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Evaluating Approaches to Fluid Management in Acute Heart Failure: Current Challenges and Novel Perspectives

  • Authors: Gregg C. Fonarow, MD, FACC, FAHA, FHFSA; Marat Fudim, MD, MHS
  • CME / ABIM MOC / CE Released: 3/16/2023
  • Valid for credit through: 3/16/2024, 11:59 PM EST
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  • Credits Available

    Physicians - maximum of 0.25 AMA PRA Category 1 Credit(s)™

    ABIM Diplomates - maximum of 0.25 ABIM MOC points

    Nurses - 0.25 ANCC Contact Hour(s) (0 contact hours are in the area of pharmacology)

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Target Audience and Goal Statement

This activity is intended for cardiologists, primary care physicians, emergency medicine physicians, nurses, and nurse practitioners.

The goal of this activity is for learners to be better able to recognize the clinical importance and challenge of optimal fluid management in the setting of acute heart failure (HF) and evaluate novel approaches to outpatient fluid management using noninvasive radiofrequency technologies to detect early evidence of HF decompensation to reduce hospital (re)admissions and improve patient outcomes.

Upon completion of this activity, participants will:

  • Have increased knowledge regarding the
    • Ability to recognize the clinical importance of optimal fluid management in the setting of acute heart failure (AHF)
    • Use of noninvasive pulmonary fluid level monitoring for the management of AHF


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  • Gregg C. Fonarow, MD, FACC, FAHA, FHFSA

    Chief (Interim), UCLA Division of Cardiology
    Director, Ahmanson-UCLA Cardiomyopathy Center
    Co-Director, UCLA Preventative Cardiology Program
    The Eliot Corday Chair in Cardiovascular Medicine and Science
    Los Angeles, California


    Gregg C. Fonarow, MD, FACC, FAHA, FHFSA, has the following relevant financial relationships: 
    Consultant or advisor for: Abbott; Amgen Inc.; AstraZeneca; Cytokinetics; Egnite; Janssen; Medtronic, Inc.; Merck; Novartis; Urovant Sciences  

  • Marat Fudim, MD, MHS

    Assistant Professor of Medicine
    Cardiologist and Advanced Heart Failure Specialist
    Duke University Medical Center
    Duke Clinical Research Institute
    Durham, North Carolina


    Marat Fudim, MD, MHS, has the following relevant financial relationships: 
    Consultant or advisor for: Alleviant Medical; Axon Therapies; Audicor; Bodyport; Boston Scientific; Daxor; Medtronic, Inc.; ZOLL
    Speaker or member of speakers bureau for: ZOLL
    Research funding from: Bayer; Bodyport; Verily
    Stock options from: Alleviant Medical; Daxor; Prehealth; Vironix


  • Joy P. Marko, MS, APN-C, CCMEP

    Senior Medical Education Director, Medscape, LLC


    Joy P. Marko, MS, APN-C, CCMEP, has no relevant financial relationships.

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  • Leigh Schmidt, MSN, RN, CNE, CHCP

    Associate Director, Accreditation and Compliance, Medscape, LLC


    Leigh Schmidt, MSN, RN, CNE, CHCP, has no relevant financial relationships.

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Evaluating Approaches to Fluid Management in Acute Heart Failure: Current Challenges and Novel Perspectives

Authors: Gregg C. Fonarow, MD, FACC, FAHA, FHFSA; Marat Fudim, MD, MHSFaculty and Disclosures

CME / ABIM MOC / CE Released: 3/16/2023

Valid for credit through: 3/16/2024, 11:59 PM EST


Activity Transcript

Gregg C. Fonarow, MD, FACC, FAHA, FHFSA: Welcome to the program, "Evaluating Approaches to Fluid Management in Acute Heart Failure: Current Challenges and Novel Perspectives." I'm Greg Fonarow, director of the Ahmanson-UCLA Cardiomyopathy Center and a professor of cardiovascular medicine at UCLA, and I'm joined by Marat Fudim, who is an assistant professor of cardiology at Duke University and also part of the Duke Clinical Research Institute. Welcome, Marat.

Marat Fudim, MD, MHS: Excited to be here.

Dr Fonarow: So we're going to be discussing noninvasive pulmonary fluid level monitoring in the management of worsened heart failure, also referred to as acute heart failure, and really talking about the burden of congestion, the role that it plays in the pathophysiology of these patients, some of the challenges of detecting fluid congestion, some of the latest in management strategies and, most importantly, detection strategies in this important patient population. I think as you all know, there are challenges in managing heart failure.

This condition is very common, is costly with hospitalizations and rehospitalizations being tremendously expensive. We have new drugs and devices to manage these patients. But really integrating this into care has been a challenge. We see a large number of hospitalizations that continue to rise. About 1 in 4 patients are rehospitalized within 30 days after a heart failure hospitalization. There's a high mortality risk. So even despite the additional medications we have to manage these patients, there are these incredible challenges.

Now, one of the things that's been recognized why patients with heart failure have multiple comorbidities are lots of processes that drive the pathophysiology can lead to decompensation and ultimately hospitalization or other types of worsened heart failure events. This really incredible role that congestion plays. So that volume overload, the systemic congestion, specifically pulmonary congestion, elevated pressures being a key trigger for that worsening or decompensation of heart failure.

And so detection of congestion, particularly early, is so critical for potentially being able to intervene prior to hospitalization or to adequately treat patients to prevent rehospitalization or re-decompensation of heart failure. So Marat, from your perspective, really, is congestion literally that key element that's driving so many of the decompensations that lead to hospitalization?

Dr Fudim: Yeah, for sure. I mean, I think maybe to take a step back even is that congestion is, everybody thinks of congestion, and has probably something different in mind. I think congestion probably as you hinted towards, could indicate a fluid overloaded state. But in many cases it's simply the state of the heart being under strain. This might be a high-pressure state. It might or might not actually be associated with significant volume overload. And maybe we'll talk a little bit about it later. But the truth to that is, at the end of the day when the patient presents the emergency room or to that clinic with complaints of shortness of breath or the inability to lie flat or swellings, that somehow that body decompensated and has now reached a state that is overloaded.

But it can mean a lot of different things. And I think when we talk about technologies is that many different technologies measure different things. So congestion means different things, and technologies measure different things. So it doesn't have to mean always the same thing. But yes, the universal truth is when that patient hits the emergency room, he or she is congested.

Dr Fonarow: And I think one of the things that technology's given us insight to be able to look back on those patients that have had various forms of monitoring, that we can often see it is in days to actually weeks prior to that decompensation that's so overt leading to hospitalization that you are starting to see subclinical elevation in filling pressures, or subclinical rise in that the volume, or other ways of detecting congestion, to where we could get a window with accurate detection to be able to intervene in a way to prevent the patient getting to the point of needing to present to the emergency room or needing an urgent outpatient visit.

So that understanding, that recognition early of congestion can be so important. But we realize there these incredible challenges if we look just by a traditional history and physical exam or monitoring daily weights, it doesn't have that sensitivity or specificity that we really need to be truly actionable. Now, your point about how congestion is really at a central theme, we've seen so many data points directly and indirectly that when no matter how you detect congestion, it's associated with worsened symptoms, higher risk of hospitalization rate, hospitalization and mortality, whether you define that by overt physical exam findings, whether you define it by pulmonary congestion on x-ray, whether it's assessed through biomarkers or more directly measured with planted hemodynamic sensors or noninvasive detection. So there's clearly symptomatic and prognostic significance to congestion. So we've got it as key characteristic, it has prognostic significance. Maybe you can tell us a little bit about some of the underlying thoughts of what are those triggers to congestion and then a little bit more of the technology that we can use to detect it.

Dr Fudim: Well, I mean you touched on so many great points. I think one of the greatest insights gained in the last 10, 20 years is like you said, that we get a window into the decompensation process quite early in its course. We just have to have the right sensors or the right measurement tools. Let's talk about what the current state of the art is. The current state of the art is that we rely on symptoms to be present for us to act on congestion and identify congestion. So it's a patient-triggered event, right? The patient calls us and tells us about the swelling or the shortness of breath, yet we know that that process probably starts weeks to months ahead of time. And that insight was provided to us really from data from intracardiac and intrapulmonary pressure sensors. There's been a lot of technologies along the way from many different companies.

The most contemporary one is the CardioMEMS™ device. It is an implantable tool that you place into a pulmonary artery. But tools of that nature have told us that pressures in the pulmonary and cardiac system increase as early as 6 weeks prior to the decompensation event. And we're not talking about 10 mm Hg, no, no doubling of pressures. We're talking subtle changes of 1, 2, maybe 3 mm Hg. But that in itself is highly prognostic of decompensation. So the paradigm shifts from relying on patient-reported signs and symptoms of decompensation to maybe even worse where we often rely, and still practice that we tell people, and you and I probably still can be accused of that, tell patients, "Call us when your weight is up by X amount of pounds or kilograms." The problem with that is that over half of the population presenting for heart failure decompensation actually does not have any significant weight gain.

So if patients are waiting for a sign to occur that will never occur and yet develop a form of congestion, we've got to ask ourselves what is driving congestion? I think that comes to your question of pathophysiology. So the thought process is that first of all, there's probably many ways you can get to a congested state leading to the measure. One of the key drivers is, yes, if your kidneys are struggling to get rid of the water and the salt because they don't get enough blood flow in the setting of a poor outflow state, or because they're getting slowly congested through right ventricular (RV) failure, then you have pure salt/water retention. So this is a kidney-driven hypothesis of how we get to the state of decompensation. In all of that there's a neurohormonal hypothesis, you know, when the body starts sensing inappropriate perfusion of the organs, it drives up hormones such as the RA systems, the renin-angiotensin system, that is retaining salt and water.

So you hear me talking a lot about salt and water, but very important is something that I personally do a lot of research on is, well, it's not just about salt/water retention. A lot of that is actually about vasoconstriction, as well. And surprise, surprise, many of the drugs that work in heart failure that many of those you have investigated, well, those drugs are in many cases actually blocking neurohormonal activation, block the harm done to the organ system. But really the primary effect is, in many cases, vasodilation or remodeling of the heart rather than a pure diuretic effect. And so if you vasoconstrict the arteries and veins, you can have just the same impact on congestion as dumping water into the tank or dumping salt in the tank. So it's multifaceted, and that makes remote monitoring or ambulatory management of heart failure patients actually quite complex because there's no one, in my opinion, no one right decision or action for one alert.

I think we need to learn a lot more about our alerts and how to act on alerts, because not every alert means that it requires a diuretic or requires a vasodilator. So maybe we get to talk a little bit more about that. But technology-wise, I think that as we recognized that pressure elevations occur early, signs, retention of microscopic amounts of water in the lungs occurs early, which is nothing else than a pressure retention, right? If the pressure goes up it starts extravasating water into the lung tissue. In a perfect world, we measure everybody in the renin-angiotensin-aldosterone (RAAS) system. Everybody gets neurohormonal testing every day. That has been sort of tested in the N-terminal pro b-type natriuretic peptide (NT-proBNP) studies as maybe panned out as much to prevent heart failure hospitalizations. But those would be the earliest signs and symptoms we can act upon. But then we can also go for bio-vitals such as heart rate and blood pressure.

Those are the more overtly noninvasively, obtainable strategies. And I think around each biometric you could think of, there's now been 20 devices developed. And what I always say in this setting, technology is no longer the limitation. Google and Apple, if there's something we can measure, they're going to make a tool around it. It's going to be small and it's going to be connected to the Cloud. So everything can be done from a bio-vital standpoint. The hard part is that how you actually integrate that signal and then act on that signal, because data that you don't act upon is worthless. So we can measure as much ambulatory blood pressure and pulmonary pressure as you want to, but if nobody acts on it, then I think it is a whole different story.

Dr Fonarow: So what do you think is some of the most promising noninvasive technology that provides data that's truly actionable that the clinician and patient can feel reliable enough to make changes in medications early?

Dr Fudim: Yeah, that is a good question. I mean, right now, probably the most used non-invasive remote monitoring tools, either standalone or combination, are actually blood pressure cuffs and weight scales, believe it or not. I mean, we made them wireless, we made them interconnected. And when arming clinician providers with this, there's some evidence to suggest you can actually improve outcomes, including in our practice. The other technologies that FDA approved and have been used successfully, I wouldn't say in every practice because I think it takes some dedicated staffing to make things happen, is the ReDS™ vest, which is one noninvasive lung measurement technology. Another one is the BMET system called μCore™, which is a patch-based technology that measures also lung water content. ReDS™ and the μCore™ technology do it slightly differently, but the outcome is the same. They are measuring how much water you have on your lungs and do it quite well when you, for example, compare it to a computed tomography (CT) scan, because the gold standard to measure water content on the lungs is just to send people in the CT and then tell you exactly how much water is in your lungs.

So those are some of the technologies that are out there, and FT approved, that can be used, and are used, clinically in a noninvasive fashion to measure decompensation. Other metrics or other tools, technologies that now take that blood pressure cuff and the heart rate and SpO2 sensor and now put that now in watches, put it now in small patches. There have been a lot of those technologies. They're currently getting tested to see whether they can predict a decompensation. Well, if your heart rate jumps by 20 points over a 40-hour period, you know that you probably [have] trouble. And same thing with a noninvasive blood pressure that you might have, or the SpO2 going down. So I think that's how it works. Those are not very specific signs and symptoms. The hope is that through the combination of those sensors, you will be able to derive a true signal for heart failure vs this is chronic obstructive pulmonary disease (COPD) exacerbation, but I think that data is still out there. We haven't proven that quite yet, that efficacy.

Dr Fonarow: Yeah, I think you've really highlighted there's this great evolution going on in the technology. But then that next stage is going to be how do we truly integrate that into the disease management for these patients where we're engaging patients or caregivers in the care team to where they're acting on that data in a way that will produce safe and effective alterations in their therapy, whether that's adjusting some of their guideline-directed medical therapy, their diuretics, sodium intake, be able to monitor their response to that, and manage them truly proactively in a way that's going to lead to better quality of life, functional status, as well as preventing unplanned emergency room visits, hospitalizations, urgent care visits. And we're on the cusp of that technology, but truly bringing that together in a way that will allow us to really proactively, effectively manage these patients beyond the sort of reactive management that, you know, you described waiting for the patient to call with worsened symptoms or show up in an outpatient center where they're clearly decompensated and where you have no choice but refer them to the emergency room.

So it's a really exciting time. It's been great discussing with you these technologies and the role that congestion plays here. So, thank you so much, and thank you for participating in this activity. Please complete the post-evaluation.

This transcript has not been copyedited.

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