S1E21 Heart Failure

<v Speaker 1>Okay, so said, they're going to be doing heart failure,
<v Speaker 1>which is pretty important for the board, so you do
<v Speaker 1>you need to be familiar with it. They give you
<v Speaker 1>some ways to remember the things that you need to
<v Speaker 1>know and just focus on the high yield stuff for today.
<v Speaker 1>As always, thank you so much for the reviews the likes,
<v Speaker 1>but thank you for everybody that's checked out my YouTube
<v Speaker 1>page as well. Seeing a lot of positive comments coming
<v Speaker 1>in there, so it's definitely much appreciated. And if you
<v Speaker 1>wouldn't mind leaving me a like or a review on
<v Speaker 1>either Apple Podcast or my YouTube channel, I would really
<v Speaker 1>appreciate it if it is helping you. So let's get
<v Speaker 1>started with heart failure. So what is heart failure. I'm
<v Speaker 1>sure all of us are pretty familiar with this, but
<v Speaker 1>heart failure is a clinical syndrome that results from either
<v Speaker 1>a structural or a functional disorder of the heart. So
<v Speaker 1>you have either an impairment of the felling of the
<v Speaker 1>heart or an impairment of the ability of the heart
<v Speaker 1>to adequately pump blood. Now predisposing factors, there's one that
<v Speaker 1>you really have to know that you have to be
<v Speaker 1>familiar with because it's the most common cause overall. Sixty
<v Speaker 1>to sixty five percent of cases of heart failure. The
<v Speaker 1>predisposing factor is coordinary art or disease, so absolutely no
<v Speaker 1>that coronary artery disease. That's really important. Majority of cases
<v Speaker 1>are from that. A few more that you need to
<v Speaker 1>be familiar with. Hypertension and valvular heart disease like aortic
<v Speaker 1>stenosis are big ones, but they're becoming less prevalent as
<v Speaker 1>the years go on to improvements in early detection and treatment,
<v Speaker 1>but they are still predisposing factors. Diabetes, diabetes, obesity, and
<v Speaker 1>then of course the lesser, the less common causes like
<v Speaker 1>dox rubisin and dilated cardia myopathy, amoidosis and restrictive restrictive cardiomiopathy.
<v Speaker 1>But overall, if you remember cordinary ardor disease, you'll probably
<v Speaker 1>get the question right on the on the exam. And
<v Speaker 1>the next thing you need to know is the different
<v Speaker 1>types of heart failure. So that's important as well because
<v Speaker 1>that's going to help you understand the clinical manifestation and
<v Speaker 1>treatment options and things like that. So obviously we have
<v Speaker 1>different parts of the heart, and like I said, the
<v Speaker 1>clinical manifestations are all dictated relating to the part of
<v Speaker 1>the heart that is affected. First, let's start with the
<v Speaker 1>sides of the heart. We have a right and we
<v Speaker 1>have a left side of the heart. And the first
<v Speaker 1>thing that you should be aware of is that you
<v Speaker 1>can only have like exclusive left sided heart failure. You
<v Speaker 1>can have exclusive right sided heart failure. It's actually not
<v Speaker 1>that common. It's more common for both to coexist. So
<v Speaker 1>most of the time you can have right and left
<v Speaker 1>sided heart failure at the same time. But it is
<v Speaker 1>possible to just have left sided only heart failure normally
<v Speaker 1>in like an acute mi so cordinary art or disease,
<v Speaker 1>long standing hypertension. And then it's also possible to just
<v Speaker 1>have right sided exclusive heart failure and patients with pulmonary
<v Speaker 1>disorders like pulmonary hypertension COPD. And actually the most common
<v Speaker 1>cause of right sided heart failure is actually left sided
<v Speaker 1>heart failure. And why is that, Well, if we think
<v Speaker 1>about the path help it makes more sense. We already
<v Speaker 1>discussed that pulmonary disorders like pulmonary hypertension can lead to
<v Speaker 1>right sided heart failure, and that's because you have this
<v Speaker 1>increased pressure in the lungs. The right side of the
<v Speaker 1>heart is pumping blood to the lungs. So you have
<v Speaker 1>this increased pressure in the lungs, it's going to hyperch
<v Speaker 1>re fee the right side of the heart, make it
<v Speaker 1>harder for it to pump, and it leads to heart failure.
<v Speaker 1>So think about left sided heart failure now causing right
<v Speaker 1>side and heart failure. Well, left sided heart failure, the
<v Speaker 1>fluid's backing up into where it came from, which is
<v Speaker 1>the lungs. So left sided heart failure is causing all
<v Speaker 1>this excess fluid to back up into the lungs. All
<v Speaker 1>that excess fluid is going to increase the pressure in
<v Speaker 1>the lungs, which is going to lead to ultimately right
<v Speaker 1>sided heart failure. So that's why left sided heart failure
<v Speaker 1>is actually the most common cause of right side and
<v Speaker 1>heart failure because of all that backed up fluid, increasing
<v Speaker 1>the pressure right side having to pump harder, and almost
<v Speaker 1>ultimately leading to a hypertrophy of the right side of
<v Speaker 1>the heart. So that's the right and the left side
<v Speaker 1>of the heart. That's the different variations with heart failure.
<v Speaker 1>With that, the other variation you're going to see is
<v Speaker 1>systolic in diastolic dysfunction or systemic and distolic heart failure. Now,
<v Speaker 1>the terms that they use for these are systolic is
<v Speaker 1>heart failure with reduced dejection fraction, and diastolic is heart
<v Speaker 1>failure with preserved dejection fraction. So that's the proper way
<v Speaker 1>to save these, but I'm not going to say that
<v Speaker 1>because it takes too long. So if I say systolic,
<v Speaker 1>think of heart failure with reduce subjection fraction diastolic preserved
<v Speaker 1>dejection fraction. So let's start with systolic aka heart failure
<v Speaker 1>with reduced ejection fraction. So systolic is a pumping problem.
<v Speaker 1>The ventricles for whatever reason, have become weak and bag
<v Speaker 1>either are stretched out, they can't pump the way they
<v Speaker 1>used to. They're just baggy. They have no strength anymore. Normally,
<v Speaker 1>this is going to be a post m I patient
<v Speaker 1>and dilated cardiomyopathy. But just thinking systolic, you have these weak,
<v Speaker 1>baggy ventricles. They can't pump the way they used to,
<v Speaker 1>and because of that, you have this decreased dejection fraction.
<v Speaker 1>An ejection fraction if you're not familiar with it, it's the
<v Speaker 1>measurement of volume of blood that's pumped out of the
<v Speaker 1>left ventricle with each contraction. Normally, is a normal patient's
<v Speaker 1>gonna be around fifty to seventy percent. These patients are
<v Speaker 1>generally going to be actually under forty percent ejection fraction,
<v Speaker 1>So systolic you're gonna have decreased dejection fraction, and then
<v Speaker 1>a physical exam be familiar that they may have an
<v Speaker 1>S three gallop. All right, let's talk about an S
<v Speaker 1>three and S three. Although it can be heard in
<v Speaker 1>healthy young children and adults, it's usually abnormal in patients
<v Speaker 1>over the age of forty years, suggesting an enlarge or
<v Speaker 1>dilated ventricular chamber. An S three gallop is often an
<v Speaker 1>early finding of heart failure associated with dilated cardiomyopathy. It's
<v Speaker 1>more frequently heard in systolic rather than diastolic heart failure.
<v Speaker 1>So if you see an S three mentioned in an
<v Speaker 1>adult on an exam question, you should be thinking systolic
<v Speaker 1>heart failure, so heart failure with reduced ejection fraction. So
<v Speaker 1>S three is more common in systolic and S four,
<v Speaker 1>which will go over in a minute, is more common
<v Speaker 1>in diastolic. How do you remember that systolic cista lick
<v Speaker 1>has three syllables, so remember it's associated with an S
<v Speaker 1>three and di stall lick has four syllables, so it's
<v Speaker 1>associated with an S four. Quick and easy way to
<v Speaker 1>remember the two. Now diastolic heart failure, which is heart
<v Speaker 1>failure with preserved ejection fraction. So as it says preserve
<v Speaker 1>the ejection fraction is normally not decrease. You have the opposite.
<v Speaker 1>The ventricles are actually stiff, they're sometimes thickened. It can't relax.
<v Speaker 1>So the problems not with pumping, but it's with receiving blood.
<v Speaker 1>They can't expand to fill the blood during diastol they're
<v Speaker 1>stiff in they're thick so again it's not a pumping problem.
<v Speaker 1>So ejection fraction is normally either normal or sometimes even elevated.
<v Speaker 1>The ventricles just can't expand to fill it thatadequate blood,
<v Speaker 1>which can also cause backup and heard other problems with
<v Speaker 1>heart failure as well. And in diastolic you're normally going
<v Speaker 1>to hear an S four gallop, all right, So S
<v Speaker 1>four S four when heard is usually an abnormal finding,
<v Speaker 1>especially in young children and adults, and a palpable S
<v Speaker 1>four is always abnormal regardless of age. Usually the presence
<v Speaker 1>of an S four is due to the forceful atrial
<v Speaker 1>contraction against a stiff non compliant ventricle like we see
<v Speaker 1>in diastolic heart failure, So it is more common in
<v Speaker 1>diastolic heart failure or heart failure with preserved dejection fraction.
<v Speaker 1>Remember diastolic has four syllables, diestolic four syllables, so think
<v Speaker 1>S four and diastolic car failure. You're normally going to
<v Speaker 1>see in different cardiomyopathies, valvular heart disease, use, hypertension. Those
<v Speaker 1>are some of the predisposing fractors for that. So again,
<v Speaker 1>systolic is a pumping problem. You have this baggy ventricle,
<v Speaker 1>it can't pump blood out. Diastolic you have this stiffened,
<v Speaker 1>thick ventricle that can't receive blood. It can't fill the
<v Speaker 1>way you used to, can't get as much blood in there,
<v Speaker 1>But no problem pumping, So ejection fraction is preserved. Now
<v Speaker 1>clinical manifestations, well, it's all related to whether it's right
<v Speaker 1>or left sided heart failure. Remember what I said before
<v Speaker 1>that normally these are going to coexist, so most of
<v Speaker 1>the time you're going to see symptoms of both right
<v Speaker 1>and left sided heart failure. But again it's possible to
<v Speaker 1>have just exclusive right or left sided heart failure. So
<v Speaker 1>in both right and left sided heart failure, the blood
<v Speaker 1>is backing up. So whether it's systolic the ventricles don't
<v Speaker 1>pump enough blood out or diastolic the ventricles don't relax,
<v Speaker 1>you can't receive all the blood from the atrium. Both cases,
<v Speaker 1>you have this backing up of blood and the symptoms
<v Speaker 1>are all related to where it's backing up to. So
<v Speaker 1>if you have and it's basically where it came from.
<v Speaker 1>So if you have left sided heart failure, well, what's
<v Speaker 1>providing the left side of the heart with blood the
<v Speaker 1>pulmonary veins from the lungs. So if you have left
<v Speaker 1>side and heart failure, the blood's going to back up
<v Speaker 1>into the pulmonary vein and back into the lungs. And
<v Speaker 1>that's why with left sided heart failure, the most common
<v Speaker 1>symptom is going to be dyspnea because you have these
<v Speaker 1>lungs full of fluid. Or thopnia is another big one.
<v Speaker 1>Or thopnia is dyspania while lying flat. So these patients
<v Speaker 1>lay down within a few minutes, they're out of breath
<v Speaker 1>and they're coughing, so they may have a chronic cough
<v Speaker 1>as well. They may have some frothy pink sputum that
<v Speaker 1>can be seen. So left sided heart failure is all
<v Speaker 1>related to the lungs. And you can remember that by
<v Speaker 1>L for left sided heart failure, think of lungs. So
<v Speaker 1>as soon as you see left side of heart failure,
<v Speaker 1>think of lungs. All pulmonary symptoms like that. That's because
<v Speaker 1>again left side of the heart connects to the lungs.
<v Speaker 1>It's going to back up into the lungs where it
<v Speaker 1>came from. Now, right side of the heart. The way
<v Speaker 1>I remember that l left sided is for lungs. R
<v Speaker 1>is going to be rest of the body because it's
<v Speaker 1>going to go everywhere else the rest of the body,
<v Speaker 1>so are so it provides the right side of the
<v Speaker 1>heart with blood. It's the inferior of be in a
<v Speaker 1>caba and the superior vena caba, which connect to pretty
<v Speaker 1>much everything. So these patients are going to have peripheral edema,
<v Speaker 1>they may have like pitting a dima on the legs,
<v Speaker 1>jugular venus distension. It's because the blood from the right
<v Speaker 1>atrium is backing up into the jugular vein. So you
<v Speaker 1>take a look at their neck, you'll see this distended
<v Speaker 1>jugular vein. Blood can also back up into the GI system.
<v Speaker 1>The liver. They may have knowledge of vomiting something known
<v Speaker 1>as a pado jugular reflux, which is when you push
<v Speaker 1>on the liver, you palpate the liver and push into it.
<v Speaker 1>It actually causes an increased JVPCE. So you push on
<v Speaker 1>their liver and you look at their neck and all
<v Speaker 1>of a sudden you see the jugular venus distended, the
<v Speaker 1>jugular vein extended. So those are your clinical manifestations of
<v Speaker 1>the right and the light the left sides. Remember left
<v Speaker 1>side lungs. Right side is going to be the rest
<v Speaker 1>of the body. But again, most of the time these
<v Speaker 1>are going to co exist. You're normally going to have both.
<v Speaker 1>One other thing I wanted to mention before you move
<v Speaker 1>on to diagnosis is something that I don't think is
<v Speaker 1>that important, but it's very easy to remember. So in
<v Speaker 1>the case they ask you one question, let's just go
<v Speaker 1>over it really quick because it's it's pretty easy to memorize.
<v Speaker 1>So that's the New York Heart Association functional class. So
<v Speaker 1>these are four classes that are used to somewhat guide
<v Speaker 1>treatment and different therapies. But you just need to know
<v Speaker 1>a few things to be able to remember this for
<v Speaker 1>the exam. So there's four classes. There's class one, two, three,
<v Speaker 1>and four. As you move along in the classes, the
<v Speaker 1>symptoms get worse. So let's knock out class one and
<v Speaker 1>four really quick because those are the easiest. So Class
<v Speaker 1>one New York Card Association Functional Class Class one no symptoms.
<v Speaker 1>They have heart failure, but they have no symptoms, no
<v Speaker 1>problems at all. Class four they're going to have symptoms
<v Speaker 1>even at rest. So they're sitting down, they're laying down,
<v Speaker 1>they can't breathe, they're having all of these problems. It
<v Speaker 1>never gets better. Even when they're resting, they're having symptoms.
<v Speaker 1>So that's class one and four. Remember one, no symptoms,
<v Speaker 1>four symptoms even at rest. Class three is going to
<v Speaker 1>be their only comfortable at rest. They have even the
<v Speaker 1>regular daily activities their ADLs. Their activity is a daily living,
<v Speaker 1>walking around, doing the dishes, minor things that you and
<v Speaker 1>me would have no issues with. They're having dyspnea and problems.
<v Speaker 1>Even with that, they're only comfortable at rest. And then
<v Speaker 1>class two is kind of like kind of in between.
<v Speaker 1>They're gonna have mild symptoms. Most of their ADLs, they're
<v Speaker 1>gonna be okay. They exert themselves a little bit more,
<v Speaker 1>they may start to develop some symptoms. They're not completely
<v Speaker 1>asymptomatic like Class one, they just have mild symptoms. So
<v Speaker 1>again Class one no symptoms, Class four symptoms at rest,
<v Speaker 1>Class three only comfortable at rest, and the Class two is
<v Speaker 1>just basically mild symptoms. That's the New York Cart Association
<v Speaker 1>class all right, So let's move onto diagnosis. There's really
<v Speaker 1>four diagnostic tests that you need to be familiar with.
<v Speaker 1>Those four tests, your best test is going to be
<v Speaker 1>an ECHO. Your first test, like your initial test is
<v Speaker 1>going to be a chess X, right, and then a
<v Speaker 1>couple other labs like your BNP, and then an ECG.
<v Speaker 1>So let's start and move our way down the line.
<v Speaker 1>So let's do your first test. If they ask you,
<v Speaker 1>what's your initial test they'll do for patients suspecting heart failure,
<v Speaker 1>it's going to be a chest X right now. Chest
<v Speaker 1>X ray is not diagnostic for congestive heart failure. It's
<v Speaker 1>just not specific enough, but it is a good initial test.
<v Speaker 1>And what are you gonna see on a chest X
<v Speaker 1>ray that you need to know to suspect congestive heart failure? Well,
<v Speaker 1>there's something known as cephalization of flow cephalization of flow,
<v Speaker 1>and what this is is due to all the back
<v Speaker 1>flow of blood into the lungs, you have this increased
<v Speaker 1>pulmonary pressure which actually causes the vascular flow to migrate
<v Speaker 1>up the lungs and go all the way to the apecs.
<v Speaker 1>So because of the cephilization of flow, you're gonna have
<v Speaker 1>two key findings, those key terms that you need to
<v Speaker 1>be familiar with, that you need to know cause from
<v Speaker 1>the cephilization of flow, that's curly B lines k E
<v Speaker 1>R L E Y B lines and then butterfly or
<v Speaker 1>bowing appearance in chest X ray. Of course you're gonna
<v Speaker 1>have cardiomegaly plural effusion, but you know they're not gonna
<v Speaker 1>ask you a question about that. They're gonna ask you
<v Speaker 1>about these key findings. So what are curly B lines.
<v Speaker 1>These are due to lymphatic encorgement or edema at the
<v Speaker 1>lung periphery, so at the sides of the lungs and
<v Speaker 1>a congestive heart failure patient. And at the sides or
<v Speaker 1>the periphery of the lungs on chest sticks where you're
<v Speaker 1>gonna see these short, little tiny one to two centimeter
<v Speaker 1>thin lines. So these one to two centimeters little radio
<v Speaker 1>opaque lines that most of the time, unless you're pretty
<v Speaker 1>good at reading chest x raason, you probably completely miss.
<v Speaker 1>But a radiologist will see that and know that it's
<v Speaker 1>related to congestive heart failure. Potentially, there's other causes again,
<v Speaker 1>and the other thing you should be familiar with is
<v Speaker 1>something known as bat wing or butterfly appearance. This is
<v Speaker 1>better with a visual, so check out my YouTube channel.
<v Speaker 1>We gonna have pictures of all of these what I'm
<v Speaker 1>going through the video. But this is another cause from
<v Speaker 1>the accumulation of fluid. But in these cases, the fluid
<v Speaker 1>is filling the high lar in the peri hyla region
<v Speaker 1>of the lungs, and because of the location of the edema,
<v Speaker 1>you're gonna have this bat wing appearance with these white
<v Speaker 1>opacities in the lungs and it looks like the wings
<v Speaker 1>of a bat wing or a bird or whatever you
<v Speaker 1>want to think of butterfly. So it's just the location
<v Speaker 1>of fluid overloaded in the lungs. So that's the initial
<v Speaker 1>test that you'll do. Again. It's not really going to
<v Speaker 1>be diagnostic, but it's a good first test to kind
<v Speaker 1>of give you an idea that maybe this patient does
<v Speaker 1>have CHF. Okay. So another initial test that you'll do,
<v Speaker 1>especially if they're coming into the ear, is something known
<v Speaker 1>as BNP. You'll also hear it known as pro BNP,
<v Speaker 1>and that is either B type naturetic peptide. It also
<v Speaker 1>used to be called brain naturetic peptide, but as the
<v Speaker 1>newer name for it is B type naturetic peptide. So
<v Speaker 1>what this is BNP is this peptide that's secreted by
<v Speaker 1>the heart to regulate blood pressure and fluid in the body,
<v Speaker 1>and it's released when you have the ventricle stretching. So
<v Speaker 1>that's the body's way of knowing, okay, the ventricles are
<v Speaker 1>stretching or being overloaded from fluid. They don't exactly know why,
<v Speaker 1>so they release this and it's pumped out to kind
<v Speaker 1>of regulate and make some changes in the blood pressure
<v Speaker 1>and regulate the fluids in the body. Now, BNP is
<v Speaker 1>also pumped out during renal failure. It can be decreased
<v Speaker 1>in obese patients. So it's not one hundred percent specific,
<v Speaker 1>but it's a good rule out test because if you
<v Speaker 1>do a BNP in a patient you suggest has heart
<v Speaker 1>failure and it's zero or it's completely normal less than
<v Speaker 1>one hundred good chance that they don't have heart failure. Generally,
<v Speaker 1>the number that you're looking for is a BNP over
<v Speaker 1>one hundred, you should be thinking there's a pretty good
<v Speaker 1>chance that this PATI could have heart failure. So BNP
<v Speaker 1>overall one hundred, you should be suspecting heart failure, but
<v Speaker 1>be aware there's other things that can elevate it as well.
<v Speaker 1>So that's another good lab test to do, and it's
<v Speaker 1>really good in guiding treatment when you have like decompensated
<v Speaker 1>heart failure to see the response that treatment. But you
<v Speaker 1>should know that one as well. That's your BNP or
<v Speaker 1>pro BNP. Another one that's it's not a bad test,
<v Speaker 1>but it's again not going to be diagnostic, is your ECG.
<v Speaker 1>So it's another good rule out test. And the reason
<v Speaker 1>it's a good rule out test is because if this
<v Speaker 1>patient has systolic heart failure so heart failure with reduced
<v Speaker 1>ejection fraction, if they have a normal ECG, there's a
<v Speaker 1>very small chance that they have heart failure. It's a
<v Speaker 1>ninety eight percent predictive value if it's a negative that
<v Speaker 1>they don't have heart failure. But yeah, on the flip
<v Speaker 1>side of that, if they have preserved ejection fraction. A
<v Speaker 1>lot of times the ECG is going to be normal,
<v Speaker 1>so get a good rule out test for systolic, but
<v Speaker 1>not so much for diestolic. And again if it's positive,
<v Speaker 1>if you do see abnormalities on ECG, doesn't mean it's
<v Speaker 1>heart failure. It's another good rule out test, but again
<v Speaker 1>non diagnostic. Now, the best test overall is going to
<v Speaker 1>be your echo. So your your echo is going to
<v Speaker 1>measure your ejection fraction. It's going to measure or evaluate
<v Speaker 1>the ventricular wall see if they're thinning like in systolic
<v Speaker 1>her failure. It's going to be able to get a
<v Speaker 1>really good idea of the function of the heart and
<v Speaker 1>to diagnose heart failure. So overall, echo is going to
<v Speaker 1>be your best test. That's the one you really need
<v Speaker 1>to be familiar with and know for the exam if
<v Speaker 1>they do ask you what your best test is. Okay,
<v Speaker 1>So let's move on to treatment. So treatment of systellic
<v Speaker 1>heart failure aka heart failure with reduced ejection fraction. Let's
<v Speaker 1>start with some lifestyle interventions. Then we'll hit the MEDS,
<v Speaker 1>which is the highest deealed component for the exam. So
<v Speaker 1>to start of course, associated conditions and underlying causes should
<v Speaker 1>be appropriately managed. Coronary art disease, valve disease associated conditions
<v Speaker 1>like hypertension diabetes should all be properly managed, and then
<v Speaker 1>as far as lifestyle modifications, of course, cessation of smoking
<v Speaker 1>is essential, abstinence from alcohol consumption or at least restricting alcohol,
<v Speaker 1>avoidance of obesity, and then restricting sodium intake. Depending on
<v Speaker 1>the source, the specific number can vary, so I wouldn't
<v Speaker 1>focus too much on a specific number, but up to
<v Speaker 1>date does suggest less than three grams a day, and
<v Speaker 1>in patients with more severe or refractory heart failure, restricted
<v Speaker 1>fluid intake to one point five to two liders a
<v Speaker 1>day may be recommended, and of course daily weight monitoring
<v Speaker 1>to detect fluid accumulation is also recommended. Let's move on
<v Speaker 1>to our pharmacologic therapy because this is what you need
<v Speaker 1>to know for the exam. So these meds are the
<v Speaker 1>primary therapy for heart failure with reduced ejection fraction. These
<v Speaker 1>are the four that you absolutely need to know. These
<v Speaker 1>meds not only improve symptoms but most importantly prolonged patients survival.
<v Speaker 1>So for meads or classes you need to know in
<v Speaker 1>patients with heart failure with reduced ejection fraction. These will
<v Speaker 1>typically be combination therapy with one agent from each of
<v Speaker 1>the following classes. So these classes are ar and i's
<v Speaker 1>beta blockers, MRAs, and sglt too inhibitors. Let's start with
<v Speaker 1>our arni's or our class, which is our rien and
<v Speaker 1>angiotenson system inhibitors. We have a number of options arnis
<v Speaker 1>ace inhibitors ARBs, which you choose that would be ar
<v Speaker 1>and I specifically cycubitril valsartan, which is also known as Intresto.
<v Speaker 1>That's the brand name and you'll see this being utilized
<v Speaker 1>very often. It's an angiotensin receptor neprilicin inhibitor, which is
<v Speaker 1>composed of an AR and B an inhibitor of neprilicin,
<v Speaker 1>which is an enzyme that degrades naturitic peptides, bradickinin and
<v Speaker 1>other phasoactive peptides. And it's preferred over aces in ARBs
<v Speaker 1>due to improved efficacy relative to these other classes, and
<v Speaker 1>in patients who can't tolerate ARNI therapy or due to costs,
<v Speaker 1>can't obtain it. Aces and urbs are an option, but
<v Speaker 1>ARNI is the preferred class, so it should be the
<v Speaker 1>focus for the exam. Next is going to be beta blockers,
<v Speaker 1>specifically metoprolol, carbadolol and bisoper law are the preferred agents
<v Speaker 1>as these beta blockers have demonstrated mortality benefit, unlike the
<v Speaker 1>other medications in the beta blocker class which lack comparable evidence.
<v Speaker 1>Next is going to be our MINERALI coord cord receptor
<v Speaker 1>antagonist that's a planinone and spirinal lactone, A playerone is
<v Speaker 1>usually preferred over spirinal lactone due to a lower risk
<v Speaker 1>of endocrine side effects like ganocomasitia and impotence. And then
<v Speaker 1>finally we have our SGLT two inhibitors. These are amazing drugs.
<v Speaker 1>We use them in diabetes CKD and of course part failure.
<v Speaker 1>So our sodium glucose cotransporter to inhibitors like dapicla flows
<v Speaker 1>in which is Farsiga or empical flows in which is Jardiance.
<v Speaker 1>So those are the four meds or classes you need
<v Speaker 1>to know. There is one other med that does have
<v Speaker 1>proven mortality benefit, that's hydrolyzene plus nitrate, but this is
<v Speaker 1>not a first line med and really just a backup
<v Speaker 1>option for patients who cannot tolerate an ar and I
<v Speaker 1>or an ASR and R. So I want you to
<v Speaker 1>remember these for the exam. This is super important. It's
<v Speaker 1>probably the highest yeald thing to know for heart failure.
<v Speaker 1>So here's anomonic to help you remember them. To remember
<v Speaker 1>the main meds you need to know for management of
<v Speaker 1>heart failure with reduced ejection fraction aka systemic heart failure,
<v Speaker 1>remember bash the heart to make it beat harder. Bash
<v Speaker 1>the heart to make it beat harder helps you remember
<v Speaker 1>the meds with proven mortality benefit in systellic heart failure.
<v Speaker 1>BASH is spelled B ashe, so let's start with B.
<v Speaker 1>That's again going to be our beta blockers mitoprol, carveatal
<v Speaker 1>olbit SOAPROLAW. Next to A stands for ar and I,
<v Speaker 1>our angiotensen receptor blocker, and aprilicin inhibitor, which is secure
<v Speaker 1>patrol of al sartan ace inhibitors or ARBs are an
<v Speaker 1>I backup, which also start with A if an AR
<v Speaker 1>and I is not appropriate or affordable. Next is going
<v Speaker 1>to be our sglt twos our sonium glucose cotransporter to
<v Speaker 1>inhibitors to epical flows in epical flows. In next hydroalyzene
<v Speaker 1>plus nitrate. Again, this is not a first line med
<v Speaker 1>but it is a medication with proven mortality benefit, so
<v Speaker 1>it is appropriate. Here also helps them on, so it's
<v Speaker 1>good to be aware of. But really we're only going
<v Speaker 1>to use this again if any of our A medications
<v Speaker 1>aar andies ACES or ARBs were not tolerated or not
<v Speaker 1>appropriate for whatever reason, maybe patients with hyperkalemia or kidney dysfunction.
<v Speaker 1>So again just know this med does have proven mortality benefit,
<v Speaker 1>but it's not first line. And then finally we have
<v Speaker 1>our MINERALI cord cooid receptor antagonists, which are a plaranone
<v Speaker 1>and spirinal lactone. And in this case we're using the
<v Speaker 1>E for BASH because a planaranone is preferred over spyirinal
<v Speaker 1>lactone due to its more favorable side effect profile, and
<v Speaker 1>therefore it's the one you should know. Okay, again, meds
<v Speaker 1>you need to know for systallic heart failure with proven
<v Speaker 1>mortality benefit, bash B ashe the hard to make it
<v Speaker 1>beat harder beta blockers aar andies sgot two hydraulazine and
<v Speaker 1>a plaranone. Know those and you should be good for
<v Speaker 1>the exam. Now there are other medications of these are
<v Speaker 1>more for symptomatic relief, so diuretics like furosamide will be
<v Speaker 1>used in patients with persistent volume overload to help eliminate
<v Speaker 1>clinical evidence of fluid retention. So obviously plays a large
<v Speaker 1>role in patience with acutely decompensated heart failure, and the
<v Speaker 1>diuretic most commonly used will be freeurosimide. And then we
<v Speaker 1>have some secondary options. So the secondary options are in
<v Speaker 1>patients who cannot tolerate the primary regimen or have residual
<v Speaker 1>heart failure symptoms despite optimal therapy. These are not commonly use,
<v Speaker 1>so I don't think you need to menimalize them, but
<v Speaker 1>just be aware that they do exist. This is going
<v Speaker 1>to be EVI a braiden verisiguat digoxin hydrouzene plus nitrate
<v Speaker 1>that we talked about before again, so don't really need
<v Speaker 1>to focus too much on these. These aren't high yield,
<v Speaker 1>but these are secondary or backup options if our primary
<v Speaker 1>therapy can't be utilized for whatever reason. Right, So, treatment
<v Speaker 1>of heart failure with preserved ejection fraction or diestolic car
<v Speaker 1>failure is a little different than systolic car failure that
<v Speaker 1>there is no clear evidence that pharmacologic therapy or other
<v Speaker 1>therapies reduce the risk of mortality in these patients. So
<v Speaker 1>if you're feeling overwhelmed and maybe want to skip a section,
<v Speaker 1>this would be the one, as there are no high
<v Speaker 1>yield meds to know here. In general, you'll treat these
<v Speaker 1>patients associated conditions just like you would anyone else. Hypertension,
<v Speaker 1>a fib coordinary ardor disease, et cetera. You'll suggest die
<v Speaker 1>in an exercise cardiac rehab. And if you want to
<v Speaker 1>just remember one med class, this would probably be as
<v Speaker 1>up to date recommends this as initial therapy for most patients,
<v Speaker 1>and that's going to be an SGLT two inhibitor like
<v Speaker 1>empical flowsen or dapical flows in. This is going to
<v Speaker 1>be initial therapy for most patients, So this would be
<v Speaker 1>the one if you want to remember one med class,
<v Speaker 1>this is the one to know. Second line would be
<v Speaker 1>a MINERALI cord chord receptor antagonist, so like spirriinalactone or
<v Speaker 1>a plaranone, And in this case there is an additional
<v Speaker 1>agent called fenerenone, which is a newer non steroidal mineral
<v Speaker 1>chord cord receptor antagonist. You're obese patients, we can use
<v Speaker 1>GLP one receptor agonists like symaglotide or two zepetide. These
<v Speaker 1>meds have shown benefit in patients with obesity and heart
<v Speaker 1>failure with preserved dejection fraction. And then the patients with
<v Speaker 1>volume overload, you'll use diuretics, just like we were talking
<v Speaker 1>about before. This is usually going to be a loop
<v Speaker 1>diuretic like thurosamide. So bottom line here, if you want
<v Speaker 1>to remember one med class for heart failure with preserved
<v Speaker 1>dejection fraction, let it be SGLT two inhibitors. But not
<v Speaker 1>a lot to know here otherwise, so I wouldn't waste
<v Speaker 1>too much time, all right, And remember one last thing
<v Speaker 1>about the treatment. Outside of your pharmacologic treatment, there's some
<v Speaker 1>mechanical devices. So as these patients progress with heart failure,
<v Speaker 1>once they get to like stage four, their rejection fractions
<v Speaker 1>under thirty five percent, the treatment in addition to pharmacologic
<v Speaker 1>therapy is actually going to include a left ventricular assist device,
<v Speaker 1>which is an implantable device that helps the failing heart
<v Speaker 1>to contract with mechanical assistance. They also may have an
<v Speaker 1>AICDM planet, which is an automatic implantable cardioverter defibrillator. These
<v Speaker 1>are patients again in the last stages, and ultimately once
<v Speaker 1>they get to stage four, death normally occurs within a
<v Speaker 1>year without heart transplant. So once you get to that point,
<v Speaker 1>you just kind of use everything you can to preserve
<v Speaker 1>life as long as possible. Okay, so that is heart failure.
<v Speaker 1>Thank you so much. As always, I know I said
<v Speaker 1>it in the beginning, and I'll say it every time
<v Speaker 1>because I do appreciate the comments. It really does make
<v Speaker 1>my day.