Next, we are going to talk about heart failure. Heart failure is a leading problem in the United States. With more than 5 million people diagnosed, it's probably actually much higher than that. A big contributing cause to death in a lot of people.
And half of those who are diagnosed will die within five years. This costs a lot of money across the United States and leads to significant loss in productivity and quality of life. So let's talk a little bit about the pathophysiology. Going back, we remember MAP, or mean arterial pressure, is derived from both the cardiac output and the systemic vascular resistance. We will remember, go back to your basic patho, that cardiac output comes from both your heart rate times your stroke volume.
And stroke volume is derived from your contractility. and your preload or the amount of fluid that you have on board. Systemic vascular resistance, back up to it, is basically blood pressure. That determines how hard the heart has to work to push against the blood flowing out of the heart to go to your body.
Your heart rate and contractility are driven by beta-1 and are compensatory, can be compensatory, if your systemic vascular resistance falls or your... preload falls, you're dehydrated, then the sympathetic nervous system works on heart and contractility. However, in instances such as heart failure, these compensatory mechanisms can go awry and lead to disease. These beta-1, these effects, these increased heart rate and contractility leads to remodeling of the ventricles, which is that is not something we do not want.
So when we think about the effect on the heart, there's both a neural and hormonal effect. The neural effect is these are these beta one receptors that contribute to heart failure. Let's talk about heart failure in terms of right or left. We have the right and the left with the lungs in between.
And of course, we have our vascular perfusion going on. One thing that happens in heart failure is that we have poor perfusion to the kidneys. And this will lead to a release of renin.
And that whole renin-angiotensin system will get going. And this leads to... when you release the angiotensin 2, this causes vasoconstriction and increased systemic vascular resistance, which of course just makes things worse.
And I'm talking about left-sided failure right now. So the problem that occurs on left side of heart failure has a lot to do with systemic vascular resistance and volume both. That vasoconstriction that occurs not only affects to the kidneys and worsens it, but it also affects perfusion to the adrenal glands.
This leads to the release of aldosterone, which then causes increased sodium reabsorption in the tubules. This, of course, only worsens the situation and causes more fluid and more symptoms. So when you think about that, you think of angiotensin 2 and aldosterone is really the hormonal issue with heart failure.
When remodeling occurs secondary to increased preload, that's when you get heart failure with reduced EF. When it occurs secondary to increased vascular resistance, you get heart failure with preserved EF. This, of course, is very basic.
Most people have some of both, but that's just a very basic idea of that. So in the case of increased fluid, the fluid will back up behind the site of failure. and if the left ventricle fails the fluid will then back up with them in the lungs leading to pulmonary edema so this is our man we're going to have to show you the symptoms of left-sided heart failure.
They will often present with dyspnea on exertion, paroxysmal nocturnal dyspnea, where they just wake up in the middle of the night, short of breath, and orthopnea, where they will require a lot of pillows to sleep at night. In addition, you may see other symptoms secondary to hypoxia, such as confusion, fatigue, restlessness, tachycardia, and tachypnea. When you're doing your assessment, what you're going to see is crackles. On the right side, when that side fails, then the fluid will back up to the superior vena cava.
um and the and and into the body and sometimes into the liver and they will then develop dependent edema that could be the feet it could be the buttocks uh it just is wherever is closer to the floor is where the problem will happen um this can also um so these individuals will present with peripheral edema, dependent edema. They'll present with weight gain, JVD, hepatojugular reflux. And some people will actually develop a congestive hepatopathy.
So it will begin to affect their liver. And when that happens, They will have elevated liver enzymes. They may also present with abdominal pain, malabsorption, and a poor appetite. So when you have all this fluid on board, you are going to see an increase in atrial stretch.
And so you'll then see an elevated BNP. Most commonly, left-sided heart failure occurs first and can lead to right-sided failure. Most people have both, though. You may only see signs of left-sided failure in more acute situations, but if it's ongoing, it will always begin to eventually affect the right side. Right-sided heart failure in isolation leads to cardiopulmonary.
This is usually secondary to a pulmonary issue such as a long-standing lung disease, long-standing COPD, pulmonary hypertension, pulmonary fibrosis. Um, so what are the symptoms secondary? Um, so what we've gone over now are the symptoms, um, related to each side of the heart. And remember, left-sided usually leads to right-sided.
So you're going to have both sets of symptoms, but on occasion, a person will have an acute left-sided failure and will only have left-sided symptoms. Remember those left-sided symptoms are relative. secondary to the fluid backing up into the lungs and causing respiratory symptoms and hypoxia. This also leads to poor perfusion to the kidneys, resulting in the whole angiotensin system being activated, which leads to vasoconstriction, further affecting the adrenal glands, causing the release of aldosterone. So a whole thing there.
In addition, when the right side is failing, you will have fluid back up into the periphery and also sometimes into the liver, causing liver problems. What you're going to see on initial in your interview. you're not only evaluating the types and symptoms and the severity of symptoms, but also you're beginning to investigate the underlying cause.
So you're asking them a lot of questions. A family history of cardiomyopathy is really important and may lead you to investigate a familial disorder. Anything such as hypertension or a history of coronary artery disease or chest pain may point you to ischemic etiologies. Alcohol is another cause of cardiomyopathy.
If they're an alcoholic, that might be part of your underlying cause. If they've had a viral illness followed by a sudden onset of symptoms, then you might be looking more at a viral myocarditis. And you're also checking their medications to see if any of these could possibly be exacerbating their symptoms. So do a thorough assessment, asking a lot of subjective questions, but also getting a really thorough history. I've written you have here on the slide some things to include your physical exam.
You want to do a complete physical exam. Some considerations in this, your vital signs. You want to know, are they hypertensive?
Are they hypoxic? Are they tachycardic? On the cardiovascular side, do they have an irregular pulse, which might point toward atrial fibrillation? Do they have any murmurs?
Do they have any extra heart sounds like S3 or S4? Is their point of maximal impulse displaced? Do they have any JBD or an hepatoducular reflux? When you're assessing the abdomen, you want to look for hepatomegaly, spleenomegaly. You want to look for any excess fluid which might be present in the periphery of the legs.
Do they have ascites? Is there extra fluid, periorbital fluid, or in their scrotum even? In the respiratory system, of course, you're looking for the presence of crackles or rails.
Patients with chronic CHF may not have them. There is a compensatory mechanism which increases the recruitment of capillaries to help take care of the extra fluid and also increases lymphatic drainage from the lungs. So people who have longstanding CHF may not have crackles, though they're still symptomatic. Other things like this periorbital purpura that you'll see on this slide. And if somebody has this periorbital purpura and they have cerebral neuropathy, these are features of amyloid cardiomyopathy.
If you see skeletal deformities, they might indicate Morphin syndrome. So these are all things you have to do a very thorough exam because you're looking at their signs and symptoms, but also Are there underlying causes? From a diagnostic standpoint, we want to look, of course, at a chest x-ray. We're looking for cardiomegaly. We're looking for pulmonary edema.
We want to look at BMP. And we'll talk a little bit more about that in a moment. But one thing to remember is that BMP is falsely low in patients with obesity.
EK gene findings may point to a cause of or an exacerbating factor such as atrial fib, frequent PVCs, runs of SVT. Those could all be contributing to the problem. You may also note left ventricular hypertrophy or a previous myocardial infarction.
Heart block and other conduction abnormalities may be a causative factor as well. They can also point to another underlying cause, such as sarcoidosis. An echocardiogram is really your way to determine which type of heart failure they have and how severe it is. So you're going to note on that their ejection fraction. Do they have a normal ejection fraction with this heart failure or is it decreased?
What's the size of their ventricle? Is there a presence of hypertrophy? If you see pericardial thickening, this might be suggested of pericarditis.
Some other things you want to look at are things such as anemia or infection, which can exacerbate CHF. You're looking at their electrolytes. Hyponatremia is very common in severe heart failure, but it can also occur secondary to excessive diuresis. So it can come both ways.
Liver function, again. As the right side is affected and you get some liver congestion, you can start affecting the liver. TSH is another thing to look at. You want to hemoglobin A1C if it hasn't been checked to make sure if there's any diabetes affecting this. Sometimes we check a SED rate, but eventually a stress test or cardiac cath may be indicated to rule out any ischemia as the cause of this heart failure.
So just a few things though. Think about with a BNP. There are some other etiologies other than heart failure to an elevated BMP. And I've got a whole list of them there for you.
Atrial fib, even some chemotherapeutic agents, recent cardiac surgery, pericardial disease. You know, if you have somebody with pericarditis, they can also, they may come in with symptoms you think. They're short of breath, they're having pain.
may think they're in heart failure, but it may just be the pericarditis. There's also some non-cardiac causes of elevated BNP. As you get older, it's more likely to be high anemia. Renal failure is a big one. Can't really trust it in somebody with significant renal failure.
Pulmonary hypertension and obstructive sleep apnea will increase it, as does any critical illness. So let's look at current recommendations. for checking BMPs. It is now recommended that a BMP is used as a screening tool for those at risk for heart failure. If the BMP is found to be greater than 50, it is recommended that they have further evaluation with a cardiologist and an echocardiogram.
But we also use it as part of our diagnostic workup for those with acute or new onset dyspnea. And we use it for our prognosis during episodes of acute decompensation. They've been admitted and now they're discharged. BMPs are recommended to assistance in how they're doing. What's their prognosis?
So we're now using BMPs for more than just somebody coming in with acute failure. So now we're going to focus on heart failure with reduced EF. or the old term is systolic heart failure.
And what we want to do is we're going to talk about the treatment for that. So when your stressor is increased volume, you end up with a hypertrophy, a centric hypertrophy. And what happens here is as the stress increases, your sacraments are added.
And... Remember, the muscle cell is the myocyte and sacramers are the contractile part of that myocyte. So as the fluid increases, you see more sacramers added and actually causes those myocytes to stretch out.
So then as they stretch out, what you get is the size of the heart gets bigger, but the walls thin out. Thus, while there are more sacramers, the wall is thinner and it doesn't contract as well. So the ventricle changes shape and it's unable to push the blood out into the aorta as well.
And this leads to a low ejection fraction. So to have heart failure with reduced CF, that is an ejection fraction, less than 40%. So what causes this? The easiest way to remember this are three words.
Leaky, floppy, and dead. So leaky, that would be leaky valves. Leaky valves, aortic insufficiency, something else going on with the valves like endocarditis.
Floppy muscles, things that can cause that are things like a viral infection, chemo, alcohol. And then a dead heart. Do they have, they had an MI, do they have that area of the heart?
that is no longer functioning. And these are the main things that can lead to this. So how will the patient present?
First, you're going to see, of course, the left-sided symptoms we talked about with the paroxysmal nocturnal dyspnea, the dyspnea on exertion, crackles, the point of maximal impulse will be displaced downward and laterally. And they often will present with that S3. This happens first in the left, and then this is followed by right-sided symptoms.
They will get JVD, the weight gain, the dependent edema, the hepatojugular reflux, and possibly it will affect their liver. So what we're going to do first, of course, is the diagnosis. We're going to get a BMP and echo in. Eventually, this will be followed by a catheterization to determine if... This is related to ischemia or to a cardiomyopathy.
Other tests that will be done are things such as a chest X-ray to determine if there's any pulmonary component to this and a 12-lead EKG antitroponin. So now that we've got that, let's look at treatment. Now we're going to get... in-depth in treatment on the next two slides, but I wanted to give you a little blip here.
So our treatment is guideline-directed medical therapy. However, if the EF is less than 35%, they have a real risk of arrhythmias. At this point, we might consider an automated internal defibrillator.
If the QRS is very wide, or you have this left bundle branch block, we may consider cardiac re-synchronization therapy, such as a biventricular pacemaker. And this line here is kind of on the way to transplants. There are things that can also be done. You know, if these two things don't work, that either you've used the biventricular pacemaker or an automated internal defibrillator where still having issues, they're on their way to a transplant.
There's some bridge things we can do. One thing is a continuous inotropes such as dobutamine or milrinone. This can be a bridge to a left ventricular assist device and ultimately a transplant. Not everybody goes down this route and many are managed medically, but this is the end result if the other measures don't work. So our goal of treatment is really we want to decrease that cardiac workload, decrease our volume and optimize that left ventricular function.
This is going to lead to reduced mortality, a better quality of life, more functionality, more functionality. We want to see if there's any underlying cause and treat that and also manage all those comorbidities. And another goal is to decrease hospitalizations. So let's talk about the medical management. at those specific guidelines directed here.
We have the New York Heart Association classifications for heart failure. These classes are based on how much activity a patient can do before becoming dyspneic. For example, a class one patient really didn't have any symptoms.
You know, they're unlimited. whereas a class four, they're going to have dyspnea at rest. And in between, you have class two and three, where two would be dyspnea with a lot of exertion, like climbing a bunch of steps, whereas class three will start to have dyspnea just walking on flat ground for a little while, so they have worsening symptoms.
So what we know is that everyone, whether symptomatic or not, should be on a beta blocker and an ARB with a nephrolysin inhibitor. These are important components of the patient's therapy. The nephrolysin inhibitor is something like cecubitril.
These are really important. It cost prohibits those, then they may go with an ARB only. We generally use an ARB over an ACE due to the angioedema and the cough.
Entresto has both an ARB and an F-glycin inhibitor in it. Again, this treatment is for all, whether they're symptomatic or not. And so how do they work?
ARBs. decrease aldosterone and decrease fluid and water retention. They also decrease vasoconstriction, thus decreasing afterload, improving their blood pressure and improving their heart rate.
So that will lead to reduced ventricular remodeling. So you always want to start at a low dose, increase every one to two weeks. You want to monitor for hyperkalemia.
and decrease renal function. Remember, in the presence of a renal artery stenosis, that would be a key, is if you put something on an acer and arm, and then they begin to have worsening renal function. Saccharine butyrol, which is a neprolysin inhibitor, it degrades vasoactive peptides, bradykinin, adrenal medullin. And so what does that do? It causes blood vessel dilatation, reduction of extracellular fluid volume, DI sodium excretion.
You don't want to give your... um, you don't want to give any Saccharbutyla or Valsartan within 36 hours of an ACE. You have to wait a while to give that. So these are the mainstays of therapy, even if you're asymptomatic.
Um, so what happens next? Those are for everybody. Again, beta blockers, uh, these are also for everybody. What do they do?
Uh, they should be started at low dose and gradually increased. They block beta-1 and beta-2, resulting in decreased heart rate and blood pressure and improved cardiac output. When should you avoid beta blockers?
You should avoid them in the presence of bradycardia, of course. Hypotension, hypoperfusion, heart blocks, peripheral arterial disease with ischemia. So... At this point, so that's for everybody, at some point they may become ischemic, I mean become symptomatic. In the past, if they became symptomatic, the next thing we added was a loop diuretic, which was either furosemide or torsemide.
They have found in some studies that torsemide is more effective. And then once they move to stage three, we had to decide between hydrolyzine and isosorbide or a mineral. corticosteroid-like Spirulactone. But a major change occurred in 2022, moving Spirulactone from a third-line agent to way up at the top of the list for a symptomatic patient. At that point, in a symptomatic patient, we now add a Spirulactone and an SGL2 inhibitor first before adding loops.
These are based on the ACA and the SGL2 inhibitor. American Heart Association, American College of Cardiology classification. And these are letters. A, of course, is no risk, no treatment.
B is when somebody has structural heart disease. Their EF is less than 40, but they are asymptomatic. They, again, they'll be put on beta block or ARB and psychobuteral. And C, they have started having symptoms.
And while we don't ignore the fluid and not give loops, we start off with spirolactone at a low dose and then that SGL inhibitor. Loops will be added if the symptoms continue once you've maximized other things. But loops, while they do help with symptoms, they don't help with remodeling.
Remember your beta blocker, your Losartan, those actually improve remodeling and decrease mortality. So again. That's what you add once they have symptoms.
There's a few other things that can be added down the road. You can then add furosemide or torsemide. You can also add some other diuretics like thiazides, metallosin can be added as well.
You can also add your hydrolyzine and isosorbate down the road if you continue to have symptoms. And we will, of course, you know, we'll give our loops as needed and then we'll add these others going forward. Again, as symptoms worsen, we're moving to a heart failure classification D. That's when we're moving more towards an automated internal defibrillator. which will be added to the therapy.
And don't forget our, and what we talked about earlier with the inotropes, if none of your other things work, continuous inotropes leading to a left ventricular assist device and eventually transplant. Now let's don't forget lifestyle changes that are going to be initiated on it. initiated on everybody.
with any heart failure. A key to this is daily weights. We do teach our patients about fluids and we teach them about sodium.
You know, in the past, we would talk about two liters of fluid and two grams of sodium. I think this goes better if talked about with daily weights. That way, people can understand that, oh, I went to Checkers and I had a hamburger and fries and Now I'm up two and a half pounds today, sodium retention.
And that lets people begin to start monitoring their sodium and their fluid kind of on their own based on their symptoms. So we do want to initiate these lifestyle changes, though, with the daily weights, looking at fluid and looking at salt. Other things that we want to do is to avoid incense because they do worsen heart failure.
Exercise is tolerated. Cardiac rehab can be very appropriate for these individuals and can improve function. You know, if they're at a stage four or stage D, depending on which classification you're using, then, you know, they may not be able to do much. You want to work at treating any ischemic issues that might be contributing to this. and work at risk factor reductions, controlling that blood pressure, their glucose, the renal function, smoking cessation, restricting alcohol are all important.
Remember over here on the left at stage D, when they're having significant dyspnea at rest, just to recap, once you have, we're going to start any patient, whether they're symptomatic or not, we'll be put on carbetolol. I mean, put on a beta blocker and an R plus secubitril. Once they have symptoms, we're going to add mineral corticosteroids, spirolactone, plus an SGL2 inhibitors. Now, I didn't talk about SGL2 inhibitors as to what they do because they don't know how they work.
But there have been multiple studies done that show that people who are on SGL2 inhibitors have much better outcomes with heart failure. than those who aren't on them. So now they're adding them.
If the Spirulactone and the other measures are not controlling their symptoms, then you're going to start adding loop diuretics and move down the line. Other considerations are of course the Thiazides, Hydralazine, Isisorbate, and even Dijoxan. If they still are not controlled, that's when you're moving toward transplant, you will try an automated internal. cardiac defibrillator or pacer.
But if you're still having significant symptoms and you've maximized everything, you're moving toward a transplant and they may have as bridge therapy before transplant, a continuous inotropes or a left ventricular assist device. And again, lifestyle treatments for everybody. What about an acute heart failure? In acute, we want to make sure that we rule out any etiology.
Are they having an arrhythmia? Do they have an MI? Are they having an MI?
Are they being adherent to their medication and diet? We want to check that. I'm not going to go deep into the treatment at the acute care facility because you won't be doing that. But, of course, they diurese. They may need oxygen.
They may need CPAP. But what I do want to say is the big thing after that, once that's been taken care of, is that you want to optimize their therapy. For example, if they were already on, you know, they weren't symptomatic before, they were on their ARB, their nephrolizumab inhibitor, their beta blocker. Well, now they're symptomatic. Then, of course, post this event, this exacerbation, you want to add.
the Spirulactone and SGL2s. If they were already on those and now have become symptomatic and had an exacerbation, then now it may be time to add daily or every other day loop diuretics. So we want to optimize their current therapy. We'll briefly talk about heart failure with preserved EF.
Remember, the primary cause of this is increased afterload, too much resistance. The heart is having to work too hard to push. And so what happens in this case is the Thackeramers line up side by side, increasing the size in a large ventricle. But instead of having a thin wall, they have a thick, beefy wall. And this in turn leads to difficulty in relaxing and letting the blood come in.
And this is also termed diastolic dysfunction. So they're not being able to relax. These people will have a normal ejection fraction, but they will have symptoms of heart failure. The etiology is usually hypertension. It's also more common as the one ages.
Having ischemic heart disease can cause this as well. And some of the cardiomyopathies can also cause heart failure with preserved EF. They're not going to present any different than a patient who has heart failure with reduced EF. And you're going to diagnose them the same. The only difference in presentation is that heart failure with preserved EF are more likely to have an S4.
But remember, heart failure with reduced CF are more likely to have an S3. Your treatment is exactly the same, but you want to pay special attention to controlling that hypertension as part of the cause. Last thing is a few comorbidities to deal with when you're talking about heart failure.
One thing that has been added to the recommendation is. For those individuals who have low iron levels and a transferrin saturation of less than 20%, it has been recommended that they receive IV iron replacement and even possibly erythropoietin. They need more oxygen carrying capacity and giving them this IV iron has been shown to improve functional status and quality of life.
Another thing which is a newer recommendation is that those who have heart failure or they're at risk for heart failure, their blood pressure should be kept at less than 130 and actually maybe even less than that, maybe less than 120 to help control remodeling and help to control this getting worse. The other thing is that it's really important to assess for... any sleep apnea because this can definitely contribute to heart failure.
All right, that's all for that. Thank you guys for listening.