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Acute Care Cardiovascular Essentials for Advanced ...
Congestive Heart Failure
Congestive Heart Failure
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Video Transcription
Welcome back. So this week, we are going to talk about congestive heart failure, which is, again, very common. I'll give you some statistics here in a minute. But CHF is a clinical syndrome resulting from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill or to eject blood. And the reason that's important, and I wanted to start with it, because it's a foundational element to really understand the difference between systolic dysfunction and diastolic dysfunction, and then how they both can lead to heart failure symptoms and the different symptoms. From a diastolic standpoint, that's the ability for that left ventricle to really fill effectively, and it needs to be compliant enough that it allows for expansion. And what happens in some of our patients is that left ventricle becomes very stiff. And there's multiple potential etiologies for that, and we're not going to go into all of that today. But what I want you to understand is those patients with diastolic dysfunction, most of them actually have a normal ejection fraction. But since that left ventricle is not able to fill effectively, their ability to continue to get blood moving forward is impaired. The flip side of that is systolic dysfunction, where that left ventricle is weak and the muscle is not able to contract effectively, whether that was from a previous MI or from an overall dilated weakened left ventricle, but it's not able to eject blood effectively. And in that case, the ejection fraction is decreased, may only be able to empty 30% of its contents, 35. I've seen some patients with a slow with 10 to 15% ejection fraction. But understanding the differences between those two is going to make a difference when it comes to therapies, and in some cases, even how they typically present. Few statistics, heart failure is very common. Millions of Americans are affected, half a million new cases each year. Certainly, incidence goes up with age, and it's the most common cause of hospitalization in those patients over 65. Mortality is high, and it's still high. It's been high. And this is regardless of diastolic or systolic dysfunction, 50% at five years. We have about 300,000 deaths per year and a significant cost, $24.3 billion annually, with $3 billion on drug therapy. So definitely a big portion of our healthcare spending, but a big portion of our mortality and morbidity with our older patient populations. A couple more concepts, preload and afterload. And the reason these are important is because when we start talking about, again, therapies, this is kind of the levers that we look to manage. So preload is the end diastolic volume and the resultant fiber length of the ventricles prior to the onset of contraction. So it's that volume after they have filled. I also think of preload as the volume that's available. So if patients are hypovolemic or dehydrated, their volume will be down and that preload will be down. Afterload, however, is the impedance to the left ventricle ejection. So every time that left ventricle contracts and it tries to empty its contents into the aorta and out into the systemic vasculature, how much pressure is it having to really push against? And this is where one of our therapies comes in. We do a lot with afterload reduction. And what that does is it vasodilates and allows and kind of offloads that left ventricle so it doesn't have to work so hard. So really understanding those concepts will make sense as we start to talk about the therapies. We go into this in a lot more detail in the longer APP essential curriculum. So if you're looking for more details, I would reference you to that. So thinking about heart failure, and we're really going to talk about the acute presentation today. So what happens when they show up in the hospital? And the typical symptoms we see, shortness of breath, fatigue, activity intolerance, and fluid retention, both pulmonary congestion and peripheral edema. And some patients only have pulmonary congestion if they really just have left-sided heart failure. Others just have right-sided heart failure. Maybe their lungs are clear, but they have a significant amount of peripheral edema. I've seen people put on 70 to 100 pounds of peripheral edema related to right-sided heart failure with very little pulmonary congestion. So they can be seen distinctly from one another. There's something else I want to talk about briefly, referring to low cardiac output state. Occasionally, we will get an end-stage patient that presents with just profound fatigue, narrow pulse pressure, tachycardic, oligarch, so minimal urine output. And they may not look that fluid overloaded or volume overloaded, but they have a very low cardiac output state and typically represents very late end-stage disease management. So if you're doing late stage C and stage D heart failure patients, these are the types of patients that you're going to be encountering. So what are some of the questions we need to ask on presentation to really kind of narrow this down or as we think about our differential diagnosis? So certainly shortness of breath on exertion. We're going to talk about New York Heart Association classification in just a minute, but we want to actually quantify how much shortness of breath that they're having and how much exertion is required for them to feel their symptoms. Orthopnea, you know, are they, when they lay flat, are they able to lay flat? Are they using pillows at night that they didn't use to use? Are they sleeping in chairs in order to maintain comfort levels? Paroxysmal nocturnal dyspnea, are they waking up in the middle of the night short of breath and maybe going to bed and sleeping okay? And then a couple hours into it, they're waking up, gasping for air. They have to sit at the side of the bed, kind of like gravitation, pull that fluid back down so they can breathe again, and then they're able to get some more sleep. Many of them will describe a cough. Sometimes that cough is dry. Sometimes it's wet, but usually if it's wet, it's more of a frothy, light sputum versus more of a heavy, thicker that you would see in a COPD patient. Many of them actually describe chest discomfort, and they describe it more as a tightness, kind of constriction around their chest, and that's usually related to the fluid and difficulty of them expanding their lungs. Some will describe palpitations, especially if they're having any issues with some arrhythmias like AFib or even short runs of non-sustained ventricular tachycardia. You need to ask about syncope or near syncope. Maybe that is a sign of orthostatic hypotension, you know, as they stand up, that kind of thing, some volume management, and then of course fatigue. Nausea and abdominal pain, oftentimes if they have low cardiac output, they will get some postprandial pain just related to the body's trying to digest the food. We don't have good blood flow to that area. Nocturia would be urination at night. Now, what's interesting about that, especially in our low cardiac output patients, is that they perfuse their organs based on the need. During the day, we need to perfuse the brain because we're awake, and we need to perfuse the GI organs because we are digesting our food, and we may have some activity, so musculoskeletal muscles, but oftentimes the perfusion to our kidneys isn't great. That body will actually shunt, and so at night, when things are quieted down, you're sleeping, and you're not digesting food, that blood flow to the kidneys will increase, and they'll start to make urine at night, so that's oftentimes one of the reasons that we see nocturia in these patients. Some of these patients have very little urine output. If they're not perfusing well, or if the GI tract is edematous, and they're not able to break down or absorb the oral Lasix or oral diuretic well, their urine output will decrease. Some will notice confusion if they're not perfusing their brains well, and then most of them have difficulties with sleeping, as well as if they've been going on a long-time depression, just for the fact they can't do the things they normally do. How do these patients present? Well, some of them will present with weight changes. Oftentimes, what we tell our patients is to call us if their weight is up by more than two pounds in a day or three pounds in a week. Some will have issues related to blood pressure, so again, some of these may have high blood pressure, especially our diastolic dysfunction patients tend to present with very high blood pressure. Our systolic dysfunction patients actually tend to present with lower blood pressure. Pulse is interesting, because once they become decompensated, oftentimes they will become quite tachycardic. They're trying to increase cardiac output, and one of the ways to do that is to increase heart rate, so tachycardia is actually kind of an ominous sign with these patients. Jugular venous distension, we're measuring that here, looking at that volume overload, and then presence of audible rales, wheezes, or signs of pleurofusion. From a cardiac perspective, looking at the PMI, sometimes that left ventricle is large and dilated and displaces the PMI over to the left. The right ventricular heave may be present if they've got a dilated right ventricle and a lot of right-sided failure or core pulmonary type patient, and you can actually feel that when you put your hand on their chest. Loosening for murmurs and gallops, again, some valvular disease and or the gallops of the S3 or the S4 showing either volume overload or even ischemic nature. Hepatomegaly, when that liver becomes congested, it will become enlarged, and you want to kind of percuss that out and understand how far through finger depth is it below the rib cage or the costophrenic angle, and then, of course, peripheral edema. The folks that I'm working with that never stop at just the tibial areas but move yourself right up their legs, look for sacral edema, and then our men look for scrotal edema, and that will help, again, give you an idea of just how much edema they actually have. So, differential diagnosis, you know, there's different patients can present similarly, so those with chronic lung disease. Another thing to think about is pulmonary embolism or pulmonary hypertension. Thyroid disease, both overactive, so hyper and hypothyroid. Arrhythmias, patients that have had AFib with rapid rates for a really long time can develop heart failure symptoms. An anemia, especially if they're severely anemic, you may find symptoms of heart failure because the heart just can't keep up with the demand. We call that high cardiac output failure. It's not so much that the heart itself is structurally abnormal, but it's because the oxygen demand is down from the lack of hemoglobin, the heart is working quite a bit harder to maintain that. Deconditioning and obesity, again, we want to rule everything else out first, but you can see some of that, and then cognitive disorders. So, where do we start when it comes to workup? Chest x-ray is a great place because we want to look for any pulmonary edema or increased vasculature. ECG to look for rhythm, any abnormal rhythms, or again, signs of structural changes. So, any Q waves that would be consistent with previous MI, any axis deviation that could potentially be a sign of some sort of structural change, LVH, those kind of things. You want to do your electrolytes, calcium, magnesium. Again, part of this, oftentimes the electrolytes are abnormal, and we need to make sure those are replaced. And then total protein albumin, looking for that protein store. One of the other potential diagnosis on your list of differentials is actually malnutrition, protein malnutrition. So, if they have had low protein stores, we lose our oncotic pressure, and that allows the fluid to seep into the interstitial space, and those patients can look very similar to a heart failure patient. And you will diurese them and just not really get very far, and it's because their protein levels are so low. So, I always recommend checking that albumin and protein. And then the B1 and CREAT, you need to understand where they are at for renal function. Liver function tests, again, kind of same. That goes along with the protein albumin. And then lipid panel, CBC, urinalysis, thyroid function, and then the brain natriuretic peptide or the pro-brain natriuretic peptide to really give you a sense of just how much volume overloaded or how much of a stretch on that left ventricle there is. A little bit about New York Heart Association classification. Earlier, I talked about getting a sense of their dyspnea and their activity levels. So we have a great way of quantifying this so we're all speaking the same language. So New York Heart Association class one means the patient may have a history of heart failure but right now they're having no symptoms. They can do all their normal activities. Classification two means I'm having symptoms with moderate exertion. So my normal activities of daily living, I'm probably fine, but going to the grocery store, doing some of those types of things, I have to stop and take a break because I get short of breath and I need to rest. Class three means even my normal daily living activities are tough, taking showers, getting dressed, I'm having to stop, catch my breath, just can't seem to even get through those normal things. And then class four means that having a conversation with you is hard. At rest, I'm having shortness of breath type symptoms and I have what's called conversational dyspnea. I'm not able to get full sentences out before I have to stop and take that breath. This is a great way to understand and to describe your patient. That way when the next provider or clinician comes through and is reading your note, this will make perfect sense. And when we think about hospitalization, it's those with class three to class four symptoms that we typically think about because they have a hard time managing themselves at home and therefore need more aggressive therapy. So thinking about goals for therapy, we really have three. There's the treatment of symptoms. Number one, we wanna halt and slow down the progression of the disease and we wanna prevent sudden cardiac death. Today we're just gonna talk about the first because that's really the goal for the hospitalization is to kind of get back on top and manage those symptoms. So when we think about initial support for these patients, certainly airway and oxygen. So if their oxygen saturations are less than 90, you need to make sure we're using supplemental oxygen. Vital signs and monitoring if there's any concern for hemodynamic instability, continuous monitoring as an option is important. Continuous cardiac monitoring, especially for those first days until they're stable, they need to be on a telemetry unit. IV access, of course. Prompt diuretic therapy. I wanna talk about that in a minute. With strict monitoring of their urine output, their I's and O's are really important to understand how effective your therapy is. And then for some of those patients that are extremely hypertensive, early vasodilator therapy is important and it's consistent with the guidelines. So let's talk about diuretic therapy. Initial dosing should be received in the emergency department. There's a time element to this. And in some cases, if we diurese them in the ED, we may be sending them home. So if your institution kind of has it set up that they're not getting their first dose of IV diuretic until they hit the floor, you're wasting or you're losing time, if you will. What do we do for diuretic therapy? Well, your loop diuretic is your agent of choice. And we wanna go IV. The reason we do IV is because most of these patients, by the time they hit the hospital, their GI tract is edematous and they therefore are not breaking down and absorbing the oral medications that they're on. And so giving them IV allows for better efficacy of those medicines. So if they've not previously been on a loop diuretic, starting with a bolus of 20 to 40 milligrams is a great place and it's consistent with the guidelines. If they have been on previous, let's say they take it at home. Let's say they're on 20 milligrams twice a day at home. Well, what you're gonna do is you're gonna double it and change it to IV. So they're gonna get 40 milligrams IV Lasix as their initial dose and likely you'll dose it BID. Severity compensation with renal failure sometimes they're tough. And you wanna go back to previous hospitalizations and see what doses were given that were effective. It's a great way to learn from what we've done before and not have to recreate the wheel. So pull those old records and kind of see what's been working. And some patients will actually end up on an IV infusion. So a continuous infusion of Lasix or Bumex or some type of a loop diuretic versus bolus BID. With effective diuresis, you should see increasing your output within 30 minutes with a peak at one to two hours. If you have not seen that, in fact, most protocols will ask the nurse to follow up with urine output within one to two hours. And without a certain amount, they should give you a call so you can redose. Because if they haven't started with that increased urine output by them, then we have not given an effective dose or something else is going on. In addition, we need to monitor their lights and renal function closely, at least daily. Excuse me, if they're diuresing significantly, if you're getting a couple liters a day, you may wanna follow their electrolytes twice a day and make sure that potassium is replaced. Because you can really run into issues with hypokalemia with these patients if you're not careful. So when is hospitalization required? Well, if there's any evidence of severely decompensated heart failure with hypotension, worsening renal function, or ulceration, that's a sign that they need to be hospitalized. Those are all signs of decreased perfusion. So their cardiac output is significantly impaired. Dyspnea at rest, or increased respiratory rate, or hypoxia. So if their SpO2 is less than 90%, they need supplemental oxygen, and you're gonna have to admit them for that. If there's any hemodynamically significant arrhythmia, including a new onset of AFib with rapid ventricular rate, or if they're having issues with VT, those are things that they need to be monitored close for. Admit them. And then if there's any evidence of an acute coronary syndrome or ischemia, they need to be admitted for further workup and management. You wanna consider hospitalization if they've got worsening congestion. So if their weights are up and they're having difficulty with their normal activities. Any signs or symptoms of pulmonary or systemic congestion. Again, if you can balance this and get them diuresing so that when you send them home, they can manage on their oral medications, they don't have to be admitted. But if that's not the case and you're not really getting very far with the initial IV dose of Lasix, you probably need to admit them for closer observation. Any major electrolyte disturbance. Again, you can set them up for bad abnormal rhythms. You need to monitor that closely. And then any associated acute comorbidities, such as PE, pulmonary embolism, pneumonia, DKA if they're diabetic and have hyperglycemia and you're worried about diabetic ketoacidosis or any evidence or concern for stroke. And then finally, if they've had repeated ICD firings, that is another indication that you may need to admit those patients for closer monitoring. So we've got them started on their diuretic. We're also gonna put them on a sodium restriction, two grams a day and a fluid restriction, 1.5 to two liters a day. And you really have to have a strict input and output monitoring system set up. That's really important for understanding just how effective your therapy is and if you're getting close to a point where you can get them home. So make sure you order those isenodes. In addition, if they're not anti-coagulated for another reason, you need to think about DVT prophylaxis as well as hyperglycemia control. And so just again, as you're thinking about managing them in the hospital, these are both very important for, make sure they don't get a DVT while they're there. Couple other things to think about. So some of these patients will present with hypertension, with severe hypertension and heart failure. That oftentimes goes along with the diastolic issue or diastolic dysfunction. So you're gonna wanna reduce that blood pressure through the use of vasodilator therapy, IV nitroglycerin or other types of agents. The guidelines do walk through several different agents. IV nitrile is probably the easiest to use, but again, working with your clinical team at your institution as to what's the best choice or the typical practice patterns. From a hypotension standpoint, you wanna consider discontinuation of any of your home meds that will lower blood pressure or potentially just decrease the dosages. This is hard because we need these patients on beta blockers and ACE inhibitors to really halt the progression of their disease. But if they show up with blood pressures in the 70s and 80s, they're not gonna be then perfusing their end organs very well. You're gonna have to back down on those meds. Don't be afraid though to re titrate back up as they stabilize and begin to develop or actually improve and become more compensated. And then there is a portion of your patients that they're so hypotensive, you're gonna need to use inotropic agents. These are typically the systolic dysfunction only patients. And the common meds are usually Dibutamine or Milrinone. Again, working closely with your care team around typical practice patterns and which patients and when. So your goals for your hospitalization or improved symptoms, optimize your volume status. It's helpful to know what your patient's dry weight is. You may not get them back completely to their dry weight before discharge, but you need to know how close you are. One of the main reasons for readmission is we didn't dry them out enough the first time so they go home and they're continuing to have problems. Identifying the etiology and precipitating factors is really important. Sometimes patients can have issues with heart failure related to ischemia, progression of ischemic disease. Sometimes it's other issues, but I think spending some time walking them through symptoms, walking them through lifestyle changes is really important. I'll give you a couple of examples. I had a patient that I was working with that came in with an exacerbation. And as I was talking, you know, she'd been stable for a long time, hadn't been in the hospital for several years, and now suddenly she shows up. So now we're trying to work through it. Well, she was one that the previous week, she was having some issues with shoulder pain and saw the nurse at her assisted living facility who recommended having her take over-the-counter ibuprofen. And she just was tenuous enough that that extra NSAID that she hadn't previously been taking caused enough sodium retention and then fluid retention that just pushed her over the edge. And so that, you know, no more ibuprofen for you. But those are the kinds of things that are important. I had another patient that we were asked to see on the cardiology service. He was admitted to the hospital service just because he had been stable and it had been a long time since he'd been in. And as I was working through the consult, realized that he had just had a birthday a few days prior. And so as I was talking to him and his family, found out that it was a big birthday and they had a big birthday party. And at the birthday party, they had a lot of salty foods. And in this case, that was enough to, that's when he started feeling bad the next day. We often refer to Christmas and Easter and Thanksgiving as the gravy holidays. And a lot of our heart failure patients show up the next day because of that extra salt load. So just take some time and try to figure out, you know, what caused this, because that can go a long way in preventing it in the future. Additional goals include initiating and optimizing oral therapy. Again, getting them switched over to more effective oral doses of their diuretic. And then beginning to optimize or really push the doses of their ACE inhibitor and their beta blockers. We wanna minimize any side effects. You know, we can follow them closely. So when we make medication adjustments, we're monitoring vital signs and we're monitoring labs. And then lots of good patient education and then setting up the transitional care plan of who's gonna be managing them after they go home and when. Those are really important goals of the stay. When they're in, things we should be monitoring daily. So I's and O's, we've talked a lot about that already. Electrolytes and renal function. Magnesium and calcium, if you've had abnormalities and you've had to replace, especially the magnesium. Vital signs and cardiac rhythm. And then begin to titrate those beta blockers and ACE inhibitors. From an ambulation standpoint, we need to make sure they're up and moving around and if they have needs for home needs, so getting the therapies involved and then symptom improvement and patient education opportunities as you're rounding on those patients on a daily basis. Discharge preparation. I talked a little bit about already understanding what their dry weight goal is and define if you're able to, do you have know what your plan or your goal is for them to get them home. Home and functional needs. So social worker and therapy evaluation. Again, I cannot stress education enough. And then those follow-up plans. If their EF is down, do they need an ICD? Do we need to monitor them for the 90 days and titrate those meds to recheck the EF? Make sure that plan is in place. Any further workup of an etiology is in place. Do they need an ischemic workup? Are there other things going on that need to be followed up on? And then we really recommend, and it's consistent with guidelines, follow-up visit within 72 hours. Again, a lot going on with these patients and after they get home, they're confused about meds. They don't know who to call, when, where, all those sorts of things. So getting them back in shortly will go a long way to reducing your readmission rate and improve your patient outcomes. So that kind of brings us to the end of heart failure. Again, if you have questions, please feel free to reach out to us or any feedback. We're always happy for feedback. But I would direct you to the readings. There's a lot of information in there and we really appreciate your time and engagement.
Video Summary
In this video, the speaker discusses congestive heart failure (CHF) and its different types and symptoms. CHF is a clinical syndrome resulting from a structural or functional cardiac disorder that impairs the ventricle's ability to fill or eject blood. The two main types of CHF are systolic dysfunction, where the left ventricle is weak and unable to contract effectively, and diastolic dysfunction, where the left ventricle becomes stiff and is unable to fill effectively. The symptoms include shortness of breath, fatigue, activity intolerance, and fluid retention. The speaker also provides statistics on the prevalence and mortality of heart failure. The importance of understanding preload and afterload in relation to therapy management is discussed. The video also covers the acute presentation of heart failure in a hospital setting and the necessary tests and therapies for managing patients. The speaker emphasizes the need for strict monitoring of urine output, electrolytes, and renal function. The goals for therapy include symptom improvement, optimization of volume status, identification of precipitating factors, and initiation and optimization of oral therapy. The speaker also highlights the importance of patient education and discharge preparation, as well as the need for follow-up visits and further workup if necessary. The video concludes with a recommendation to reference additional readings for more information on the topic.
Keywords
congestive heart failure
types of CHF
systolic dysfunction
diastolic dysfunction
symptoms of CHF
therapy management
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