All right, well, good evening, everyone. Welcome or welcome back to Heart Failure Search Virtual Bootcamp. Tonight is day three, which is management parts one and two. So we're gonna be concluding our series, our bootcamp series this evening. So we're so glad that you've joined us. So on behalf of the program chairs, I'm Jennifer Cook from the University of Cincinnati where I serve as a section head. And I also am the chair of the Education Committee for Heart Failure Society of America. With my program chairs here with Dr. Mallory Maragian that's going to be speaking with us this evening. And then of course, you've seen both Terry and Franny earlier in the series. And we have Courtney Schakowsky this evening with us tonight as well to discuss management. So this evening, we're gonna be getting started with opening remarks and introductions. And then we're gonna have some audience response questions followed by didactic presentation and then question and answer. And then we'll do it all over again with prepared questions, didactic and then question and answer. And then we'll wrap up the evening right on time. Just a reminder to everyone that after we're finished with the recording of this session tonight, the entire bootcamp series will be available on demand in the Heart Failure Society of America Learning Center. And to access it, you log on to the Heart Failure Society of America Learning Center and click my courses and you will have access to this enduring material based on your registration for the series. And so now we'll move on to our first set of audience response questions. And we have Mallory joining us. Okay, good afternoon everyone. I have the first question here will be which of the following does not represent a social barrier to implementation of appropriate heart failure management? Is it A, lack of social support, B, financial burden of heart failure treatments, C, abnormal renal function or D, transportation limitations? Let's go ahead and move on to the next question. Okay, moving on to question two for the management part one, which of the following should prompt a referral to an advanced heart failure specialist? Is it A, a systolic blood pressure above goal despite maximally tolerated guideline directed medical therapy, B, recurrent heart failure hospitalizations within the past year, C, persistent NYHA class two symptoms or D, need for lower diuretic doses over time? Okay, let's go ahead and move on to the next one. Okay, question three, which patient would most likely be a candidate for cardiac transplantation? Is it A, a patient with a 10-pack year smoking history that quit two years ago, B, a patient with cancer and a life expectancy less than two years, C, a patient with pulmonary hypertension and a pulmonary vascular resistance of six woods units or D, a patient with severe peripheral vascular disease and A1C of 9.1%. Okay, we can move on. And then question four, which of the following would be the most appropriate to counsel a patient on regarding heart failure self-care? Is it A, to avoid regular physical activity to prevent symptoms, B, restrict dietary sodium to less than 1.5 grams per day, C, monitor symptoms regularly and know when to call your provider or D, maintain strict fluid restriction to less than 1.5 liters per day? Okay, great. So we can go ahead and close that poll and move on to your presentation now. This is great to get our minds flowing and ready to go for our learning. And we're gonna be coming back to these questions after the presentation to test our knowledge again. Thank you. Hello and welcome to management part one of the HFSA HF-CERT virtual bootcamp. My name is Mallory Maragian and I'm a cardiology clinical pharmacy specialist at the University of Maryland Medical Center in Baltimore, Maryland. Here are our program chairs for the virtual bootcamp as well as our program faculty. I do not have any conflicts of interest to disclose. During the management part one portion of this virtual bootcamp, we will focus on overall management and trajectory for heart failure rather than focusing on the specific treatment options and interventions which will be covered in management part two. More specifically, we'll focus on management of patients with symptomatic heart failure. So when looking at the ACC AHA stages of heart failure, we're really talking about stage C, which is patients with structural heart disease as well as symptomatic and symptoms of heart failure and patients with stage D, which are patients that have more advanced symptoms that are refractory to medical management. This image illustrates the typical disease course for a patient with heart failure with time on the X-axis and physical function on the Y-axis. A patient will present with initial drop in physical function or decompensation, which may coincide with the initial diagnosis of heart failure. Patients then hopefully will reach a state of clinical stability where the guideline directed medical therapy is optimized and they reach their baseline physical function. However, over time, heart failure is progressive and patients will likely ultimately start to have decompensations where they don't necessarily get back to their functional baseline and no longer respond to or not able to tolerate guideline directed medical therapy or GDMT and they move towards stage D heart failure. We will first discuss the management principles and best practices during stage C when the goal is really to maintain clinical stability. When thinking of heart failure management following that initial diagnosis or decompensation, it can be thought of as three phases. So after that initial diagnosis or decompensation, a patient will move into the transitional care phase where the patient transitions from inpatient to outpatient management. Then the patient will move to an intensification phase where the patient is followed up very frequently and is titrated to target doses of guideline directed medical therapy. Then the patient will move to stabilization phase where the patient establishes and maintains clinical stability. Jumping into the transitional care phase, we really care about this phase a lot because it is a complex time for the patient and a lot of errors and omissions can occur during this time. So creating a strong transitional care plan prior to discharge is critical and should be communicated with the patient and caregiver as well as their outpatient provider. Some components of the transitional care plan should include identifying precipitating causes of worsening heart failure, volume assessment and plan for adjusting diuretic therapy, coordination of safety laboratory checks, any further changes to guideline medical therapy that might be planned for outpatient, identifying and addressing if possible any barriers to management, as well as providing heart failure education on lifestyle modification, self-care measures and medication on adherence. In order to ensure a complete transitional care plan and establish discharge checklists such as the AHA Target HF Discharge Checklist may be useful to use, or some institutions will develop an institution-specific checklist that is tailored to their needs. Once a patient has transitioned to follow up with an outpatient provider, the intensification phase begins. During this time, titration of guideline-directed medical therapy, and when I say guideline-directed medical therapy or GDMT, I'm really talking about RAS inhibition, evidence-based beta blocker, mineralocorticoid receptor antagonist and SGLT2 inhibitor, titration to trial-defined target doses should be prioritized. This is a class 1A recommendation in the ACC AHA guideline, and use of all four classes has been estimated to reduce all cause mortality by 73% compared with no treatment. The sequence of initiation of the four classes should be based on patient characteristics and not based on the sequence of trial publication. The intensification phase generally takes two to four months, and during this time, a patient should be evaluated frequently, as frequently as every one to two weeks, either in a physical clinical visit or via tele-visit. And during this time, patients should be evaluated based on their symptoms, their vital signs, their functional status, their physical exam, as well as their lab abnormalities to see if GDMT can be titrated and initiated. Patients may also need adjustments to their diuretics during this phase, so a thorough assessment of volume status should also be attained at each visit. The intensification phase continues until no further adjustments are tolerated or needed for guideline-directed medical therapy, and patients reach a uvolemic state. The stabilization phase occurs around three months or may take longer, depending on the patient's ability to follow up and tolerate guideline-directed medical therapy, as well as their ability to maintain a uvolemic state. At this point, follow-up can shift to every three to six months, and with the patient maintaining good self-care practices in the meantime. Also during this phase, ongoing assessment and referral to other specialties can occur as needed, such as referral to palliative care or electrophysiology colleagues for device therapy. At each phase of management, it is important to recognize and address high-risk characteristics or barriers that may be associated with poor discharge clinical outcomes. Some medical barriers and social barriers are listed on this slide. So medical barriers can include patients with cognitive impairment or depression, if they have active substance use disorder, frailty, or abnormal either renal function or hyperkalemia, which may prevent up titration of certain medications. Social barriers include things such as financial burden of heart failure treatments, if the patients have food insecurity or housing insecurity, if there's a language barrier or patients that have low health literacy. Patient education and counseling on heart failure self-care is also crucial to optimizing appropriate management for heart failure. Patients with heart failure and more effective self-care behaviors have better quality of life and lower all-cause mortality and readmission rates than those that have lower levels of self-care. And meta-analyses evaluating this found that self-care interventions and multidisciplinary management teams that focus on enhancing heart failure self-care actually reduce time to heart failure-related hospitalizations and all-cause death. And they improve heart failure-related quality of life. So really crucial to ensure that patients have really great heart failure self-care. Heart failure self-care can be thought of as three key concepts. And it should be noted that heart failure self-care really applies to any patient with heart failure, regardless of their left ventricular ejection fraction. So first we have self-care maintenance activities. And these are activities that are meant to maintain stability such as taking or adjusting their medications, engaging in physical activity or adhering to healthy diet. Next, we have self-care monitoring activities. And these are activities that are meant to, for the patient to notice that they have any changes in their clinical status, such as weighing themselves daily, observing their signs and symptoms and monitoring for adverse drug events from medications. And then lastly, we have self-care management. And these are activities meant to respond to any changes in signs and symptoms as they occur, such as adjusting their diuretic dose or knowing when to contact a health care provider. I would now like to highlight some specific recommendations from the guidelines, recommendations on self-care, starting with dietary sodium and fluid restriction. As a reminder, heart failure pathophysiology makes it difficult for a patient to effectively rid the body of salt or sodium, which ultimately leads to volume overload as water tends to follow salt in the body. Therefore, restricting dietary sodium and fluid has always been a common non-pharmacologic treatment for patients with heart failure symptoms due to congestion. But these specific recommendations have been based on low quality evidence. And the current guideline, given the conflicting data, strict salt intake reduction is not recommended further than the recommendations for the general population, which is to avoid excessive sodium intake. Similarly, for fluid restriction, when evaluating this in trials and meta-analyses, restrictive fluid intake compared with free fluid consumption has not been shown to reduce hospitalizations or mortality rates or have effects on patients' quality of life. Therefore, the guideline recommendation is that fluid restriction is of uncertain benefit and generally not recommended. Exercise training or regular physical activity is recommended, however, for patients with heart failure and is associated with improved functional status, exercise performance, and quality of life. Cardiac rehab programs are also recommended for patients with heart failure. A self-care tool for patients, such as the self-check care plan that is provided by the AHA, can be useful and offers easy guidance with tips to maintain stability. This also helps patients monitor themselves and know how to self-manage based on the category that they're placed in. So a patient would look at the self-care check plan. They would monitor themselves for their weight, any changes that they've had in their symptoms, and place themselves into a category, either green, yellow, or red, based on those symptoms and weight changes. Based on that, they would know what to do, either continue on the course that they're on, either call their doctor, or they may need to call 911 and be seen right away. The frequency of monitoring should depend on the clinical status and stability of the patient and can range from daily to every several days, self-care checks in those that are recently diagnosed or have a recent hospitalization, and at a minimum, every six months for those that are more stable. Getting back to the typical disease course for a patient with heart failure, unfortunately, a subset of patients with heart failure will continue to have symptoms and rapid disease progression, despite being on maximally tolerated guideline direct medical therapy. This transition to stage D, or advanced heart failure, is important to recognize and is a time where treatment decisions need to be made, whether to pursue advanced therapies or more supportive in a palliative approach. On the right-hand side of the screen, you can see the ESE definition of advanced heart failure. This was updated recently and includes four distinct criteria. The revised definition focuses on refractory symptoms rather than cardiac function and more clearly acknowledges that advanced heart failure can occur in patients without severely reduced ejection fraction. So that can include patients that have isolated RV dysfunction, if they have severe valvular or congenital heart disease that's not repairable, and in patients with preserved or mildly reduced ejection fraction. The four criteria are that patients need to have severe and persistent symptoms of heart failure, severe cardiac dysfunction, as I mentioned previously, if they've had recurrent hospitalizations within the last 12 months, and they need to have severe impairment of their exercise capacity, either based on a six-minute walk test or a peak VO2. And in patients with advanced heart failure, patients should be referred in a timely manner to a heart failure specialist. The I NEED HELP acronym was created to assist in decision making and when to refer to heart failure specialty care. Clinical indicators of advanced heart failure that should trigger possible referral include if patients need IV inotropes, if they've had persistent NYHA class 3b or 4 symptoms, or persistently elevated natriuretic peptides, but they have evidence of end organ dysfunction or severely reduced ejection fraction, if they have had defibrillator shocks or recurrent hospitalizations within the past year, if they are having worsening edema despite escalating diuretics doses, or based on their vitals, if they have low blood pressure and high heart rate, which could indicate that they're compensating for a low output state. And then lastly, if they are needing progressive down titration or having intolerance of guideline directed medical therapy. All of these are indicators that a patient may be moving toward advanced heart failure. And timely referral for review and consideration for advanced heart failure therapies is really crucial to achieve optimal patient outcomes because delaying referral could be detrimental. Once a patient develops cardiogenic shock or end organ dysfunction, it may limit their abilities to be a candidate for advanced therapies. So referral to an advanced heart failure specialist really represents a decision point, where patients either are a candidate and decide to pursue evaluation for advanced therapies, such as a left ventricular assist device, cardiac transplantation, or palliative inotropes, or if they decide to focus more on palliative care up to hospice care. And palliative care and shared decision making should be paramount during this time. And decisions around the evaluation and use of advanced therapies should be informed by the patient's values, goals, and preferences. Palliative care has a role across all stages of heart failure, starting early in the course of the disease and intensifying in the end stage of the disease, and even extending into caregiver bereavement after death. It's important to distinguish between palliative care and hospice care, as palliative care can coexist with invasive treatments and curative or life prolonging therapy. Also, palliative care services are not always provided by specialty palliative providers and are often provided by patients' primary provider. And some examples of palliative care services include providing prognosis discussion and clarifying goals of care, participating in shared decision making, and focusing on patients' symptoms, whether they are going to pursue advanced therapies or they're going to pursue more of a comfort approach. Next, we'll move on to discuss some specific eligibility for advanced therapies, starting with durable mechanical circulatory support or a left ventricular assist device or an LVAD. So in thinking of an LVAD, it essentially replaces the function of the left ventricle, pumping blood from the left ventricle into the aorta. Therefore, broadly speaking, they are most useful for patients with sole LV dysfunction. Per the ACC AHA guidelines, patients with advanced heart failure with reduced ejection fraction and NYHA class 4 symptoms who are deemed to be dependent on continuous IV inotropes or temporary mechanical circulatory support, i.e. these patients are unrecoverable, then a durable LVAD is considered a class 1 indication to improve functional status, quality of life, and survival. And I'd like to take a minute to point out that in recent trials, two-year survival is greater than 80% in patients with LVADs. And with the modern centrifugal flow devices, survival is estimated to be about 50% at five years after implementation. LVADs may also be used for hemodynamically unstable patients as a bridge to recovery or a bridge to decision. And that's a 2A recommendation in the guideline. LVADs are often classified by intent of treatment as either destination therapy, bridge to recovery, or bridge to decision. Destination therapy meaning that if a patient is deemed to have heart failure that is likely unrecoverable and the patient is not a candidate for a heart transplant. Bridge to recovery would be where the patient may have cardiac function that may improve enough to eventually be able to have the VAD decommissioned or explanted. And bridge to decision where a patient may have modifiable relative contraindications to cardiac transplantation or more time is needed to deem the patient a candidate for cardiac transplantation. Listed on the right-hand side of the slide, you'll also see a list of absolute and relative contraindications to durable LVAD devices. Some absolute would include patients with irreversible hepatic, renal, or neurologic disease as these patients tend to have worse outcomes after implantation. And then you can see also patients have a history of medical non-adherence or severe psychosocial limitations. Cardiac transplantation is also recommended for select patients with advanced heart failure despite guideline-directed medical therapy to improve survival and quality of life. And the median survival of an adult transplant recipient now is estimated to be greater than 12 years. Generally speaking, cardiac transplant is indicated in patients with end-stage heart failure with an estimated one-year survival as calculated by the Seattle Heart Failure Model, less than 80%, or a heart failure survival score in the high-risk or medium-risk range. Notably, cardiac transplantation, unlike LVAD, can be useful not only for those that have heart failure that's primarily due to LV dysfunction, but also those with end-stage heart failure due to other causes, such as congenital heart disease or hypertrophic cardiomyopathy, as well as patients with anginal symptoms that's refractory to medical therapy and is not amenable to revascularization, or patients with refractory ventricular arrhythmias. I've also listed here the absolute and relative contraindications to cardiac transplantation. So you can see some absolute contraindications include patients that have systemic illness that would lead them to have a life expectancy less than two years, other than their heart failure. If they have irreversible pulmonary hypertension, as this could cause the right side of the new heart to fail. If they have a heart failure that's causing the new heart to fail. If they have clinically severe symptomatic cerebrovascular disease, if they have active substance abuse, and if they have inability to comply with drug therapy, as well as multi-system disease with severe extracardiac dysfunction. Patients may be able to get a dual organ transplant, but if they have multi-system failure, then they likely would not be a candidate for cardiac transplantation. Some relative that I will point out, some relative contraindications. Patients that are greater than age 70, generally it's not a hard cut off, but generally are not considered cardiac transplant candidates. And if they've had active tobacco or recent substance abuse within the last six months, then they're generally considered not cardiac transplant candidates. Continuous IV inotropic agents may be considered for some patients. And appropriate use include as a bridge to LVAD or cardiac transplantation, or as palliative therapy for symptom control and improvement in functional status. It's important to consider that inotrope use has not been found to extend life, and using outside of these indications could cause harm. Some considerations for use of inotropes before starting these in a patient should be that continuous IV access and manipulation of the pump is required. So patients need to be able to take care of the access site, as well as the pump itself. And there are some risks associated with this, including the risk of arrhythmias and catheter-related infections. Lastly, we'll discuss hospice care, which is really a model of subspecialty palliative care that is offered to patients with terminal disease. So in order to be a candidate for hospice care, the patient needs to have a life expectancy less than six months. Hospice care is not only a philosophy of care, but also insurance benefit that covers the cost of care that maintains or improves quality of life. So different than palliative care, hospice care therapies are non-curative and focus on comfort only. And hospice care can also provide care to family and provide caregiver support and bereavement support. That concludes the management part one portion of this virtual boot camp. I'd like to thank you for listening. These are my references. And we'll move into the questions shortly. Bye, everyone. All right. So we're back live. And we're going to go through our audience response questions again. So if we could pull those up, share that deck again. So we also have some great questions in the chat. Chat. Specializing heart and laryngeal cardiology. So let me pull that up while we're, oh, here we go. OK. Let's go ahead and share the slides that are coming up. All right. So we'll go through the questions again. They'll be the same questions from before to retest your knowledge and see if you learned things. So the first question, which of the following does not represent a social barrier to implementation of appropriate heart failure management? So A, lack of social support. B, financial burden of heart failure treatments. C, abnormal renal dysfunction. And D, transportation limitations. So let's have more participants answer. This is an interesting one because we see so much of this in the clinic, don't we, Mallory? As far as patients that have social barriers to implementation, it seems like we spend those first visits post-discharge navigating this just as much as we navigate our guideline-directed medical therapy. Yeah, it's really, really crucial. And I know the population that I see, and I'm sure all of you see, really do tend to have a lot of those social barriers. And unfortunately, they also do have some medical barriers. Those tend to be a little bit more fixed, and we can't necessarily do as much for them. But hopefully, we have resources for some more of the social barriers. So it looks like the majority picked up on that abnormal renal function would be the medical barrier rather than a social barrier. Unfortunately, we can do some medications to help prevent the progression, but we can't do much about if they have abnormal renal function at baseline. But if they have financial burden, we can try to help manage medication costs for them, see if there's different programs for them, as well as transportation limitations, see if we can provide rides for the patients and things like that. So some of those social barriers, at least, we can try to address and find out what they are and see if we can address them when we're caring for patients. One of the things that our PharmDs are able to do in the inpatient setting at the time of discharge is do pre-auths to certify whether the patients can get the medications at discharge. Courtney, do you guys do that type of thing in your system as well? And how is that assisting your patients? Yeah. We implemented, probably two years ago, a pharmacy program that's called a cost consult. And our providers are able to prescribe GDMT through this cost consult and see what the co-pays or if patients are in the donut hole or what their out-of-pocket max is. And that way, we can help navigate GDMT at discharge and see if we can't get a coupon to buy us some time. But I think it has been practice-changing in making sure these patients are discharged on appropriate therapies and address the financial burden if there is one. All right. Well, let's go on to the next question. OK. So question two, which of the following should prompt a referral to an advanced heart failure specialist? If we have systolic blood pressures above gold despite maximally tolerated guideline-directed medical therapy, B, recurrent heart failure hospitalizations within the past year, C, persistent NYHA class 2 symptoms, and then D, need for lower diuretic doses over time? This one's a little bit tricky in places with just one word switch. It has a different meaning. Yeah, it's kind of some of them are in the opposite direction of what we think of for advanced heart failure. So it looks like the group did answer mostly correctly with the recurrent heart failure hospitalizations being an indicator for advanced heart failure. Patients with an SPP above gold actually would probably be doing quite well on their maximally tolerated guideline-directed medical therapy and likely would not be considered advanced heart failure. And the same thing, if they're needing lower diuretic doses over time, they're also doing probably pretty well, likely due to their guideline-directed medical therapy. And then NYHA class 2 symptoms tends to be the goal for a lot of patients. So you'd really be looking for those class 3B or 4 symptoms, so more severe symptoms than that for advanced heart failure. One of the things that I love to do in rounds, when we're in the CVICU and we have a team with learners at different levels, is we talk about how do you distinguish these patients in the heart failure clinic that have class 3 symptoms? Because we have hundreds and maybe thousands of patients in our heart failure clinic that have class 3 symptoms. And how do you pick out those that are going to progress to need advanced therapies versus those that you continue just to titrate their guideline directed medical therapy? And then what I always like to do with everyone is go around in a circle and see who can come up with the different things. And then eventually point to, I need help at the end. And this really reminds me of that. And the recurrent hospitalizations is such a great time to bring this up, because essentially there's this aha moment when everybody realizes that every single patient who's on our service needs help. Essentially, yes. If you're having heart failure hospitalizations, that's the time to help them. Absolutely. Absolutely. Yeah, and it's definitely that big picture. There's not just one thing that necessarily is pointing you in that direction. It's looking at the whole patient and seeing that a lot of these things are actually occurring simultaneously. All right, let's go on to the next question. OK. OK, question three. Which patient would most likely be a candidate for cardiac transplantation? Is it a patient with a 10-pack year smoking history that quit two years ago, a patient with cancer and a life expectancy less than two years, a patient with a pulmonary hypertension and a PVR of six woods units, or D, a patient with severe peripheral vascular disease and an A1C of 9.1%? Well, we can go ahead. And this one's perfect. So does this surprise you at all? I think so. There's a couple of, it's a little bit more split. It looks like the majority still got the answer we're looking for here, which is the patient with the 10-pack year smoking history that quit. The key is two years ago. So we don't want to limit patients that have been able to quit smoking. Just having a history isn't necessarily a reason we would transplant them. But anytime anybody has any active smoking or substance use disorder, then they wouldn't necessarily be a candidate. The other ones are a little bit tricky, just depending. But a patient with cancer and a life expectancy less than two years, you want the life-limiting disease to be the heart failure and not anything else. Because patients with a transplant should be able to live about 12 years, the median patient at least. And then pulmonary hypertension and that PVR, we'd like it to be as low as possible, really, before transplant. Because the new heart tends to fail if we have too high of a pulmonary vascular resistance. So three is the cutoff that was in the guidelines. And sometimes our surgeons even want it to be a little bit less than that, two or less. And then this is kind of these on their own, a patient with severe peripheral vascular disease, or A1C of 9.1%. They're relative contraindications. But once you start having multiple relative contraindications, then they're probably not necessarily a candidate for transplantation. So yeah, that's kind of most of the people that are correct there. Yeah, that's terrific. And we actually had in the previous test, we had more people who went with the choice for pulmonary hypertension in the pretest. And so we have more that have answer A correct this time. So that's really terrific. And I do think it can be confusing using the PVR. It makes me wonder sometimes how we use the PVR in Woods units for pulmonary vascular resistance, but we use Dynes per minute squared for systemic vascular resistance. And I always like to say, it's because the heart failure doctors can calculate a PVR in Wood units in our head. And we need to do that at the bedside whenever we have this swans in and stuff. Yeah, we're always doing that on rounds every day. We're trying to get their PVR down before listing them for transplant. So, all right, let's go on to the last question. Okay, and then question four, which of the following would be the most appropriate to counsel a patient on regarding heart failure self-care? Is it to A, avoid regular physical activity to prevent symptoms? B, restrict dietary sodium less than 1.5 grams per day. C, monitor symptoms regularly and know when to call your provider. And D, maintain strict fluid restriction less than 1.5 liters per day. Thank you. I really liked your self-care slide, Mallory. Thank you. I thought that was really elegant. Yeah, and I liked how you had it split up in the three different categories. And so if we share the results here, very good. So the majority of people said monitor symptoms regularly and restrict dietary sodium less than 1.5 grams per day. And so I thought that's really interesting that everybody seemed to be on the right page with that one. Yeah, definitely. That's something that we're gonna be asking our patients to do. And depending on their health literacy, hopefully they may need to do this in different ways for different patients, but hopefully they're able to monitor their symptoms, let you know. Restricting dietary sodium and fluid restriction is something that's kind of always, we always tell, it's been a little bit more controversial lately, especially the sodium. There's been some studies coming out showing that there's no difference and that strict sodium restriction might actually be harmful for patients with heart failure. There's also some studies looking at acute heart failure and giving a sodium load actually too. So I think that that's kind of something that always was in practice and now is kind of coming out of practice as we have more and more data about sodium restriction. Well, if you need some brownie points from your patients, give them some license for sodium. Yeah, yeah, definitely. You can salt your food a little bit more than we used to let you. Yeah. All right, great. Well, we can go ahead and take these slides down and we'll go ahead and address some of the questions that are in the chat. And so actually I think we'll go ahead and Mallory, since you've been in the hot seat, we'll ask this question to Courtney. This is coming from Diane. And she wonders, have you had success in using a plurinone instead of spironolactone in a patient with hyperkalemia on spironolactone? Is the first part of the question. And the second question is, what if they have a rash with spironolactone? Sure, great questions. The risk of hyperkalemia is the same with a plurinone and spironolactone, but they are structurally different. So if you do have a patient who has a rash on spironolactone, you can definitely try a plurinone and hopefully that rash is no longer. It's so interesting now that a plurinone is generic as well. Yeah. And when did that happen? Which is great. A couple of years ago or something? Yeah. The young faculty that have joined us use a plurinone all the time. I'm like, why don't I do that? I'm like, oh, because it used to be expensive. I know it was so ingrained and we were just prioritizing our male patients who failed spironolactone a few years ago. And now I do think it is becoming more and more popular because of the side effects associated with spironolactone. And so this one goes back to Mallory because we talked a little bit about sodium, but what about weighing yourself? So Diane has a question. What are the perils for identification of a dry weight for patients when it is unknown at early diagnosis? That's a great question. And a dry weight is kind of a tricky, we like to have at least some sort of range for a patient to say they're a dry weight, but that sometimes can be a moving target because patients as they're starting to feel better might gain weight, like caloric weight rather than fluid. And they may, if their disease is progressing, their dry weight may actually go down as they have more cardiac cachexia. So during that early stage though, it can be a little bit difficult and the hospital will usually wait until we think that they're euvolemic and then we can just decide that based on their physical exam. And usually we diurese them until eventually their serum creatinine will bump and then we know that they're dry. On the outpatient side, it could be a little bit more difficult. You're gonna be looking for symptoms, I think more so. And you can still do a physical exam if the patient's in clinic with you, but it might be a little bit more difficult for a patient to do that on their own. So you might have to go more based on their symptoms. Are you feeling like based on how they're sleeping at night, are you able to sleep through the night? Are you needing to sit up in a chair or use more pillows? Are you feeling like you're not able to get around your house as much? And then if they're feeling better in those ways, then you might declare that their dry weight is if they're starting to feel better. And you might just have to go based on that rather than having a specific number knowing exactly that they're dry at that time. Yeah, that's terrific. The next question is during inpatient admission, any perils on ensuring I's and O's and daily weights by nursing? So that's always a struggle, right? Seems like a typical struggle, Diane says. And I can take that one. I know that we have different units. Our critical care unit is excellent with I's and O's and daily weights. It's just ingrained in the culture and we really get that information. So it's a lot of comfort, especially, of course, if you add that to a SWAN, you're really following all the data. But then as we decrease the level of care, at least in our hospital, we have a step-down unit that also is fairly good with I's and O's and daily weights, but then we have a mixed med surge floor where the nurses are taking care of a hip replacement next to a heart failure patient and a little bit more difficult on that floor to get I's and O's and daily weights. But as a clinician, it's so helpful for me to add that information to how they're doing clinically, how the blood pressure is responding to guideline-directed medical therapy and parameters of end-organ function. So any tips and tricks from either of you to working with nurses and maintaining education on our floors? I agree. It still can sometimes even be, even on our heart failure floors lately, we've had a lot of turnover and things. So one thing that we've done is we've tried to decide which shift it will be responsible for it because our shifts change at 7 a.m. And we were trying to have day shift nurse do it, but they had a lot after sign out and then they need to start getting the 8 a.m. meds in. So it was a little bit too much for them to try and fit. So now we're trying to have the end of the night shift start doing those daily weights. So maybe finding out what time there's like a little bit of a lull for nursing, not that they have a ton of time to be doing everything, but trying to figure out when might work better for which shift. So that way they know it's night shift's responsibility. I'm not assuming that the day shift is gonna do it. And then hopefully day shift will still see if they didn't get one and they can still get one, but having it kind of designated is kind of been helping us to try and get the daily weights still sometimes as a struggle though. Changing gears a little bit. This question is from Carol. Can you address your impression using CardiMems to better manage volume status and weight. And, you know, in our hands, you know, CardioMEMS has been quite a benefit for patients that have admissions to the hospital. You know, we knew early on that there are decreased hospital readmissions with CardioMEMS amongst patients who had been admitted to the hospital. And then more recent data emerged that suggests that patients that are congested benefit as well. And so we do have, you know, indication for CardioMEMS in our, in our patients that have HFREF, but more importantly with HFPEF as well, because we have fewer choices and fewer things that we can do in HFPEF patients. One of the things that has been important in my experience with CardioMEMS, one is not implanting too late in the disease process. So we want to be able to treat the congestion in patients that have volume overload, but if they're dying from pump failure, that's a little bit too late in the pump, in the disease progression. So I recommend, you know, a little bit earlier in disease progression. And the second learning point for CardioMEMS is really selecting patients that are going to be uploading data because of course the necessity for the device is that they have data on a daily basis. And in addition to that, having systems in our clinics that are able to monitor the data and give the patient feedback. I have a time for, let's see where we're at. Oh, well, actually let's go ahead and we can come back to the rest of these questions. And I'm so excited to see all these questions in the chat. So we will get to the rest of them, but let's keep moving right now because some of them might be answered in Courtney's presentation. So let's go ahead and move on to the prepared questions. The stimulating thought for the next session. All right, everybody. Now let's change gears a little bit and we're going to talk mostly about the medication management. So here is a patient who comes to clinic for follow-up. They, she has an EF of 20%, New York Heart Association, three stage C. She takes lisinopril, 2.5 milligrams daily, furosemide, 40 milligrams daily, and carbadol, 2.5 milligrams twice daily. Her blood pressure is 120 over 70 and a heart rate of 60 beats per minute. Which of the following could be done to potentially improve this patient's mortality? A, would you increase lisinopril to 10 milligrams daily? B, add digoxin 0.125 milligrams daily. C, start impagliflozin 10 milligrams daily. Or D, increase carbadol to 25 milligrams twice daily. Okay, let's go to the next one. All right, question two. A patient with HFREF and no known drug allergies has been stabilized on lisinopril 20 milligrams for two months. His primary care doctor wishes to begin Secubitril Valsartan or Entresto. What is your recommendation regarding the ACE inhibitor? Is it A, continue the lisinopril with Secubitril Valsartan? B, stop the lisinopril within 24 hours of beginning Secubitril Valsartan? C, stop the lisinopril within 36 hours of beginning Secubitril Valsartan? Or D, reduce the dose of lisinopril to 10 milligrams and then begin Secubitril Valsartan? And we can move on. All right, and the last question is the advanced heart failure team would like to start digoxin on a 59-year-old man with a New York Heart Association functional class 3 symptoms and an EF of 33 percent. He has had three previous heart failure related admissions in the past three months. What information is most appropriate to relay to the patient regarding his digoxin? A, digoxin may increase the risk of hypokalemia, therefore avoid potassium-containing foods. B, digoxin will decrease the risk of heart failure related hospitalizations. C, digoxin will decrease the risk of all-cause mortality. Or D, digoxin may increase the risk for phosphine, therefore stay current on annual eye exams. It looks like this is a great question. Yeah. All right, let's quickly move on. Hi, everyone. Welcome back to the Heart Failure Society of America virtual boot camp. My name is Courtney Schakowsky, and I'd like to thank the program chairs for inviting me to give this section of your virtual boot camp, which is management part two. I work as the clinical pharmacy specialist at the University of Colorado Hospital specializing heart failure and cardiology. I have no financial or conflicts of interest to disclose. And let's jump right into our long list of learning objectives that we hope to accomplish in 20 minutes. Admittedly, we're just going to touch on things that are important to know, or at least refer back to as you're studying for the heart failure certification exam. So let's jump right into it. Guideline-directed medical therapy. This is consisting of the four pillars of heart failure for reduced ejection fraction, and we know that these four pillars improve outcomes for patients with heart failure. And the four pillars are ARNIs, beta blockers, MRAs, and SGLT2s on top of our diuretics for symptom management. The guidelines outline in a stepwise fashion a really great from steps one through six on starting with the establishing your diagnosis of heart failure and addressing your congestion, and then getting GDMT on board right away. And we're going to talk about specifically GDMT throughout this lecture. Steps two through six are also important and definitely deserve some attention as you're studying for these exams, but given the time constraints, we're mostly focusing on step one. So what we know is the evidence-based heart failure with reduced ejection fraction medications provide varying benefits and reducing risk, and that risk reduction is in mortality and also heart failure hospitalizations. I've listed the GDMT medications here, and the relative risk reduction in mortality ranges from 16 to 20 percent. And the mortality benefit is seen from nine months to over 42 months. And we know that that number needed to treat for the mortality benefit when it's standardized to 36 months is quite low, so we should definitely get all of our heart failure medication patients on these medications. I don't have time to go through the pharmacology of really any of our medications in detail, so we're just going to touch on high-level information. What we know is that the ACEs and ARBs and ARNIs and MRAs all affect different aspects of our renin-angiotensin system. And as you know, aldosterone promotes sodium and water retention, and the goal of blocking different aspects of this renin-angiotensin system ultimately inhibits aldosterone production, and in doing so decreases afterload, reduces ventricular remodeling, and also provides some cardioprotective effects. The evidence that we have from ACE inhibitors with our heart failure population is that we know that these medications reduce all-cause mortality and mortality related to heart failure, hospitalizations for heart failure, and also improve overall symptoms, and that data comes from the SOLVE and SOLVED treatment trials. We know that there's a greater benefit with using an ACE or HARB in patients who have worsening heart failure, and that data is from the CONSENSUS and SOLVED prevention trials. Angiotensin receptor blockers are at least as effective as ACE inhibitors in reducing all-cause mortality and sudden death or hospitalization, and that data comes from the ELITE and ELITE 2 trials. A few pearls from these medications is that we know that ARBs are better tolerated, and by that I mean there's about a 10% cross-reactivity that patients who had an angioedema to an ACE inhibitor will likely not get angioedema to an ARB, and so we feel safe starting that in those patients. We know that ARBs also aren't related to that ACE inhibitor-associated cough. Both of these medications can cause hyperkalemia, and they're both contraindicated in pregnancy, and both of them can cause a transient increase in the patient's serum creatinine by roughly 0.3 milligrams per deciliter, but it's definitely not a reason to pause or decrease the dose of these medications. ARNI pharmacology, as you know, is a little bit similar to an ARB, but it's a combination medication. So not only does it contain an angiotensin receptor blocker, but it also has an effect on the natriuretic peptide system, and that's with Secubitril. So ARNI's brand name is called Entresto, and it's the combination of Valsartan and Secubitril. So with all of the ARB benefits, we also inhibit neprilysin, and ARNI's allow natriuretic peptides to be active, which help promote diuresis and basodilation and sodium excretion. Data from the trials for Entresto or Secubitril-Valsartan demonstrated a significant reduction in cardiovascular death and all-cause mortality versus ACE inhibitors for patients with HF-REF, and the majority or the data that is out now is from the Paradigm-HF and Pioneer-HF trials, and you can see that the combined cardiovascular or the combined endpoint, which was cardiovascular death and heart failure hospitalizations, patients in the Entresto or the Secubitril-Valsartan group had a statistically significant better reduction in that cumulative endpoint, but even when you break down these endpoints in terms of cardiovascular death and all-cause mortality, patients in the Entresto or Secubitril-Valsartan group had a greater risk of reduction as well. Pearls about Entresto. It's not a medication that you're going to titrate each dose, so once you get patients started on it, it'll probably titrate every two to four weeks as tolerated. This medication can also cause angioedema, and because of that, it's very important that you have a 36-hour washout period for patients who are transitioning from an ACE inhibitor to Entresto. The medication Entresto is also contraindicated for patients who have any history of angioedema, whether or not that angioedema was because of an ACE or an ARB, and the data also demonstrates, and just real-world clinical practice, we know that the incidence of hypotension occurs more with patients who are on an ARNI than an ACE inhibitor. Moving right along to our next pillar for heart failure is beta blocker therapy. Patients who have heart failure ramp up the CNS sympathetic outflow, and you can see what happens when this sympathetic outflow is ramped up. When we start beta blocker therapy, we antagonize the system, and hopefully in doing so, we get, just to name a few, reductions in heart rate that allow for more filling time, improved cardiac function, and again, also decrease the cardiac remodeling. Data for beta blockers in heart failure has been around for a while. The majority of these trials were done in the 1990s, and these landmark trials include the U.S. CARBETA Law Study, MERIT-HS, CBIS-2, and Comperticus, and all of these trials demonstrated a reduction in mortality for patients who were started on beta blockers, and I've outlined here at baseline the number of patients who are also on an ACE or an ARB, which is quite high in the majority of these trials, ranging, you know, 95-97%. Some pearls to think about, there's only three guideline-directed medical therapy beta blockers that are approved for the treatment in heart failure. That's bisoprolol, carbetolol, metoprolol succinate, so not metoprolol tartrate. We know that higher doses of a beta blocker are associated with greater reductions in mortality and improvement in left ventricular ejection fraction, and that data comes from the MOCA trial, so we will prioritize titration of a beta blocker over other GDMT therapies. Definitely, these beta blockers can cause fatigue in the first three months. Really encourage your patients to stick with it because that will hopefully get better over time, and you'll hold when patients are in cardiogenic shock. Obviously, treat the shock, and when patients are out of their shock, symptoms will get them back on board. If patients have a history of bronchospastic disease, we encourage bisoprolol as the GDMT beta blocker of choice. Our next pillar that we're going to touch on are the aldosterone receptor antagonists, and these medications, there's two of them, so spironolactone and aplerinone, and I mentioned, I like to note that spironolactone is a non-selective aldosterone antagonist, and that means that it is going to affect not only your mineral corticoid receptors, but also your androgen receptors, and this is where some of the side effects of sexual dysfunction and gynecomastia will result from. Our selective aldosterone antagonist is aplerinone, and we can favor that medication if our patients are experiencing these androgen receptor side effects because we only really affect the mineral corticoid receptors. Data for the MRAs, we know that they have demonstrated a higher probability of survival across different severities of heart failure. First was the RAILS trial, and that trial was placebo versus spironolactone in patients with severe heart failure with reduced ejection fraction. The majority of these patients in the trial were on an ACE inhibitor, but not many of them were able to tolerate a beta blocker, I imagine, because of the severity of their disease, but spironolactone, as you can see here, was statistically significant in the probability of survival. A few later, we looked at aplerinone in the EMPHASIS heart failure trial, and this patient population had mild HFREF, and more patients in this study were actually on a beta blocker than compared to the RAILS trial, but you can see there's the similar benefit in terms of survival probability. So both of these MRAs are great for your patients with HFREF. It's spironolactone and aplerinone. Before you start these medications, you need to make sure that patients have pretty good renal function and serum potassiums less than five because these medications can elevate the potassium. In that sense, it requires close monitoring of renal function and also serum potassium. It will usually get checked three days after it's initiated and may or may not affect your diuretic dosing. Because spironolactone is that non-selective MRA, it can cause gynecomastia, and for patients who are experiencing that, we'll switch them over to aplerinone. The last pillar of our GDMT that we're going to talk about are the SGLT2 inhibitors, and these medications are pretty new. They were initially studied for diabetes and were great anti-diabetic medications. They work in the S1 segment of the proximal tubule and really promote sodium and water excretion, and what we found, though, is that these medications also have great benefits for patients with heart failure and may actually even create some renal protection. The data for our SGLT2 inhibitors is, we know that they reduce heart failure hospitalizations and cardiovascular mortality irrespective of the presence of type 2 diabetes, and that data comes from the DAPA-HS trial with tapagliflozin and also the EMPEROR-REDUCE trial with impagliflozin. More recent data for our patients who have HEF-PEF, SGLT2 inhibitors also demonstrate a mortality benefit in that patient population. So whether you have HEF-PEF or HEF-REF, SGLT2 inhibitors are a great medication that have mortality benefit for our patients. A few pearls. Caution use of these medications for patients who have frequent genital mycotic infections. Because it promotes that sodium and water excretion, you may actually see a small diuretic effect, and so it's important to assess volume status of your patients when you initiate these medications, and over time you do have to stop the SGLT2 inhibitors three days prior to a scheduled surgery, and that's because with prolonged fasting there's a risk of ketoacidosis. You can start these medications for inpatients who have an EGFR as low as 20 mls per minute per meter squared. Similar to our ACEs and ARBs, they can also cause a transient increase in your serum creatinine of 0.3 mg per deciliter, but it's not a reason to stop or adjust your dose. And a big takeaway point here is that the risk of diabetic ketoacidosis is not seen in our patients who do not have diabetes, and that was something that took a while for us to determine. The effects of adding each one of these GDMT pillars to another are fully additive. So each one of these medications bring its own mortality and decreased hospitalization benefit, and all of these trials for beta blockers, MRAs, ARNIs, and SGLT2 inhibitors demonstrate a clinically relevant benefit within 30 days of initiation. And it's data from these trials that what we now recommend is a simultaneous rapid sequence strategy of initiating the pillars from day one in order to improve benefits. So get your ARNI, get the beta blocker, get the MRA, and get the SGLT2 on board at the lowest possible dose. And because we know that beta blockers have a greater benefit at higher doses, that's the medication that we're going to prioritize titrating. But cumulatively, these medications within 30 days reduce the risk of death by 73 percent over two years. It's important to note though, and we don't have a lot of time to focus on during this presentation, but caring for our heart failure patients doesn't stop here. And it's really important for the team and for us to evaluate what other optimizations can we make. Do they need to be referred to EP for potential procedures? Do we need to add on additional therapies or consider advanced therapies? And most importantly, really get comorbidities under control as well because we know that shows benefit in our heart failure symptoms. I often get asked, you know, how do we manage or what are some of the common barriers to initiating GDMT and how can we overcome that? And I think this is a really great table that demonstrates what are some of those common barriers, which include acute kidney injury, hyperkalemia, symptomatic hypotension, even adherence and cost insurance, and what are some first line strategies. So it's not just stopping a medication and it's not switching them to something that might not have as much mortality benefit, but not only does it offer a first line strategy, there's also a second line strategy. And I think it's a really great resource to become familiar with as you're caring for these heart failure patients in order to provide solutions to the barriers that they may or may not be experiencing. Just as I mentioned previously, in addition to GDMT, we really need to make sure that we're managing comorbidities, whether that's hypertension, diabetes. Many of our patients have atrial fibrillation and also need anticoagulation. So you can see how the list and the number of medications that these patients will take just keeps going up. What happens after you optimize GDMT? The guidelines have a really great table that I've outlined here. And we should consider, once you've optimized GDMT, you should consider whether or not these patients also qualify for additional therapies, whether that's ivabredine or variciguat. We're gonna touch a little bit on digoxin, maybe a potassium binder, and then do they need some of these procedures in order to improve their outcome? So I recommend that you definitely familiarize yourself with what the guidelines say here. Touching base a little bit on digoxin, because many of our patients do qualify. Remember that digoxin inhibits the sodium potassium ATPase enzyme. And this enzyme is responsible for maintaining the balance of sodium and potassium within the heart. When we do affect it, what we end up creating is an increase in intracellular calcium. And that intracellular calcium actually enhances our myocardial contractility for our heart failure patients. The data for digoxin basically provides and what we know that digoxin will keep our patients out of the hospital. And who benefits the most from starting digoxin? And that's outlined here in red. It's really your sickest patients. It's the patients who have New York Heart Association class three or four with an EF less than 25%. That's definitely somebody that I would consider starting digoxin on. Big thing to note that I suggest you evaluate a little bit are the drug-drug interactions with digoxin, whether they're P-glycoprotein inhibitors or inducers or potentially just have effects on absorption like our bile acid sequestrants. It's really important that we monitor and make adjustments as needed because digoxin does affect other medications as well. It can cause toxicity. And the majority of these toxicities are related to electrolyte imbalances. And in order to treat this life-threatening or potentially life-threatening digoxin toxicity or overdose, we would use digoxin immune fab or digibind. And the indication for that really comes down to do the patients have severe ventricular arrhythmias, progressive bradycardia, second or third degree heart block that's unresponsive to atropine, a potassium level greater than five, five or six with signs of a rapidly progressing digoxin toxicity. And that's when you would consider using the digoxin immune fab. One key thing to note, if you were to give this medication in order to reverse the toxicity, you can no longer check digoxin serum levels because you will also be checking the digibind. And last but not least, so we're running out of time, but I do want you guys to familiar yourself with some of the cardiac amyloidosis. And I think this is a really great clinical science statement that reviews treatment for wild type and variant cardiomyopathies based on whether or not they have neuropathy and which medications that you should consider. We don't have time to go into the details, but it's definitely a great resource as you're preparing for this certification. And I know that was a lot in a few short minutes, but I'm looking forward to your questions during the live session. Courtney, that was terrific. Really rapid fire to be able to get through all of that, but that's really- It's a lot to cover, I just realized. All right, let's go back to our questions again. All right, everyone. Question one, a patient comes to clinic for follow-up. She's got an EF of 20%, New York Heart Association, three stage C. She takes lisinopril 2.5 milligrams daily, furosemide 40 milligrams daily, and parvatalol 12.5 milligrams twice daily. She's got a blood pressure of 120 over 70 and a heart rate of 60 beats per minute. Which of the following could be done to potentially improve this patient's mortality? Is it A, increase lisinopril to 10 milligrams daily, B, add digoxin 0.125 milligrams daily, C, start n-pagloflosin 10 milligrams daily, or D, increase carvatalol to 25 milligrams twice daily? So I can see with the responses to this that the wording is really important here. All right, I think the majority of you guys got that right. Remember, our SGLT2 inhibitors are the last, I would say, pillar with recent data in terms of mortality. And it's definitely a pillar that you wanna get started on patients in order to improve their mortality. I don't disagree that titrating a beta blocker could be a next step, but I do believe that we need to get started and I do believe that we need to get the pillars on board before we can consider titrating to our optimal doses. And then let me ask, in your practice, is there a preference over impipigliflozacin versus dapagliflozacin, or is it just an- Insurance. I see. Yeah, yeah, it's really, just as Mallory alluded to, in terms of the barriers, whatever their insurance will pay for. Do you guys have a preference? I would say, I would answer the exact same thing. Okay. And I saw a question actually in the chat about EGFR is down to 20 for both Impag and DAPA. And we practice for both SGLT2 inhibitors down to an EGFR to 20. I think one of the package inserts does to 25, but we extrapolate the data for both. Do you guys practice differently? We do the same at University of Maryland. We'll use either one. We have Impagliflozacin on formulary, so we tend to use Impagliflozacin more, which has the lower GFR cutoff just as a default, but we would use either. A couple other questions while we're here on the SGLT2 inhibitors. So scheduled surgery, does this include cardiac cath or ablation for holding these medications? It does. At our institution, we consider it a scheduled surgery. You just don't want that risk of any sort of hypoglycemic event and missing three days of the medication. It isn't harmful. Next question about the SGLT2 inhibitors. Is there any limitation of an SGLT2 inhibitor with type 1 diabetes on insulin? Yes. It's, I would caution use of SGLT2 inhibitors in patients with type 1 diabetes. We always get our endocrine colleagues on board before we would consider starting that medication because of the risks associated with ketoacidosis. Do you guys have a different practice at your institutions? We also tend to use with caution, especially if anybody's had a history of DKA, which a lot of our type 1 diabetes patients have had a history, we may actually consider not starting it just because of the increased risk for DKA and that could be another hospitalization. So a little counterintuitive. So we tend to be very cautious in type 1 diabetes. All right, let's move to the next question. Okay. All right, so next question. A patient with HEP-REF and no known drug allergies has been stabilized on lisinopril, 20 milligrams daily for two months. His primary care doctor wishes to begin Secubitril-Valsartan. What is your recommendation regarding the ACE inhibitor? Is it A, continue the lisinopril with Secubitril-Valsartan? B, stop the lisinopril within 24 hours of beginning Secubitril-Valsartan? C, stop the lisinopril within 36 hours of beginning Secubitril-Valsartan? Or D, reduce the dose of lisinopril to 10 milligrams and begin Secubitril-Valsartan? And it looks like you guys nailed this question. There was a little bit of confusion at the beginning but you definitely want that 36 hour washout period in order to decrease the risk of angioedema. I know our electronic healthcare medics, we use Epic. It's a hard stop for providers to enter whether or not the patients have taken an ACE inhibitor dose within the last 36 hours for that safety reason. So be sure that transition is safe. I wonder, has anyone else seen a transition to using more ARBs in the hospital? You know, that's something that's really surprised me that we have started to do, you know, where we used to start lisinopril as an inpatient, you know, for a new start, a new diagnosis of heart failure or even captopril if we were worried about titration but now we're getting much more comfortable titrating the ARBs so that we don't have to do the washout period. Yeah, us too. All right, let's move on. Okay, last but not least, and I apologize. I just noticed some typos in here, so my apologies. The advanced heart failure team would like to start digoxin on a 59-year-old man with New York Heart Association functional class three symptoms and an EF of 33%. He has had three previous heart failure related admissions in the past three months. What information is most appropriate to relay to the patient regarding his digoxin? Is it A, digoxin may increase the risk for hypokalemia, therefore avoid potassium-containing foods? B, digoxin will decrease the risk of heart failure-related hospitalizations? C, digoxin will decrease the risk of all-cause mortality? Or D, digoxin may increase the risk for phosphine, therefore stay current on annual eye exams? Okay, let us show them the results. There we go. All right, great job. I think the majority of you got this. The data with digoxin really is only related to heart failure hospitalizations. It's why it's not one of the four pillars, but there is a place in therapy for digoxin for some heart failure patients. I'm sure Dr. Fook and Mallory have seen that there is a place in therapy for digoxin. Dr. Fook and Mallory have seen it within their practice. We all still use it. So I think nobody answered D, which is associated with ivabradine, which is one of the medications that are a potential medication that you could use for a heart failure patient once you have GDMT on board. It does not decrease the risk of mortality, and it's actually not associated with hypokalemia. Courtney, I have a question for you about digoxin. Would your enthusiasm wane or change at all if the patient was 80 years old? Yes, I do not like digoxin in our elderly patients for a couple of reasons. You know, they don't have the best renal function at baseline, and so I worry about digoxin toxicity accumulating. And so I am very hesitant to start digoxin in our elderly patients. Excellent. All right, let's go ahead and close the questions, and we'll go, we have time left so that we can just tackle the chat. All right, so when calculating renal function, should EGFR be used or creatinine clearance? I think Mallory and I could tackle this one probably together, but there, I would say that the majority, as pharmacists, we function with creatinine clearance, and you'll see us calculate creatinine clearance, and we ask our students always to calculate creatinine clearance. But a lot of drug studies and the way drugs were trialed, it was with an EGFR cutoff. I think creatinine clearance, I think creatinine clearance in my practice is more specific in terms of really estimating a patient's renal function, and so I tend to favor creatinine clearance. There's even some data, I don't know if you guys are using in your practice, and not necessarily with our heart failure medications, but Cystatin C in order to gauge a patient's renal function. So I think there's a lot of tools out there, and each institution is a little bit different in terms of what they prefer. Yeah, just to piggyback, I would say it depends on the medication too sometimes, for empaglifolazone, a lot of the diabetes medications specifically have used EGFR in their more recent studies. So I do use EGFR for that, and especially when they're helping reduce the rate of decline of EGFR. But other medications, I tend to use creatinine clearance. I think per the guidelines, technically spironolactone is EGFR, but I will kind of look at their overall picture what their actual serum creatinine is, and what their creatinine clearance is, what their EGFR is when I'm kind of deciding about that. And Jack asks, do you use both EMPA and DAPA down to a GFR of 20? Yes. So we'll drive that home, thank you for that. Next question, so spironolactone, I've seen recommendations to check potassium at three days and a week, but I can barely get some of my patients to come in for labs, any suggestions? It's tough, because I think that three days and then one week is from the 2005 guidelines that we still sort of practice, but I'm more inpatient, so maybe you guys have help with how to get patients to come in for labs as an outpatient. Well, there are some things from the electronic medical record that can help. I don't know if you're an Epic house, something that I do when I'm seeing my patients is I will put in a reminder to myself or to my nurse that the patient has labs due, and you can actually send an automated message to remind them within Epic, and so that's a suggestion that you could try. Typically, I am having patients come back for their labs and then I'm looking for them, and if I don't see them, I have my nurse call them, and then they usually drag themselves, probably an additional 50% drag themselves to the lab after the reminder call. I'm also more on the inpatient side, so I really like your suggestions for the outpatient side because we can obviously get our labs on the inpatient side. All right, let's see the questions that we have. Oh, this is good. This is another one about spironolactone. Would you have any concerns about starting an MRI in someone with hyponatremia? That's an interesting one. That's an interesting one. I find that hyponatremia tends to either just mean the patient is more volume overloaded or perhaps is having more severe heart failure, and although if you, based on its mechanism, it could cause some hyponatremia, I would still use it because it could improve their overall heart failure, which actually might improve their hyponatremia. So if it's really severe, like they're hospitalized and it's in the teens, I might hold it for a couple of days, but otherwise, if it's just a chronic heart failure and they have low sodium, then I probably would continue it in the hopes that it might help improve their heart failure. I often look at the serum sodium, and the gold dose or the dose that we use a lot of the time is 25 milligrams, but a low sodium might be a reason why I would start at 12 1⁄2 in someone and titrate them up, and so that's kind of a tip or a trick that I've learned over the years. This is also from Tammy. With SGLT2 inhibitors, would you have any concerns starting on someone with a lower extremity amputation? I would still tend to favor to use it. I know that the older studies looking at canagliflozin did see an increased risk of lower extremity amputation. However, in all of the newer studies, there hasn't actually been that risk, especially with dapagliflozin and embagliflozin, so I would still use them. They should still be, you know, practicing good foot care and making sure that they're checking for ulcers and things of that sort if they have a concomitant diabetes, but I would still favor using it for the mortality benefit and heart failure. And then for Courtney, is age a factor to start all the four pillars at once? Yeah, it can be. I think just like we talked about age with digoxin, you know, I would keep it in mind, but I think you can get very low doses of all of these medications on board safely with patients of any age. And like Mallory and I tend to practice in an inpatient setting, so it's easier for us to say that we can do that in those patients that are in the hospital since we know we can monitor them. But I think, you know, you still want that mortality benefit and want to advocate for GDMT being on board in order to have those benefits. All right, now we have a couple of questions at the end about our last session. So in our part two of the three-part series, Terri mentioned nursing protocols that they use that she's developed. And we collected a group of email addresses and we shared those with Terri. And so if you haven't received the protocols yet, they're still on their way. So, and I'll make sure of that after today. And let's go ahead and go to our closing slides. So you will receive a brief survey by email following the webinar for feedback. So please fill it out. Also feel free to visit our Heart Failure Cert Bootcamp and the on-demand listing will be posted there for you to revisit this as it gets closer to test taking time. And to apply for the Heart Failure Certification exam, you can go to SMTT Test Candidate Management Systems here as to register for the exam. If you would like more information about Heart Failure Certification testing, you could reach either Don or Kelly at the Heart Failure Cert headquarters. And the next testing windows open August 14th and are open until September 29th. And then again, opens October 30th through December 8th. If you're interested in the first Heart Failure Certification cohort, the first exam window was between January to March of 2023. We had 82 test takers with a 95% pass rate. You can see the provider breakdown here as far as the number of nurses versus physicians and pharmacists that took the exam. And a list of the Heart Failure Certified members can be found on the Heart Failure Society of America website. Finally, this is the Heart Failure Certification website where you can register for the exam and you can also access the learning issues that were used to develop each of the presentations in the bootcamp series. And so with that, we thank you all for participating. Thank you so much for joining us on these evenings with the live presentations and question and answer, and we wish you the very best of luck on the exam.

accurate measurements

inputs and outputs

daily weights

clear communication

physicians and nurses

accurate documentation

questioning measurements

verifying measurements

sudden changes in patient's output

urine concentration

electrolyte losses

family involvement in patient discussions

sensitivity to patient's wishes