Hi, welcome back to Cardiovascular Nurse Essentials. Today, we are gonna do heart failure part one. These are my disclosures. As you can see, we have a lot of objectives to get through, lots of information, and again, readings, but I encourage you to break it up or use them as references. Heart failure is very complex, so it's important that you do understand some of these main components. And you may not understand it all immediately, and that's just fine, but use these as references as you're learning and you're prepared to go back and kind of be refreshed. You'll pick more things up. I hear people all the time talking and I learn every day, so there's no shame in that. So again, starting with some facts and prevalence, you can see a little bit of a shift, not much, still kind of in the South region where we have our most common diagnosis of heart failure. Now, the difference here is these are actually death rates. So you can see where we have more causes of death by heart failure in the Southern region there. And I've always found it interesting that really it doesn't discriminate between men and women. So for the most part, you're gonna see fairly close numbers of diagnoses based between men and women. You will note it does increase with age. So that is a common trend, obviously, like many cardiovascular and other diseases, your risk increases with age. So current statistics say about 6.2 million Americans have heart failure. And it's really the only form of heart disease that we see that is just continuing to grow by leaps and bounds. And we anticipate really a peak by 2030, so not too far in the future. And you can see all these facts, but one of the most kind of eye-opening ones is that when a person is diagnosed with heart failure, the death rate is usually within five years. So if you're diagnosed, your chances of being dead in five years is 50%. So that's pretty shocking statistic, and it's up to us to help not only treat these patients, but engage them so that they can make changes to their life and their lifestyles to help as well. And it is a high cost disease. Obviously, our main thing is caring for patients, but it does come at a hefty price directly and indirectly. So as you're gonna find, it does take multiple team members to adequately care for these patients. And then obviously there's a lot of indirect costs from this care as well, things like mortality, loss productivity, things of that nature. So let's talk about what heart failure is. I think on the surface, many people understand it, but I want you to know the true definition, meaning that it is a complex clinical syndrome. So it's not just about the heart. It is about the entire body, and it's complicated because it involves a number of organ systems and hormones. And it's really anything that causes your heart to not fill or pump well. So it's not just about the squeeze. It's not just about the left ventricle pumping ineffectively. It could be an issue with being able to relax and fill. There is a difference in chronic versus acute. Your patients are typically number one complaint is gonna be, I can't breathe well, and I'm very tired. But number one, they can tend to overlook a lot of symptoms, but by the time they get to the point where they can't breathe, that's generally when they're calling for help. And we wanna get them to call a little bit before that. And then obviously there's a lot of clinical symptoms and that you can see on assessment as well. So we're gonna get in the weeds here a bit. And there's a lot of risk factors for heart failure, okay? The obvious ones are hypertension, things we spent time on, CAD. The things that are not really heart related would be things like drug and alcohol use, chemotherapies. So chemotherapies can damage good cells as we know. So that can put a patient at risk for developing heart failure and other endocrine issues. So diabetes, thyroid, hyper or hypo can increase risk for heart failure. Again, just looking at all the various etiologies, there's a vast number of reasons people can be at risk and develop heart failure. So wanting to be educated on what all of those are. So let's talk about the pathophysiology because it is complicated and it starts by some sort of response. So your body's responding to some sort of stress or whether that's just the aging process, whether that's elevated blood pressure or an endocrine issue. And your body actually compensates. So we're really good at compensating and that's good in emergency situations, but when that becomes the current state, your body can only keep up so much. And we have what's called ventricular remodeling. So it's actually on the cellular level where our body changes. And that can result in that ventricular dysfunction that we're gonna look at a little bit more. So we got this whole response system, right? So our body notices that something's off and we've got more blood volume than we should. So it's like, okay, I can handle this. So I'm gonna stretch a little bit more. So the heart muscle actually stretches a little bit more so it can increase that force to get that blood volume out of the LV, okay? So that's great, as I said, for a short term, but under long circumstances, what happens is it actually gets to a point where now the shape of my heart has gone from more of a football shape to more of a basketball or round shape, which impacts its ability to pump or effectively. So it's actually physically changing the shape and that's what we call remodeling. So this is really not a response we want, okay? And so it gets into all the little myocytes start changing and can really modify the shape of your heart. And then from that, it also triggers a neurohormonal response in the RAS system, which we're gonna talk about in a bit. So there are different types of heart failure and some funny acronyms, but to get us started, our systolic heart failure is really probably what you would think would be most common, but there's really about 50% systolic and 50% diastolic. So we know during systole, it's when our heart is squeezing. So think systole squeeze, that's the contraction part. That's when the blood is leaving the left ventricle, going through your aorta to the body. And it's carrying that blood that's rich in oxygen. So if you have systolic heart failure, it's not pumping as well. So it's a weaker heart muscle. It's the thinner heart muscle you can see here. So it's not pumping as well. So that's why we call it systolic heart failure. It's a pumping issue. Diastolic heart failure on the other hand, we know that during diastole, the heart is relaxed. So it's trying to relax so it can fill up with blood. It's getting ready for systole or that squeeze. So you can see with the diastolic heart failure, it's actually hypertrophic. So the muscle has been usually pumping against some sort of pressure. So think pulmonary hypertension or just general hypertension. And our heart muscles become big. So when it becomes big like that, it's stiff. It's non-compliant. It will not move. So when it goes to relax, think of a bodybuilder. It can't relax as well. So it can't fill up the tank. So it's not a pumping issue so much as a filling issue. Now we do have patients that can actually have combined systolic heart failure and diastolic. And those are more of our advanced heart failure patients that we'll talk about towards the end of this. So beyond the heart, like we talked about, there's this neurohormonal response. So our sympathetic nervous system is what keeps us in check in times of stress. Heart failure puts the body at stress. So it's responding by releasing hormones. And if you look back or think back to our hypertension talk, we did discuss this a little bit, but basically what happens is in our liver and our kidneys, we detect a higher volume of fluid or maybe even a drop in blood pressure and it responds by releasing these hormones. So we have angiotensin I, which converts to angiotensin II after it goes through the lungs and picks up the angiotensin converting enzyme. And then it turns into, we also have aldosterone. And what happens is angiotensin II causes vasoconstriction. Aldosterone causes us to retain water and sodium. So obviously if somebody has heart failure, we do not want to increase the workload of the heart by pumping against constricted blood vessels. And we do not wanna add volume to that. So part of our strategies are going to be working on a hormonal level to block these hormones. And this is just, I'm not gonna go too much in detail, but this is a good reference to help you understand the importance of hormones and where they play in heart failure so that you understand the severity and just the whole impact it has on the body. So it's very important that we know what kind of heart failure we're dealing with. And when your patient presents to you, you're not gonna be able to look at them and say, oh, you have systolic or diastolic heart failure. Typically they can present the same. So obviously number one is generally they're having a hard time breathing, extreme fatigue, exercise intolerance, meaning they're even having a hard time doing their activities of daily living. So maybe you have to take lots of rest breaks between getting up and doing showers, brushing teeth, shaving, getting dressed, things like that. Fluid retention. So that means swelling, not just in the feet, but also is it in their abdomen? Is it in their fingers? Is it in their eyes? So there are different areas where edema can happen. Some other things that maybe you wouldn't think of offhand would be a cough, okay? Is it wet? Is it wheezing? Either of those are possibilities. Are they having abdominal issues like bloating, constipation, discomfort, nausea, vomiting? Do they have any chest discomfort that can be related to heart failure? Maybe they're not making urine or putting out as much urine as they should. And then confusion. So altered mental status. If we think about what blood flow does, right? Blood carries oxygen to the body. So if you're not getting the blood flow, you're not getting the oxygen to your organs. If you don't get the oxygen to your brain, you can have confusion, lightheaded, busyness, things of that nature. So we're looking way beyond the scope of just the heart. It's really a head-to-toe assessment in this population. So this is just an example of our algorithm of how to work up. So obviously everything starts with a clinical assessment. There's labs, there's EKGs, echoes, all of these things to help us decide, is it HFREF or HFPEF, which we'll talk about. I will say BNPs, this is probably more important in initial diagnosing. We don't use this as much on patients that we know have heart failure. You can, but it's not always reliable. Things like obesity or chronic heart failure can alter those numbers, but initially it can be very helpful. So our assessment, we talked about the causes and so obviously your assessment, you want to hit on a lot of those things that you can look at are valvular heart disease. Sometimes it's a valve issue causing it, some other important things would be like exposure to cardiotoxic agents. That would be maybe a new chemo patient or someone who just went through chemo. Anemia, anemia can be related to heart failure probably a lot more than we would like to acknowledge. So thinking about all of these different possibilities and seeing what the history is. And again, family history is very insightful and helps us. So looking, is there any kind of predisposition in their, in their family to atherosclerotic disease, sudden death, any kind of arrhythmias or unexplained cardiomyopathies, things of that nature that might give us a reason to, to dig a little bit deeper in terms of diagnosis. Our physical assessment is really important. We always want to check the basics though. These are telling, and we've talked about the importance of that. So accurate weights and are they changing? That is a key indicator of fluid. Now, caveat is not every patient weight will change with fluid but it is our number one starting point that we want to educate and look for those weight changes. What's their heart rate? You know, commonly heart failure is, is associated with AFib. Is that something that could be put into play here? We've talked about PMI and how that can be displaced with LVH, left ventricle hypertrophy. Now having LVH does not automatically mean heart failure, but it can be a sign. So understanding what's putting them at risk. S3 murmur is, is considered the sound of heart failure. And that just is a sign that there's extra fluid that the heart is dealing with. Looking at things like JVD, jugular venous distinction, breast sounds are really important. So if you've got a patient and you're listening to their sounds, do they have crackles? It could also be wheezing. It could be diminished. It could be coarse. So there's a variety of lung sounds that can indicate fluid. So I know a lot of times we, the initial thought is rails or crackles. Yes. But just because they have something else does not negate that they may have heart failure. And we talked about edema. You know, we, we want to look at the whole body. So a lot of patients will hold fluid in their abdomen. So are there, is their abdomen tender? Is it is it firm? Are they nauseous? Are they not able to eat? Those are all indicators that they have extra fluid. Cause if you've got extra swelling and fluid in your abdomen, you're going to, you're not going to be comfortable. You're not going to have an appetite. Things are going to really slow down. So don't discount those those things. So a lot of things that we're going to ask, and we've talked about a lot of these things and obviously you want to, you want to kind of, as you're assessing and you're talking to your patient, you may pick up on these things. So again, breathing things you're listening for while you're talking to your patients are those cues of, I had to use pillows, more pillows, or I had to sleep in the recliner. I just felt off. I felt flutters in my chest. Have you been able to eat? Have you been able to hold down food? Are you urinating at night a lot? Is that keeping you from sleeping? Or maybe, you know, just picking up on some cues. So really it's a range of things that you're wanting to look for that are going to give you a lot of information. So the most common ways are things we start with, obviously EKGs, ECHOs, and chest x-rays. Those are kind of our baseline with some labs. Okay, so common labs, we're looking at electrolytes, kidney function, liver, blood count, and then remember what I said about thyroid. We want to check their thyroid if that's not been done recently because sometimes a hyper or hypoactive thyroid, if we get that into check, that can help alleviate things. So there's a lot of things we can look at to give us this picture. So the main thing we use to diagnose is usually an ECHO, and we're looking at their ejection fraction or EF. So what does that number actually mean? It's actually the percentage of blood that goes out with each contraction. So every time the heart pumps, we're looking for a certain amount of blood to go out, and that number is 55 to 65 or 70 percent. So we're not looking for 100. We're not looking for the heart to completely empty, but we're looking for 55 to 65 percent as a normal range, and that's important because it tells us kind of what kind of heart failure they have, and we'll talk a little bit more about that. There are what we call classifications. I like to call this a two-way street because this is really assessing and aligning a patient's functional state with a NYHA score, so anywhere from one to four. So a patient that is one is ideal. They're not having any issues, no symptoms, no shortness of breath. They're able to do all their activities. Class two is somebody that's having symptoms with moderate exertion, and so that means they can do most of the things. They may have to take a few breaks here or there. It just depends on they're able to get through most of their day. Now class three is when they're going to typically start calling you or considering going to the hospital, and that's symptoms with minimal exertion. So I get up out of bed in the morning, walk into the bathroom. I'm winded. I go to the restroom. That gives me a break. I get up, wash my hands, get dressed, and then I'm just completely beat. So these are patients that are pretty significantly impacted in their ability to function. Four is somebody who cannot catch their breath at rest, so they're sitting and they feel winded. This is an emergency situation. So I say this is a two-way street because I can go from feeling a three where I'm calling you because I can't do my day-to-day activity. You tell me to increase my Lasix, and you check on me the next day, and I'm back down to maybe a two. It's not realistic for everybody to be a one, but I'm feeling better, and that gives you an indication that I'm moving in the right direction. Stages, on the other hand, are what we call a one-way street. So if I progress from A to B to C, I cannot go back. So stage A is really someone who's at risk, and I want you to think of when they updated these stages recently, they kind of aligned them more with oncology stages, and that's intentional because heart failure mimics probably oncology more than most of our general or usual cardiology diagnoses. So that stage A is somebody who is at risk. They don't actually have any functional or structural disorders, but these are those hypertensive patients we've talked about, those metabolic syndrome, diabetes, thyroid, all of those patients who can be at risk. Stage B is what we call pre-heart failure. So they may have some indications, but they're not really feeling any, they're not complaining. They don't actually feel signs or symptoms. So it's kind of those early stages where changes are occurring, and it's a warning, a precursor to stage C, which is symptomatic heart failure, meaning if we don't do something, they will progress. So stage C are your patients that actually have current or have had symptoms. So stage D is what we call advanced heart failure, and these are marked symptoms, and they interfere with their daily life. So they really have had optimal guideline-directed medical therapy, but they're still symptomatic. So obviously stage D is the worst stage, and that's where we have to look at alternative therapies. And so when you think about heart failure, there's a couple different verbs or adjectives. We've got new or de novo, which is that new initially diagnosed heart failure patient. You've got maybe a patient that's got resolved heart failure, meaning they're not symptomatic. So maybe they had admitted to the hospital with stage C. Now they're following up in your clinic with their seven-day post-discharge follow-up, but they're not having symptoms. Persistent heart failure is really kind of that chronic heart failure. They always have some limitations in functional capacity and some symptoms, and then we have worsening where we're trying to make adjustments, maybe changing meds, and they're still having increasing symptoms of their heart failure, and this is really a sign that they're deteriorating. So our different types, as I mentioned, are all based on the ejection fraction. So most commonly, you're going to hear HEF-REF and HEF-PEF. Funny acronyms, but really it relates back to that systolic and diastolic heart failure. So our HEF-REF simply means heart failure with reduced ejection fraction. This is the systolic heart failure, and the reason that makes sense is we see their EF is low. It's less than 40 percent, so that means my ventricle, my heart is not pumping as well, so I know that it's a weakened muscle. Makes sense it's not getting enough blood out of the ventricle. So HEF-REF, reduced EF. HEF-PEF, which is heart failure with preserved ejection fraction, think about that diastolic. It's not a problem with the squeeze, it's a problem with being able to relax and fill with blood. So their EF is going to be normal, so for the purpose of the definition it's greater than 50 percent, but the heart is not able to relax and get enough blood in for that next squeeze. Now that gray area between 41 and 49, where they're not really reduced but they're not really preserved, is what we call HEF-MEREF, or heart failure with mildly reduced ejection fraction. And this is an important period, so patients that fall in that range, you're really trying to do your best to prevent them from moving backwards and to reduce EF and get them stabilized or even improved, which you can do. So we do have patients that have heart failure with improved ejection fraction, so they were previously HEF-REF and now their ejection fraction has improved and may be greater than 40 percent. That does not mean that they are cured. Nobody is ever really cured. They can be stabilized, but once you have a diagnosis of heart failure, whether you've had one exacerbation or 10, that person always has a heart failure diagnosis. So I know sometimes patients will ask, does that mean I'm cured? Unfortunately, they're stable, but they are not ever really cured. And this is just kind of an interesting graphic I want you to get used to, because patients can either be warm and wet, cold and wet, warm and dry, cold and dry, and that really will tell our teams, our clinical teams, how we want to treat them. So if somebody's warm, that means they're getting perfusion, so they're getting blood flow, right? So then cold is if they're not getting perfusion, and then obviously dry is if they're not overloaded and wet is if they are. So depending on what they're presenting with, is it a perfusion issue, is it a volume issue, or is it both, will drive the therapies, because sometimes we need to get rid of the congestion, and sometimes we need to help with perfusion, and sometimes we have to do both. So how they present and their symptomatology will help drive what therapies they need. Okay, so next module in part two, we will talk about what those therapies will look like for our heart failure population.

heart failure

prevalence

risk factors

pathophysiology

diagnostic tools

therapies