antagonists, you know, clinically, even though the guidelines give the two recommendations for more driven towards reducing rehospitalization, We know that evidence from some of the subgroups and also real-life factors that they're very helpful to reduce re-hospitalization and achieve more direct, and especially if somebody is hypokalemic as well, to improve the potassium levels too. So that really is useful there. And then beta blocker is very different compared to HEFREF. So the role of beta blocker is there is no really a direct role of beta blocker in HEFREF unless there's another reason. So if somebody has arrhythmias, atrial pepillation, or ventricular arrhythmias, or PVCs, or they may have coronary artery disease. So there's another primary indication for a beta blocker that would be there. Then you would use that. But compared to HFREF, 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 etiologies. And obviously, this patient has a lot of risk factors for coronary disease. I assume she needs an ischemic 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, let me get them decongested and started on these meds, and then they can get that as an outpatient? So, yeah, so that's the question about ischemic evaluation. That's the one which comes up all the time. So first thing, it should be predicated to what are the risk factors. So not everybody wants or warrants ischemic 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, you know, now you have hephra, whether it's hypotensive or, you know, depending on where your practice is familial, not everybody really needs to run into an ischemic evaluation. and even the guidelines are pretty clear on that. But if you have risk factors and then, you know, 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're 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 revascularization, especially if they have no symptoms? Because that's where that topic comes up. 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 routinely at Kashuk Memorial will do ischemic evaluation on patients who have risk factors, especially because we also serve a lot of underserved patients. So from a totally logistics perspective, it's easier for them to get it done while they're there. But it's okay that if their risk factors are not much and 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 ischemic evaluation, does it have to be a cardiac catheterization? No. And today's day and age, not necessary at all. Again, depending on your pre-test probability and age and everything, what else is going on to somebody, you do not expect too advanced 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 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 ischemia. So if you're really doing a true evaluation, it should be either a CTA or a cardiac catheterization. Okay, 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 its 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 medical therapies early, but being cognizant of their other comorbidities. And so it seems like kind of across the board, reasonable to start SGLT2s early, often on these patients and everyone else. You're going to kind of have to be considerate 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, Moni? No, SGLT2s for everyone. I know. I think it was at SHM we were like, oh man, SGLT2 is having a party. And I just feel like we're reiterating that on this episode. The ride continues. Yeah, the HLT2 is a stat in for heart failure. I'm going to be putting it in the water soon. It's a t-shirt right there. All right. I'll advance the case. So on hospital to day three, Miss Breast's condition worsens. Her blood pressure is now 95 over 60. Her heart rate's 120, and her oxygen saturation is 92% with two liters. And her urine output has significantly declined 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 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. well. 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 inotropes, which I can't start on the floor. So are there situations, so that to me 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, it all will depend on 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 diaroses? It's 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're in low output failure. So those are two things which go hand in hand. Their 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 worry that maybe, oh, maybe the diuretic is causing the low blood pressure. We start holding the diuretic in these patients. When the answer is, you know, supportive therapy of blood pressure, whether inotropes, 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 neurohormonal agents, which may have been started on. So making sure that we stop those. Because that's kind of sometimes is because there are new therapies, they've been started on them, and now they're hypotensive as well. But in this particular case, if you, you know, 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 artery catheter as well as, you know, inotropes or pressors, 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 may need an inotrope or something else alongside for renal perfusion too. Okay. And how do you think through which ones to start? I know I getting bold as hospitalist here but which ones to start and then is there any to avoid in this situation Yeah I mean because here you are doing empiric right Right now because assuming that you don have a swan you don have a right cat on them So you doing empiric therapy assuming they are low output failure. So you want it depending on the blood pressure. If they are totally hypotensive, if they are like getting hypotensive, they have lactic acid doses from the hypotension, you really need to maintain their blood pressure and perfusion, which is across the board. As much as we hate that, you need a kind of a vasopressor, you know, and that's going to be your first one, just to maintain the blood pressure above a certain map. From an inotropy perspective, you can do, you know, if you are hypotensive, 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 melanin or dubitmin, depending on, you know, if I am suspecting that's low output failure in a cardiomyopathy patient, those are the two ones I would usually go to, melanin or dubitmin, again, depending on blood pressure. If they're already hypotensive, melanin is not going to be tolerated well, or if they are very tachycardic, you're not going to, you know, tolerate these either dobitamine or dopamine or even melanin 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, arrhythmia or 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 hypotensive. but if this could be somebody in shock and hypertensive, goes back to, Meredith, your vasodilator story, and that's where you would use things such as nitroglystin and nitride. Again, not possible on the floor because no floor will allow you to start a nitroglystin and nitride across the, I don't think, anywhere across the board, but that could be an option. If somebody was in shock, their lactic acid is going up, They're in pulmonary edema and they still are, if you really, and they're still very hypertensive and that's the case where you would use a pure, pure visotilator. Definitely thankful we don't work in an open ICU, but there are certainly hospitals that, hospitalists that do. So I think that's helpful to have that conversation. 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 when that is actually the most helpful to you as like trying to figure out what's going on and 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 a patient you're upgrading to the CCU or 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 one. Now, 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 are getting hypotensive. Or you have to peel back on therapy. They came on therapy. This is acute on chronic heart failure. They're already on good medications to begin with. You're just diuresing them, doing, you know, all the things. And now, suddenly, you're peeling off medication. So this is where you should really think about, okay, why am I having to cut back on medication or stop medication? Or they're not responding to your dietic 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 foot cat. Okay. So let's go back to Ms. Breath. She briefly requires her stay in the CCU. She gets her inotropic 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 air. Edema 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, you know, assuming this was all cardiogenic shock from low output failure, and, you know, somehow she was in 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 you're going to start medication. So again, the most tolerable medication would be an SGLT-doinnovator. And then depending on your blood pressure, you could do Alderson antagonist. If your blood pressure is reasonable, you can add an ARNI. I will be a little cautious on introduction of beta blocker at this point. If they were truly in shock, they were in ICU on inotropes, 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 is she going to be in there, what else is going on. But, you know, if she's 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. But now if 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 titrate them higher on the medications that they can tolerate? Yeah, no, this is an absolutely super important question. And it's being addressed everywhere, you know, again, in documents, on the podiums, on everywhere, because more and more evidence is that low dose of all is much superior than higher dose of a few. because you think about it, you're addressing different pathways. So you're getting incremental benefit, additive benefit of different pathways of blockade or 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 merrier would be the principle. 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 answer that. Yeah, that's definitely the one. I think the reason that Meredith 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 readmitted with like presyncope. And I, you know, I sent them out on all these medications and it's probably just like probably not happened very often. But that's the one. 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 because I think it happens. it will happen and I think that's where nuances will come in nuances like you got to look at the patient age you know what else is going on is there something which is causing the autonomic dysfunction are they dehydrated so what happens is it goes back to what we had initially talked about you know you started as glt2 in the past we didn't have that now you have glt2 and can give a pre-protein diuresis you started the albastro antagonist in the past you know if you look at the Medicaid data, anywhere 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 going to help you with diuretic too. 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 ARNIs are going to help also with the after low reduction, accentuate your diarcesis. So as you are getting those three glasses 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 want to 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 durations around the world for heart failure. And the duration of heart failure stay is 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, the four classes, and by the end of one year, a majority of them were either not on medication or there was a reduction in dose. Two-thirds 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 presyncope. It's usually because we didn't address the diuretic dose before they went out. And we, you know, maybe we adjusted the dose the day off and 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 like 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 like the other guideline therapies. And I think because of the recent studies kind of recommending, you know, 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 you know there's other things the things you can do is uh obviously you know you have to be careful with the age the octogenarians and and you have to be careful because you know 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 you you know one size doesn't always fit all even though we we want that thing to happen other thing you can do is uh the you You know, you can always do orthostatic vitals on these patients, especially the elderly patients before discharge. We'll kind of get you an idea other than just clinical exam, which we don't utilize orthostatic vitals as much because usually that's what kind of makes them fall in is that orthostasis. So that will also get you a little bit more comfortable whether they are, what's the volume 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 up, 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 a 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 Kashluk Memorial, we actually do. And I think a lot of the centers who are now focused on quality of care around readmissions and everything are investing in those systems. We actually have our patients seen in our discharge clinics by our care providers and, you know, extenders and APPs within a week of discharge. So they are, unless there's 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 on blood pressure, getting their blood work done, making sure they're no renal injury or hypotermia or anything like that. I think one of the things that caught me off guard early when we were kind of implementing all these new guideline-directed therapies was this washout period for 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, that's for another episode, but specifically about the washout period. So the washout period is very important. I don't think there's any question about that, especially coming off an ACE into an ARNI, because there's an actual risk of, you know, angio-dema. 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 issue, 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. So 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 ARNI. 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 ARNI has become kind of prohibitive for a lot of patients, I think. And so just kind of keeping that in mind is important. And obviously, we have other options that aren't as good, but obviously, it's better than not having anything at all. Yeah. So, you know, and that's actually what even the guideline writers acknowledge that, that, you know, because of different either side effects or costs could be a factor in some patients. If that's withstanding those two factors, everybody should preferably an RNA as 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 cost for patients after that. So that's definitely there. But that is still a problem, which can be for some people that much amount as well. In that case, making sure they are on an R-bit set. But they are assistance programs, you know, I think. And that's kind of key is, you know, working with the case managers, the transition coordinators or outpatient clinics to make sure you can tap into those assistance programs. because whether from the vendor itself, whether from, you know, if somebody cannot really afford to cover the cost of it, we actually 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 try to stress with my teams 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 going to be low because there's so much going on that time. So it's not just once and done kind of, you know, deal. this is an ongoing journey and ongoing effort. And this is where that team effort comes in between inpatient and outpatient teams. And if obviously they're 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 medication's perceived side effect could be. Because that's where a lot of the discontinuation 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 what I find very commonly is when you talk through and you explain to 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, dizziness sometimes, and especially in your hormonal blockers, if they're 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 prognosis. 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 scary thing to kind of start with. But then also utilizing your pharmacist, depending on, again, each system, there may be pharmacists, there may be care coordinators, there may be social workers, bedside nursing, all of them. So having different layers of education is important because one person, just the cardiologist, the hospice is not enough because that's just, you're going in, you're talking, it needs recurrent reinforcement of the diagnosis, the change in lifestyle, all those kinds 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, depending on the system, there'll be things such as community navigators. We have community health workers. We should go to the house right after discharge, 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 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 maybe your three take-home points for the listeners from what you want to make sure they take away from this episode? Yeah, I think one other thing is, I would say decongestive therapy. You've got to go aggressive. If somebody's all overloaded, just don't, I say, don't massage the same thing till death. Escalate therapy quickly. If non-responsive, go to the next level. So if it's bullous, then increase the frequency if it continues, but do something different, number one. Institute, some of those medication classes we talked about early on, especially HGLT2 as we talked about, they are, you know, you can really strategize based on blood pressure, you know, whether MRAs. It's not like one or none kind of phenomena. There's a gray area in there. So if you cannot tolerate ARNIs or beta blockers, you still can do HGLT2 and MRA. 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 transitional period, making sure patients have the right medications, that the doses are if somebody was already on before and now they really know what they're going home on. they didn't really have those, if there's a possibility, have those medicines at bedside. If they don't have it, making sure that when the pharmacy you're sending it, they have those medications. A lot of times we send patients home and, you know, they get, we send them to the pharmacy. A lot of pharmacies may not even have the medication or they need a prior authorization. And so patient shows up to the after discharge and there's no medications now. And then we know what that results in. So that's kind of what I would say. Awesome. This has been another episode of The Curbsiders, bringing you a little knowledge food for your brain hole. Yummy. Still hungry for more? Yep. Join our Patreon and get all episodes ad-free, plus twice monthly bonus episodes at patreon.com slash curbsiders. You can find show notes at thecurbsiders.com and sign up for our mailing list to get our weekly show notes in your inbox, including our Curbsiders Digest, recapping the latest practice-changing articles, guidelines, and news in internal medicine. And here at the Curbsiders, we're committed to high value, practice changing, knowledge, and to do that, we need your feedback. So please email us at askcurbsiders at gmail.com. It also helps a ton when you subscribe, rate, and review the show on YouTube, Spotify, or Apple Podcasts. A special thanks to our writer, producers for the episode, RJ Blackburn, and to our whole Curbsiders team. Our technical production is done by the team at podpace elizabeth proto does our social media jen waddo runs our patreon chris the two manchoo moderates our discord stewart brigham composed the theme music and with all of that until next time i've been meredith trubit and as always i've been moni amin thank you and good night Thank you.