So today, we're going to talk about congestive heart failure. And then I'm hoping, based on your work last week, that you're very comfortable related to cardiomyopathies. And now we're going to talk about is that feeling myocardium and left ventricle and even right ventricle at times begins to fail. What are we seeing from a symptom and a sign type management for our patients? So the first thing I want to describe, and again, it's more of semantics, but heart failure is really a clinical syndrome, a syndrome. It results from any structural or functional cardiac disorder that impairs the ability of the ventricles to fill or eject blood. So what that means is you don't have to have a reduced ejection fraction to see heart failure. In fact, we see it very often in patients with more of a diastolic dysfunction type picture where they're not filling well. We can also see it in patients with an increased cardiac output needs where, again, the demand doesn't meet the need. And so they're not able to keep up. So patients with high cardiac output failure, oftentimes we'll see in patients that are anemic or have some sort of a toxic thyroid issue going on. But again, just remember that heart failure is not tied to a specific ejection fraction. Certainly, low ejection fractions increase risk, but you're going to see it in a multitude of different issues related to the myocardium. We're also going to see a chronic versus acute. And so we have acute times of exacerbations or decompensations, and then we've got those patients that are living with just long-term poor cardiac output and function and are just managing to get by. A few statistics, because frankly, it is one of the major health issues of our current environment. So it affects just under 5 million Americans. We have half a million new cases each year that fill into that. It increases with age and the most common cause of hospitalization in patients over 65. It's also the most common cause of readmission in patients over 65. So if you haven't picked up on it yet, heart failure is a major initiative around readmissions, decrease hospitalizations, simply because it is such a high cost. Mortality is high. It's 50% at five years. We see about 300,000 deaths per year with a price tag of $24.3 billion annually, with $3 billion of that being on drug therapy. So again, significant cost, significant morbidity and mortality. And so you can imagine we spend a lot of time talking about heart failure. What is a little frustrating is that we have come a long way when it comes to our pharmacologic therapies, the way we treat heart failure, and understanding the mechanisms behind heart failure. And yet, it doesn't seem that we've done a very good job of actually budging any of these numbers. The costs are still high. The morbidity, the mortality is still very high. So we have a lot of work to do. So the next topic I want to cover, really, to cardiomyopathies and heart failure is the concept of afterload versus preload. So again, when you start talking about heart failure therapies, we're going to talk a lot about afterload reduction. And what does that really mean? What are we doing physiologically when we reduce somebody's afterload? So I'm going to take, and we're going to talk about the flow, the blood flow through the cycle. And I'm going to split the heart up into two sections. So first, we're going to have our right-sided. So this is the right ventricle. We're going to have the right atrium. And if you remember, we've got the IVC coming up this way and the SVC coming down this way. And this is the venous return. So the next thing we're going to talk about is we've got our lungs. So from the right ventricle, the blood flows into the right lung and the left lung. And then from the lungs, we move into the left side. So you've got your left atrium and your left ventricle. So when we think about preload and afterload, and again, I'm going to make this pretty elementary. But again, it is really, I think, what makes sense. So out of that left ventricle, we've got the aorta. Your preload is really about the volumes that are going in over here. It's what the volume is related to that venous return. I'm going to put over here venous return volume. So in order to affect our preload, we're going to affect it by giving more volume. So by giving IV fluids, that's going to increase preload. If you want to decrease preload, no IV fluids, and we start thinking a little bit about the diuretic piece of it. Although, I'm going to show diuretic also can affect afterload. Afterload is really the pressure that's on the backside. So it's the pressure that the left ventricle is contracting against to move into the periphery. So it's about that systemic vascular resistance, or SVR, that we talk about. So this is your afterload. So when we think about afterload and we talk about heart failure, one of our goals is we're taking a left ventricle that's not doing very well, contractility is down, and we're trying to offload it so it doesn't have to work so hard. So how can we do that? Well, number one, we can do it with vasodilatation. So your vasodilators, that's your ACE inhibitors, that's your hydralazine. We vasodilate our aortic and our arterial beds, make them bigger, decreases the pressure. We decrease the afterload. We offload the left ventricle. And now that ventricle can contract a little bit easier because it doesn't have to contract against so much pressure. The other way we can do it, and again, you could argue it's a little bit of preload, a little bit of afterload, but it's through the use of diuretics where we're decreasing volume. So again, when we start thinking about heart failure management, that concept of afterload and what that really means and the medications that we're using starts to make a lot of sense. The next thing we're going to talk about is the concept of left-sided versus right-sided failure and this whole congestion and what happens within congestive heart failure. So again, if we go back to our schematic here where we've got our right atrium, our right ventricle, you've got your blood venous return coming up through here. We go into the lungs. I'm actually going to draw the SVC. We've got the lungs, and then we're moving over into the left side. We've got our left atria and our left ventricle, and then we've got our aorta for our cardiac output. So when we think about right-sided versus left-sided, it's really just that. So left ventricular failure, if we've got a pump that's not moving things forward, and then when I work with the students, one of the things that I describe, it's kind of like the heart is just like a pump in your house. It's meant to move things forward. If it doesn't move things forward, the volume, the water in your home, or the blood in the body starts to back up. So when we have left-sided failure, where does the blood back up to? Where does that pressure and volume back up to? First, it backs up into the left atrium. When the left atrium can't handle that extra pressure, and I'll tell you, the muscle mass of the left atrium is pretty small, so it doesn't handle extra pressure very well. Then it backs up into the lungs. So once we move into, let me put left-sided failure, once we start to have issues where the congestion, or that volume, or that blood has backed up into the lungs, we start to get increased vasculature. Those capillaries get full, they get congested, and then they start to leak. And that's where we get our pleural effusions. So when you think about the symptoms on this, that patient is your paroxysmal nocturnal dysmea type patient. It's your orthopnea patient. It's the cough. It's the rails on exam. That's left-sided failure, backing up into the lungs. When we start to think about right-sided failure, so again, we have a right ventricle now that's not contracting well. And moving forward, we start to get back up into the periphery and into the venous system. When we do that, we have our jugular veins up here. So we start to see increased jugular venous distension. And we've got our IVC coming up from our liver. So we start to get liver congestion and lower extremity edema because it's all backing up into that venous system. So again, you start to think about what's happening here. It makes perfect sense now what we're going to see on exam. So right-sided failure, left-sided failure. Now, the reality of it is we very seldom see just left-sided failure because once the lungs get congested, the pressures go up. The right ventricle is supposed to be moving fluid forward. It's a low-pressure side. There's not a lot of muscle mass over here. It starts to back up because it can't handle the increased pressure in the lungs. So we very rarely see just left-sided failure. Commonly, we might see right-sided failure for patients that have pulmonary hypertension for reasons other than cardiac. But again, you see a lot of that fluid backing up into the body. We see the edema. We see the JVD. We see the hepatomegaly and the ascites. So again, if you understand the concepts of what's happening, then the signs and symptoms make perfect sense. So we think about congestive heart failure. There's multiple risk factors. So I'm just going to walk through these. But hypertension, and we see hypertension leads to coronary disease, but it also leads to a hypertensive cardiomyopathy, where, again, over years of high blood pressures, that heart has to work harder. As we described last week, it initially does create a level of hypertrophy. So if you look at a patient with hypertensive heart, initially, you will see a hypertrophic heart. But eventually, it'll start to break down, and you'll end up with a dilated left ventricle. So what I call burned-out hypertensive heart can cause significant amounts of heart failure. And it had nothing to do with any coronary disease. The second one is coronary disease. So the most common cause of a secondary dilated cardiomyopathy is ischemic heart disease, or ischemic cardiomyopathy, specifically here in the US. And again, it's related to our incidence of coronary disease and MI. The third one is diabetes. Again, it's a risk factor for coronary disease, but it's also a risk factor for a diabetic cardiomyopathy related to glucose toxicity. And over time, that muscle will begin to break down. The fourth one is obesity. The fifth one is cardiotoxic drug therapy. And I put here any time. And the concept with this one is think about your chemotherapeutic agent, patient that had some sort of cancer. And 10 years later, they're showing up with now heart failure and a dilated cardiomyopathy. They did not necessarily have that when they were getting their chemo or initially finished their chemo. But over time, that left ventricle begins to break down. So again, I don't think at this point, there's a ton of correlation between time. Now, there is a correlation between dose amounts and certainly there's certain types of chemo, adriomyosin, the big ones, but there's others. Again, you'll get some of that in your reading, so not to go into a lot of details there. But I think the key is there is they could have had that 10 years ago or even 20 years ago and are just now showing up with their heart failure and reduced ejection fraction. The next one is alcohol and cocaine. Alcohol's interesting because it's one of the few etiologies of heart, of left ventricular dysfunction that will actually get better when you sustain from the alcohol. And so, and it's typically dose related. So these are patients that drink like a fifth a day. And so, it's one of those things though, but if we can kind of get in front of that and decrease the alcohol consumption, oftentimes that may improve. Cocaine is another one. We can see it's got a direct toxic effect to the myocardium. And then finally, family history of cardiomyopathy. We've got several different familial genetic disorders that cause primary dilated cardiomyopathies or even some interesting types of hypertrophic cardiomyopathies. And so, if you have a family history, there's a risk then for you to end up developing a cardiomyopathy. So etiology, I kind of touched on a lot of these already. You know, this is really, what are the things that causes structural changes? So we have all of the different things that can cause systolic dysfunction. So I mentioned coronary disease already. That's the most common reason you see left ventricular dysfunction in the US. Hypertension, and you know, when I think about the patient populations for this, it's much greater in our African-Americans and in older women. And then we also have idiopathic, where we don't really know, although there's a good chance likely it was a viral. And I've got here a history of myocarditis. So as our diagnostics are becoming more advanced, I think we're finding more incidents of myocarditis. Likely it's a viral type infection, where before we would have called those idiopathic and we're now finding that many of them are related to a viral issue. Diabetes, we talked about. Alcohol, we talked about. Infection, I just mentioned. Now, you know, there's a couple things. Viral is kind of the big one, but there are some other, there's some parasites, and certainly there's some bacterial infections that can cause systolic dysfunction. And then the last one is tachyarrhythmia. So this one's interesting as well. Specifically, you know, the one that I think of the most common is patients with atrial fibrillation with poor rate control. Over time, if they're living with a heart rate of 130 to 150 all the time, you actually develop a left ventricular systolic dysfunction related to that. The good news is, again, on that one, if we can catch it and get rid of, you know, and treat the arrhythmia, or at least slow the heart rate down, many times that myocardium will recover and we can see some improvement. Other things to think about are valvular heart disease. So aortic stenosis, mitral regurgitation, that kind of thing. Certainly peripartum cardiomyopathy. So those that occur in late pregnancy and after the baby was born. And then we've got all sorts of things that can cause diastolic dysfunction. Myocardial ischemia, myocardial fibrosis, pressure overload hypertrophy, genetic hypertrophy, infiltrative cardiomyopathies such as sarcoidosis or amyloidosis, and then the constrictive pericarditis. So again, you've got that pericardium and if it becomes fibrosed and starts to sclerose down, we have, it really kind of impinges and can inhibit the filling mechanism of those ventricles. So let's talk about presentation. So the typical presentation we see with patients that have an exacerbation of their heart failure, certainly a shortness of breath. Whether that's dyspnea on exertion or orthopnea at night or paroxysmal nocturnal dyspnea, oftentimes it's a cough. We also, they describe significant amounts of fatigue, not being able to do their normal activities, stop needing to rest, take more naps. Some of that is they're not even sleeping that well at night. So their sleep-wake patterns start to become disturbed. We've got exercise intolerance. Again, that dyspnea on exertion, not able to keep up with their normal activities and we've got fluid retention. So the pulmonary congestion and those symptoms I already described and then certainly the peripheral edema, weight gain, that kind of thing. I don't want you to forget about low cardiac output state because what's interesting about these patients is they may have an absence of fluid overload. There may not be any swelling, but what we do see is profound fatigue. They have an interesting, they have a narrow pulse pressure. Oftentimes they're very tachycardic unless we've got them beta-blocked down. And then oliguric, because you think about that low cardiac output, we are not perfusing end organs. So kidneys are not being perfused. So we're not making urine. They oftentimes will have issues with postprandial abdominal pain. So after they eat, they can get some abdominal pain and then they oftentimes may have some mental status changes. So I often ask the spouse if they've noticed issues with completing thoughts or some mild confusion, because we can see all of those as well. So what are sort of the things that we ask when we see these patients? So dyspnea on exertion. One of the things is sometimes it kind of creeps up on them as far as activity tolerance, if it's kind of been a longstanding deal. So I'll usually ask, kind of get an idea of what their current activity level is, but I'll ask them about activities of daily living. So I usually start with, are you still going to the grocery store? When you go to the grocery store, are you pushing your cart around? Are you finding that you're having a hard time getting through the store and using one of the motorized vehicles? How are you doing with just getting ready in the morning? When you get up in the morning, can you get your shower and get dressed? Or are you finding you have to stop several times or even once to catch your breath and really get your energy back? So I try to ask them typical type of activities. And are they able to complete them? Orthopnea, again, when they lay down at night, are they're sleeping on more than one or two pillows? You have to ask clarifying questions around these because oftentimes you'll get a, oh, I sleep on three pillows. And then, well, is that new? No, I've been doing that for years because I have back pain. Okay, well, I can't count that as orthopnea, but in a patient that's truly decompensated, they will say, yeah, in the last week, I have found that in order to get any kind of decent sleep, I've got to either sleep in my chair or I need to really prop the pillows up to keep my head up so that I don't, otherwise I wake up short of breath and coughing. That paroxysmal nocturnal dyspnea, I'm going to sleep okay, but two hours into it, I'm waking up, I can hardly breathe, and I have to sit at the side of the bed in order to catch my breath. Cough is a big one. I think sometimes we forget about this, but even that tickly type cough, is it productive? Is it not productive? Is it coughing at night versus during the day? Chest discomfort, oftentimes they'll describe, and it's not necessarily ischemic discomfort, it's more of a, they say they feel like there's a band around their chest. It makes it hard for them to expand their lungs and take a deep breath, and they just have this generalized tightness, and some women will describe, it feels like my bra is too tight, or I have this band and I just can't take a really good deep breath. Palpitations, are they feeling like their heart's racing or skipping? Any syncope or near syncope, so any passing out or feeling like they're gonna pass out. When related to the near syncope, you know, you find out if it's positional or not, because again, these patients are at risk for arrhythmias as well, so if they're having non-sustained runs of VT, and having, you know, sitting in the chair, and suddenly becoming near syncopal, that's very different than they've been sitting in the chair and they go to stand up, and now they become very dizzy and lightheaded. You got two different issues going on. So make sure you ask clarifying questions, if they answer yes to those. And then finally, fatigue. Nausea, we talked about a little bit as well as the abdominal pain. Oftentimes, these patients with the lower cardiac outputs will describe postprandial abdominal issues. They'll have a decrease in appetite. We have something called cardiac cachexia, and that's where patients tend to lose a lot of weight related to low appetites and inability to really digest their food well because of lack of perfusion to the GI organs. Nocturia is interesting in that during the day when we are about, you know, up and about, we're really, especially if you've got a lower cardiac output, we're shunting the blood to the GI organs, to the periphery, to the skeletal muscles to allow for movement. And then at night, when all of that's quieted down, we're not eating, we're not moving, the blood then gets shunted to the kidneys. So guess what happens? Well, the kidneys start to kick in, we get a bunch of urine made, and people have to get up in the night for the urine in order to urinate. Now, there's other comorbidities that can cause similar symptoms, especially in men like prostate issues. But that's one of your questions is, are they getting up more than once or twice a night to urinate? And is that new? Oliguria, so maybe they're not urinating at all. One of the big questions that we ask related to their diuretic is, if you take an oral Lasix, you should be using the bathroom between 60 and 90 minutes after intake of that medication. And if they're like, it's two or three hours before I have to use the restroom, then that is not an effective dose for them. Sometimes it's related to edema in the gut lining, and that's why oral's not working, and you gotta switch them over to IV. And other times, it's just not a high enough dose. But when you're looking at a patient who has decompensated, and you're trying to figure out what's the next plan, if they're not responding to the oral Lasix or oral diuretic you're giving them within that 60-minute kind of period, then you've got an opportunity there. Confusion, we talked a little bit about that already. Insomnia, again, they're sleep-wake cycles. They're fatigued, but they're not sleeping well. And then finally, depression is really common because they simply can't do the activities that they're used to. It's a tough, you know, they don't feel well, and over time, you can get issues with depression. And that sort of just creates more of a spiral because they don't feel good, they're not mentally feeling well, they don't wanna do much, and so it just kind of builds on itself. Some of the signs to assess for would be weight changes. So these would be the, usually, why I usually say, if you've gained three pounds in a day or five pounds in a week, and then, you know, go back to the providers that you work with in your organization, but it's usually somewhere around that range. And the reason is is because you typically, no matter how much you eat, you can't put on that kind of weight related to increased calorie intake. When your weight's going up that much, it's related to fluid. And although it's not an exact indicator, it does provide some early signs that volume's going up and the heart is beginning to struggle. Certainly, blood pressure. Is the blood pressure too high? And that's one of the reasons that the heart is struggling. Or are they hypotensive? So when you start to get into some low cardiac output states these patients can get pretty hypotensive. What's their heart rate? Is it too fast or is it too slow? Any jugular venous distension on exam. So you wanna get, if you're gonna be managing heart failure patients on a regular basis, you need to get good at looking for JVD. And there's, you know, very scientific ways of doing it. And I would, again, work with your team to develop those skills and make sure you have a good handle on identifying JVD. On a lung exam, you're looking for audible rails, wheezes, decrease in the bases, or decrease even, you know, a ways up in those lung fields, looking for pleural effusions. I will mention the wheezes because there is something that we describe as cardiac asthma, where when you get fluid buildup around those alveoli, what happens is they kind of get, between the alveoli, which actually causes the rails, and then you can get fluid buildup kind of coming up into the bronchioles. You can get a fair amount of wheezing. And it isn't because they have reactive airway disease, it's because they've got extra fluid and pulmonary congestion. So it's not uncommon to hear these patients wheeze. From a cardiac standpoint, they may have a displaced PMI or pulse of max, I'm sorry, place of maximal impulse. They may have a right ventricular heave. So put your hand on their chest and are you feeling that heart rocking? In patients that have right ventricular dilatation and significant right heart failure, you may very well, I've got some memories of some patients that it was very significant RV heave. Any presence of murmurs or gallops, so anything related to aortic stenosis or mitral regurgitation or other types of valvular disease. And then certainly your gallops, your S3 and your S4. S3 is more common for volume overload. S4 is more related to ischemic changes. But again, anytime that myocardium and that flow is disrupted or is not flowing normally, you can get some of those extra sounds. You wanna assess for hepatomegaly and then you wanna measure it. How many centimeters below the intercostal space is that liver? And then certainly peripheral edema. And I know this was mentioned one other time in the course, but don't just stop at the tibia area. You wanna, I've seen patients that have pitting edema all the way up past their sacral area. So I always check lower extremities. I do the pre-tibial pitting edema, but I go up to the knees. I look in the thighs. And then if your patients are laying in the bed, I always have them lean forward and I look for any sacral edema. Now for your male patients, I have seen some really significant scrotal edema. So don't be afraid to ask and look there because they can really run into issues with that. And that's a common place if they're pretty sedentary and not doing a lot of ambulation for that fluid to settle. So differential diagnosis. You know, you're thinking about heart failure, but what are some of the other things that can cause some of these symptoms? Lung disease, you know, intrinsic lung disease, pulmonary embolus, you know, PE, pulmonary hypertension, thyroid disease, different arrhythmias, anemia. We talked about that high cardiac output failure, just simple deconditioning, although you want to rule everything else out first, obesity, and then cognitive disorders. So what's your diagnostic approach? You've taken a good history, you're kind of thinking, oh, this might be volume overload, this might be heart failure. What are the things you need to check? So chest X-ray, you want to look at those lung fields. Is there increased vascularity? Any pleural effusion? Do you have fluid along the fissures? You know, some of that, maybe an increased cardiac silhouette for indicating cardiomyopathy. You want to check an EKG. You're looking for ischemic changes. You're looking for left axis deviation that might show some structural changes. You're looking for tachycardia, although you're going to get a little bit of that on exam, but, you know, are they in sinus rhythm or are they in a different rhythm? Then you want to check some labs. You're going to look at their electrolytes of calcium, magnesium. The reason those are important is because if you begin to diurese, you need to know what their potassium, magnesium is before you start. Here's an interesting one. So total protein and albumin. One of the things that can get a little bit tricky with patients that have significant peripheral edema is protein malnutrition. So I have seen lots of patients that are quote-unquote volume overloaded. We think might be in heart failure, but when we actually do some labs, we find out that their protein and albumin levels are so below normal that what's happening is they're getting that edemas related to lack of oncotic pressure. So it's a vascular issue due to poor protein intake. We especially see these on patients that have been hospitalized for GI issues, but they've been NPO for a while, or maybe they were critically ill and we didn't do a very good job of nourishing them through TPN or that kind of thing. So don't be afraid, you know, please check those because what happens is you'll start diuresing them, but if their protein levels are low, you can't get in front of it. And you'll actually end up with some renal dysfunction in the process of trying to diurese when you're not really seeing any improvement in the edema. And because the issue is not so much volume overload from a cardiac poor perfusion issue, as it is a volume overload from poor oncotic pressure, from protein malnutrition. You also wanna check a BUN and a creatinine so you wanna understand where your kidney function is. Liver function tests, so again, AST, ALT, that kind of goes back to that protein piece because if you have poor liver function and you're not creating enough protein, it's the liver that is one of our sources of protein, then you can run into some very similar symptoms. Lipid panel, you know, that just is looking for risk factor related to coronary disease. CBC, you're looking for anemia or any white count. Urinalysis is also interesting. Here, what you're looking for is not so much a UTI, but are they spilling protein? Do you have a lot of protein in the urine? Because again, that might be another way that they're losing protein. Thyroid function tests, another, you know, if you've got a hypothyroid state or a hyperthyroid state, again, the same concept is there. You can try to treat the heart failure, but until you get the thyroid under control, you're gonna have a hard time managing it. And then finally, BNP or proBNP. So that brain natriuretic peptide is a great indicator of left ventricular volume overload and stretch. And so when that's elevated, it's a good sign that the left ventricle is struggling and that you truly do have a patient with heart failure. So your next job after making the diagnosis is to decide the type and degree of LV dysfunction. So we can do that a couple of ways. Echocardiogram, so that's your easiest, most non-invasive, cheapest way. We'll assess your ejection fraction. It will look at any valve disease that might be there. It'll look at your myocardium, so it'll show any hypertrophy. And it will also look at diastology, so the ability for those ventricles to relax. Another way to look would be cardiac MR. We can now, again, we can see the myocardium. We can see the fibrosis in the myocardium. So if we have an area of hypocontractility or lack of movement, and we want to know, I had a cardiologist that I work with, and he said, is it dead or is it almost dead? Because if it's almost dead, we can work with it. If it's dead, there's not much we can do. So a lot of times in our LV systolic dysfunction patients, a cardiac MR can be very helpful in understanding what their long-term prognosis is, especially in the non-ischemics. Is that myocardium something that we can, through some of the remodeling management and neurohormonal management, can we get that improvement? And then just kind of a systolic dysfunction, by definition, is an ejection fraction less than 40%. Certainly, we also describe, and this is where I'm like, well, we kind of don't say the same thing. We also describe ejection fraction being normal, 50 to 65%. So there is a little bit of a gray area in that. Is it what happens when it's less than 50% or greater than 40%? And again, because we've got so much heart failure related to diastolic dysfunction, don't get hung up on that ejection fraction, especially when the BNP is elevated. You've got signs and symptoms that are consistent with heart failure. They may very well have a level of both systolic and diastolic dysfunction. So then you need to define the etiology. So are they ischemic? This needs to be excluded in all patients. An angiogram or an exercise pharmacologic stress testing with imaging is indicated. So again, unless they're 16 years old, we need to really get a good handle on their coronary arteries and make sure that this is not an ischemic issue. Any cardiac toxicities, you want to do really good history. Any chemotherapeutic agents, any illicit drug use, what are the things that may have had some toxicity issues? Tachyarrhythmia, any issues with heart rate, tachycardia. The valvular disease piece of it, you're gonna be able to tell by your echo. If you have a question on one of those valves, you may need to do a TEE to see those valves better. And then a good history related to familial cardiomyopathy. Any family members that had sudden cardiac death at a young age or had an early age of heart failure, you really want to have a good understanding of what their primary family history is. So a couple other things I want to go over with you that I think are really important concepts. So the first one is New York Heart Association functional classification. This is how we can all think about these patients and measure them objectively and talk amongst each other as providers. So if you are a New York Heart Association class one, that means I may have some structural changes, but my overall symptoms are zero and my activity level is completely normal. I am asymptomatic. For classification two, I have symptoms, but with moderate exertion. So when I think about a class two, these are patients that are still doing their activities of daily living. They're still going to the grocery store, but maybe they're describing things like, you know, six months ago, I could play tennis. Now I'm not doing that because I just get too short of breath when I do those things. So it's moderate exertion is limiting, but they're things they do every day. They still do pretty good. For classification three, these patients have symptoms with minimal exertion. When they're sitting in front of you, they're talking just fine. They feel okay at rest, but these are the patients that are, yeah, I have a hard time at the grocery store. Yep, I'm not really vacuuming in the house anymore. If somebody coming over, yeah, I struggle a little bit when I'm up and getting my shower in the mornings, I have to stop and rest a couple of times. And then class four, these are the patients that physically look ill when you walk in the room. They are short of breath at rest. They have what we call conversational dyspnea, meaning that they can't get a whole sentence out before they need to take a breath. So if you're hearing a lot of rapid respirations and they're having a hard time communicating because they're so short of breath, that is a class four. And typically you're starting to think about hospitalization in a class three. And certainly if they're class four, likely they're end up gonna be hospitalized in order to get on top of it. The other thing I wanted you to be kind of aware of and be familiar with is some of the staging. So AHA, ACC several years ago came up with heart failure stage, stage A, B, C, and D. And I'm not gonna go through all of this with you, but almost everything you need to know about heart failure and managing LV dysfunction is in this chart. So we not only have what a stage A is, and I'll just kind of go through the stages and the rest of it I'm gonna let you read, but stage A means I'm at risk. I have hypertension, I have diabetes, but my heart is structurally normal. This is kind of what happens in primary care. You need to be managing those risk factors. Stage B means I've now got some changes. So maybe I had hypertension and now I've got some hypertensive changes, but I don't have any symptoms yet. So this one, I always kind of like, how do they figure out who has stage B? Because if they don't have symptoms, maybe we didn't look, or how would we know to look? But these are your patients that have had an MI and the rejection fraction might be 35%, but they really haven't developed any symptoms yet. Or for whatever other reason, you've checked maybe they had a murmur and you checked an echo and you find that their EF is down a little bit, or they've got some other changes, but they've not had symptoms. Now, stage three means the heart is now still structurally abnormal, but we're getting symptoms. So we have known structural heart disease and we have shortness of breath and fatigue with reduced exercise and tolerance. And when you think about our therapies, this is where the therapies really, I mean, before we're using our ACE inhibitors, our beta blockers, now we're adding in aldosterone antagonists, we're looking at devices like biventricular pacing, we're thinking about ICDs if they're at risk and the rejection fraction is down. And then stage D is where we've got heart failure symptoms, even though we're on the right meds, we might have our biventricular pacer, we've had all the right things done, but the disease has progressed to the point that we still have symptoms. Stage D is where we start thinking about the advanced therapies. So VAD, transplant or hospice, it's kind of, do we move over to advanced therapies or we're starting to get to end of life once we've gotten to stage D. But I think, again, we talk a lot about these. And so as you move through and begin to manage heart failure patients, your ability to stage them effectively and understand the therapy goals for each stage, I think is really helpful. So if you get nothing else out of this talk, if you can get a good handle on your New York Heart Association classification and your ACC stages, I think you'll be in a good place. And then the final thing, this has nothing to do with heart failure in and of itself, but I do want you to be aware of, if you haven't already been, is when you're looking, there's a ton of research and literature on not only heart failure, but everything else we do in cardiology. And we have all these guidelines. And so one of the things that I've included in the curriculum is guidelines. And one of them is the heart failure guidelines. Well, embedded in these guidelines, you will see things like, this is a class one recommendation. This is a class 2A, class 2B, or class three. Class three means it's not recommended. It's not indicated you shouldn't do it. Class one is, you absolutely should. The evidence is strong. The benefit far outweighs the risk. And then you can kind of see class 2A, the benefit's still greater than the risk. Class 2B, it's kind of a, oh, we think the benefit's greater than the risk. Maybe consider it. So again, I just want you, because you'll hear a lot about, that's a class one recommendation. That's a class 2A recommendation. I want you to understand what all of that means. So when we think about heart failure and our management and therapy goals, we've really got three goals. So the first one is to treat the symptoms. So we just need to get this patient in front of us feeling better, so they can get back to better activities. We need to halt and slow down the progression of disease. So we need to stop that remodeling. So when we talked about the cardiomyopathy lecture, we talked a lot about that remodeling and maladaptive response, the ACE inhibitors, the beta blockers. We need to minimize any further damage. And then the third one is preventing sudden cardiac death. So remember, in patients with any reduced ejection fraction, they're at increased risk for ventricular arrhythmias. We need to manage that. So if they are a candidate for an ICD, if they are, we need to get them over to our EP partners or whoever might be implanting those in your program and get that taken care of. So you get a lot of reading this time because congestive heart failure is a really big topic. And it's a lot of what we do. So whether you're working in general cardiology or heart failure program, even if you're working EP or interventional, we all see a lot of heart failure. So I think there's some great concepts here that if you can get a handle on them, you'll find that managing these heart failure patients isn't quite as complex. Again, feel free to reach out with any questions that you might have, and we'll be happy to point you in the right direction or get you some answers. Thank you.

Congestive heart failure

Management

Symptoms

Preload

Afterload

Staging

Etiologies

Treatment