Valvular Heart Diseases | Clinical Medicine

Foreign, what's up Ninja nerds? In this video today, we're going to be talking about valvular heart disease, also abbreviated VHDs. This is going to be part of our clinical medicine section.

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All right, let's get into VHDs. So, valvular heart diseases. There are a couple more that aren't really listed here. They are just super uncommon, they're not very high yield, so I'm not going to spend time on those. That's your tricuspid stenosis, your tricuspid regurgitation, pulmonary stenosis, pulmonary regurgitation. Those aren't super common. And the left heart disease, those valvular disorders are much, much more common and more likely to be tested on. So let's focus on those.

That includes your mitral stenosis, regurgitation, aortic stenosis, aortic regurgitation. And then we'll talk about this like little random guy here called rheumatic fever. One little note: tricuspid regurgitation may be the only one that could potentially be mentioned on your exams. Only thing to remember for that one, it's highly associated with IV drug abuse. Other than that, that's really it.

Let's start talking about these. So, mitral stenosis. Within the name, it's telling me that there is some fibrosis, there's tough, there's sclerosis of this mitral valve. So this is the valve that is actually between the left atrium and left ventricle. That's the basic anatomy, right? What I want you to associate with mitral stenosis is there's difficulty in being able to get blood where? From the left atrium to the left ventricle because this valve is not allowing that. That is honestly the basic pathophysiological process. So there is a decreased blood flow from where? Blood flow from the left atrium to the left ventricle. And really, that's about as simple as it needs to be.

But the question then kind of arises, what generally causes this valve to become super stenotic and tough and hard and not just allowing it to open normally? It should open, allow blood to go from the left atrium to the left ventricle. It's not opening properly. Why? By far the most common cause of this is going to be rheumatic fever. So that's why I will mention rheumatic fever a little bit later. All right, this is going to be the associated causes that are particularly associated with mitral stenosis. All right, good enough.

Let's talk about mitral regurgitation. Mitral regurgitation is a little bit more interesting. And what happens with mitral regurgitation is the opposite. The mitral valve is not functioning, and it's causing blood to go from the what? Left ventricle into the left atrium. That generally should not be happening. Now, the valves, mitral valves should open during diastole, allow blood to go from left atrium to left ventricle. Should snap shut during systole, blocking blood from going from left ventricle to left atrium. The question then arises, all right, so we know that from this pathophysiological process, there is an increased blood flow from the left ventricle to the left atrium. And that's the pathophysiological process that occurs in both of these diseases, right? So this is the concept here.

Now, what I want us to be able to ask ourselves the question is, is what is causing these valves to not function and block blood from going back up? One of the causes for this particular thing is you have some type of dilated left ventricle. Causes. All right, so there's a dilated left ventricle. What are diseases that would cause dilation of the left ventricle? Systolic heart failure. Systolic heart failure. What's another terminology, just so we're clear for systolic heart failure? This is also known as heart failure with a reduced ejection fraction. What happens is you dilate these ventricles, and if they dilate, look, they're dilated. It's going to stretch these valve flaps farther away from one another. Now, there's not, there's too much distance between them to snap shut during systole. That's one cause.

Another one is called dilated cardiomyopathy. This is another particular cause that I want you guys to associate it with. But basically, the whole concept is they're dilating the ventricles and not allowing for the valve flaps to come together nicely. This one is there some type of mitral valve damage or like destruction? Generally, but in general, there's direct damage to the mitral valve. The question that we have to ask is, what are the reasons why there is mitral valve damage? And there is a couple. The biggest one is sometimes you can get an infection. And if you have an infection, particularly something called infective endocarditis, it can destroy these valves. It can literally chew them away, and now you don't have a valve flap that can actually meet the other one and completely close. So I want you to remember a big one here is going to be infective endocarditis. Super common, especially in the IV drug use population, or those who have some type of underlying cardiac surgery or prosthetic valves.

The other one here is that the mitral valve has some type of like underlying genetic connective tissue dysfunction. So it's naturally weak and it's degenerate. We call this myxomatous degeneration. Remember that from pathology. So the valve is naturally weak that it can pop, it can prolapse, and when it prolapses, it can bow up into the left atrium. You guys know what that's called? We call that mitral valve prolapse. This is extremely common in patients who have some type of like connective tissue disorder. Do you guys remember some of them? Things like Marfan syndrome, Ehlers-Danlos syndrome. These are big things to remember here.

All right, so to recap this: Mitral stenosis, decreased blood going from the left atrium to the left ventricle because of a stenotic valve. Rheumatic fever happens to be pretty much one of the most common. Mitral regurgitation, increased blood flow going back into the left atrium because you dilate your left ventricle or you damage the mitral valve. Pretty straightforward. We'll come back to this in a second.

So over to aortic stenosis. Aortic stenosis is this valve. It's supposed to allow blood to go from the left ventricle into the aorta during systole and then block the blood flow from the aorta into the left ventricle during diastole. Aortic stenosis, it's not allowing blood to flow forward. So it's supposed to go here, and it is not allowing for that process to occur. And the reason is, there's some type of hardening or sclerosis or just intense fibrosis of the aortic valve. And the problem with this disease is there is a decreased blood flow from the left ventricle to the aorta. And that is really the pathophysiological process that I want you guys to understand here.

But then the question then arises, like all of these, what is causing this valve to become super sclerotic and hard and difficult being able to open up and allow blood to leave the left ventricle? The causes here is it's twofold. I want you to remember it like this: those patients who are less than 70 years of age and those that are greater than 70 years of age. And those who are less than 70 years of age, they may have a gen, some type of problem with the valve development. And we call this a bicuspid aortic valve. A bicuspid, I'm going to put aortic valve. That's an abbreviation for the aortic valve. For those greater than 70, it's just calcification over time. This happens to be probably one of the most common causes. It's just dystrophic calcification. So we call this dystrophic calcification, and this is just wear and tear on the valve over time. And that is generally the problem for this disorder.

The last one of these left ventricular valvular heart diseases is aortic regurgitation. For this one, it's very interesting. So what happens in this disease is again, the aortic valve should open during systole, close during diastole. During diastole, for some reason, the blood decides to shoot back into the left ventricle from the aorta. Shoot back from the aorta, sorry, into the left ventricle. That's the correct terminology. So again, with these particular scenarios, what's the pathophysiological process? There is an increase in blood flow from the aorta to the left ventricle. And that is the pathophysiological process that I want you guys to understand.

Now, with that being said, we then say, okay, there's something wrong with the valves. Pretty straightforward. For mitral regurgitation, it was a dilated left ventricle. Aortic regurgitation, it's a dilated aorta. So anything that causes dilation of the aorta. So dilated aorta causes. It doesn't take a genius to figure out these. What's the dilation of the aorta called? An aortic aneurysm. So when patients have an ascending aortic aneurysm, this is a very, very common cause. And anything else that causes dilation. There is a, it is not very common, and I want you guys to worry too much about it. But anything that causes aortic inflammation. So there is some rarities out there like syphilis and things like Takayasu's arteritis and reactive arthritis, which you can see sometimes in Reiter's syndrome. But this is by far going to be much more common for you to have an ascending aortic aneurysm. And it's pretty straightforward. If this aorta is super dilated, just like it was for the left ventricle and mitral regurgitation, it's pulling the valve flaps farther away from one another. They can't completely close.

In this particular scenario, it was damaged mitral valve, aortic valve damage. So there is some type of aortic valve damage. And so we have to ask ourselves the question, what is causing this aortic valve damage? And it's relatively similar. One is infective endocarditis, right? Infective endocarditis can damage the mitral valves, it can damage the aortic valves. And remember I told you that little pearl, the only thing pertinent for tricuspid regurgitation is in MRSA and IV drug abusers, that can attack the tricuspid valve. But generally, these are the most commonly attacked valves. So infective endocarditis is an infection of those valves where the bacteria literally, I'm not even kidding, can chew away the actual valve.

Another one is, this one's an interesting one. Sometimes if patients get aortic dissections, like ascending aortic dissection, or proximal aortic dissections, it can literally tear away in the media and then move into the valve and cause it to literally dysfunction. So sometimes another one would be a, a proximal aortic dissection or a Stanford A proximal aortic dissection. These would be some of the big things that I would really want you guys to remember for the causes of aortic regurgitation.

So with that being said, we've covered all the valvular heart diseases. But I got this rando thing here mentioned, you're like, okay, I saw rheumatic fever, particularly with mitral stenosis. It can attack other valves. It loves the mitral valve. We'll talk about that. Then it loves the aortic valve. So let's talk a teensy bit about this because you can see this in some of these valvular disorders. Rheumatic fever usually, this happens in younger patients who get strep throat. All right, so they get a bacteria that causes an infection here. So here we're going to have an infection here of the actual pharynx. Here's the bacteria that's wreaking all this havoc. This is called, I'm abbreviated, Group A beta-hemolytic Streptococcus bacteria. So this is some type of bacteria, and it causes a nasty infection of the pharynx. Now, naturally, what will happen is your body will have these things called plasma cells that'll become eventually activated. And what they're going to try to do is, is they're going to try to pump out some autoantibodies, right? Some anti-streptolysin antibodies, some anti-DNase B antibodies, a bunch of these puppies. And when they try to pump these out, these are supposed to go and eradicate or destroy, let's put a little inhibitory sign, inhibit the actual Group A beta-hemolytic Streptococcus bacteria, destroy it. But sometimes what happens is these autoantibodies like to go and destroy other tissues. And one of those tissues that we have discussed here is particularly what? The heart.

And with that being said, the most commonly affected valves that when it actually goes, these autoantibodies, they go and attack the heart, they love to attack a couple different valves. The most prominent valve that they love to attack is going to be the mitral valve. Then after that, it would be the aortic valve. So with that being said, what you're going to see is you're going to see some type of valvular heart damage. You're going to see a lot of damage to the actual valves, but it's going to prefer to hit the mitral valve, and then after that, hit the aortic valve. So sometimes what you may see in certain textbooks is that rheumatic fever, which can lead to rheumatic heart disease. So this is eventually what happens is if you damage the actual hearts, we actually give this a terminology here, and we call this rheumatic heart disease once you actually start exhibiting some cardiac destruction. When we see this, you may see, oh, this causes mitral stenosis and it causes mitral regurgitation. Yeah. And it can even cause aortic stenosis and sometimes aortic regurgitation. But I just want you guys to remember that it really loves to attack the valves.

All right, my friends, that covers the pathophysiology of valvular heart diseases. Now I want you guys to understand what happens when these valvular heart diseases wreak havoc on our body. All right, my friends, now let's talk about the complications associated with valvular heart diseases. First thing, mitral stenosis. We already know there's a problem going from left atrium to left ventricle, right? Rheumatic fever is a big trigger here. What I want you guys to understand, though, is that if we can't get blood from the left atrium to the left ventricle, the problem is, is what? It's going to kind of start backing up from the left atrium into the pulmonary veins. And so what happens is, is these patients generally have like a very high left atrial pressure that transmits to a high pulmonary capillary wedge pressure. And that leads to that hydrostatic pressure being high and pushing that fluid out into the interstitial spaces, into the alveoli. When fluid accumulates there, what is that called? Pulmonary edema. And then that pulmonary edema, depending upon the severity of it, can cause features of dyspnea, paroxysmal nocturnal dyspnea, it can cause orthopnea. And in certain severe cases, it may cause respiratory distress, causing hypoxia, increased work of breathing, increased respiratory rate, etc. But it's again, a concept of this pathophysiological process. So again, blood can't go from here to here because of that, the pressure in the left atrium rises. That then transmits to what? The pulmonary capillaries, which causes their pressure to increase. That then stimulates fluid to accumulate here, which leads to pulmonary edema, which leads to the symptomatic features of left heart failure, which you may see.

The other concept here is that because you can't get blood from the left atrium into the left ventricle, again, blood will stay in this area, right? But you know what else will stay in here? A lot of that blood will actually start causing the left atrium to say, hey man, left atrial pressure is pretty high, and the volume inside of the left atrium is pretty high. I need to dilate. And so what happens is, is because of all of this, you develop something called left atrial dilation. Now, look at how honking big this dang atrium is. It's gargantuan. And because of that big old atrium, now you stretch out the myocardium. When you stretch the atrial tissue, it alters the circuitry there, and it increases the risk for patients developing atrial fibrillation. So then this causes atrial fibrillation to be way more prominent in these patients. Now, what's the problem with atrial fibrillation? It doesn't contract very well because of those reentrant circuits, and it causes clots to begin to form in the left atrium. And then those clots can flick off, and you can form emboli, and these emboli can travel via the systemic circulation. So look at this, some of these are going to slip out here, they're going to run out here and into the systemic circulation. If they run into the systemic circulation, what is that called? They're called embolic phenomenon. So then you're going to get these thromboemboli, which are going to go and spread to multiple areas of the body. Some of those under the brain, this is the most terrifying, you can end up with a stroke. It can go to the gut and cause acute mesenteric ischemia. It could go to a vessel in the leg and block off the blood flow of the leg and cause acute limb ischemia. So these are all potential features that can happen in a patient who has mitral stenosis.

Now, this type of AFib that they usually develop, we'll talk about it more in the AFib lecture, but I'll put it here in kind of like a little parentheses, if you will. It's like a little, little spacer. It's called valvular, valvular atrial fibrillation. Very important because that determines the type of treatment we'll give to these patients. All right, cool. Mitral stenosis, remember pulmonary edema due to high left atrial pressure, left atrial dilation, increasing risk of AFib and thromboemboli.

All right, what's next? Mitral regurgitation. With mitral regurgitation, the problem is blood is pumping back up into the left atrium from the left ventricle. So now, look, two things happen here. Normally, when you contract your left ventricle, blood should go this way. Should not be going this way. But both of these things have become unfortunate events here where this occurs pretty rapidly. So then what happens to your left atrial pressure? Goes up. What happens to your pulmonary capillary wedge pressure? Goes up. What do you then stimulate? Pulmonary edema. So all of these things happen because of this flood of blood, this jet backing up into the left atrium. Left atrial pressure goes up, pulmonary capillary wedge pressure goes up, you stimulate pulmonary edema, and this presents, we'll just put for now, but the same thing is above: dyspnea, paroxysmal nocturnal dyspnea, orthopnea, or in severe cases, it can cause respiratory failure. So then again, fluid will accumulate here and all in these particular areas here, precipitating this, which may precipitate this or worsening respiratory failure.

The other downside of mitral regurgitation, especially this is acute. So if a patient develops an acute mitral regurgitation, what happens is, is a lot of blood backs up here and causes overt pulmonary edema. But also, you have less blood. There is a decrease, per se, in the volume of blood that is leaving the heart within each heartbeat, your stroke volume. That thing can drop. The cardiac output can drop. The blood pressure and can lead to shock. These patients may go into overt cardiogenic shock if it is acute. So this is more prominent in patients who have acute mitral regurgitation, whereas those who are more of the chronic mitral regurgitation, they may compensate in some type of way. They may dilate their ventricles to try to have a bigger preload. But in these scenarios of acute mitral regurgitation, it can progress to a type of shock which we call cardiogenic shock. So these are the big things that I want you to watch out for with mitral regurgitation is the possibility of cardiogenic shock and pulmonary edema. Okay, we're going to come back to rheumatic fever in just a second. All right, remember that this is a big trigger of mitral valve disease, aortic disease, but what's the most common one? Mitral valve, first, like mitral stenosis.

All right, aortic stenosis. This is a really interesting one. It's similar to one of those we call hypertrophic cardiomyopathy. Similar pathophysiology, just a little bit difference in the underlying cause. In hypertrophic, it was a big septal hypertrophy. And in aortic stenosis, the valve is super hard and sclerotic and not allowing blood to leave. So it's the same concept, if you will. So in this disease, it's hard getting blood out, right? So there definitely will be a reduction in the amount of blood leaving the heart. So we'll call this the cardiac output, which will lead to a reduction in your systemic perfusion. Now, in patients who have this, we like to call this, like, you know how we said that this is kind of like your left ventricular outflow tract? This can act, it can act as what's called, we're going to call this a LVOT, or a left ventricular outflow tract obstruction. So it's kind of preventing blood from getting out of the left ventricle into the aorta. That leads to this reduction in cardiac output, that leads to the reduction in systemic perfusion. And this can be very quick. And so because of that, this can affect tissues very abruptly. Some of these are very interesting. First one here is the carotids. So a patient who has aortic stenosis, when you palpate their carotid during systole, it's very weak because it's hard for them to get blood out of the heart, and it's also delayed because the heart is really having to squeeze and squeeze and squeeze. So it takes a longer time for them to push out the appropriate volume of blood into the carotid. So it's a delayed and weak pulse. We always got to make things more difficult though, and so we use a term, we call it pulses parvus et tardus. All we're saying is is its weak and delayed pulse. That's all it is. And that's usually because again, very little blood is reaching the carotids.

All right, the next concept here is that it also can cause a transient reduction in perfusion to the brain, and sometimes these patients can transiently lose consciousness. What is this called? This is called syncope. Another very, very common feature here that we can see. And the last one here is whenever you don't perfuse the coronaries. The aortic stenosis is a really powerful trigger. If you can't get blood out of the left ventricle into the aorta, you won't be able to perfuse those coronaries, which is right off the base of the aorta. And so this can cause a reduction in coronary perfusion, which may lead to a little bit of ischemia, and that ischemia may present with angina. And so watch out for anginal symptoms here as another prominent feature.

The last thing that I want you guys to remember here is, is if it's hard to get blood out of the left ventricle, it's going to start causing blood to unfortunately back up. And so it may, so this is being inhibited, right? But unfortunately, because it can't get out, the blood will start to back up, and the left atrial pressures will go up, the pulmonary capillary wedge pressures will go up. This will precipitate, oh my gosh, it's like a, a repeat all the time. This will be ingrained into your brains forever, guys. Dyspnea, paroxysmal nocturnal dyspnea, orthopnea, etc. It can even be terribly, especially if it's really, really bad, it can precipitate respiratory failure, right? And this is some of the big features here due to that blood backing up into the left atrium, right? So those left ventricular end-diastolic pressures will be really, really high, and it's hard to fill it.

Okay, with that being said, the common theme that you want to remember is aortic stenosis is SAD. I know that's corny, but remember syncope, angina, and dyspnea tend to be the common features in aortic stenosis due to the left ventricular tract obstruction, similar to hypertrophic cardiomyopathy. Now, there will be a murmur that is also present in all of these. I don't, we didn't, we're not skipping over it. We're going to talk about it in great detail in a second, but for right now, that's another really big way to differentiate aortic stenosis from hypertrophic cardiomyopathy is the murmur, and also age. Age is another really big factor. One other thing that I want you guys to remember here with aortic stenosis is whenever this difficulty in getting blood out of the left ventricle occurs, the afterload is high, right? It's hard to get blood out. After those high, that will trigger the ventricle to have to get thicker, and that'll lead to something called left ventricular hypertrophy. It'll thicken it. You guys remember in the heart failure lecture, when the ventricle gets really, really thick, it doesn't feel well. What type of heart failure is that? Heart failure with a preserved ejection fraction. We call that a diastolic heart failure, just because of room here. I'm going to put HFpEF. Oftentimes, this will be another potential thing that you can see in these patients, the aortic stenosis.

Okay, aortic regurgitation. Problem is blood is flooding back into the left ventricle. So you're trying your best to push blood out, but a lot of it is just flooding back in. What will this do? Okay, well, let's focus first on if I can't get blood out. So let's say that I'm pushing blood out, but a lot of it's flooding back in, and the total volume of blood that you're pushing out of the heart in that one kind of cardiac cycle is what? It's reduced because you're pushing it out, but a lot's just flooding right back in. So that's a reduction in the cardiac output. And what the problem with this is, is if this is acute. So I have to remember to tell you guys this again. If this is an acute, and I'm going to abbreviate this, aortic regurgitation, this will drop the blood pressure and this will put the patient into cardiogenic shock very quickly. This one's a terrifying one. Okay, so if the patient does have an acute aortic regurgitation and they drop their cardiac output enough, they'll drop their blood pressure and they will present with cardiogenic shock. So that's a big thing to be able to remember.

All right, the other concept here is that we're pushing very little blood out because a lot of it's flooding back in. So what you're going to start noticing is, is that the blood, I'm going to do it like this because of room with all these arrows, the blood will start to kind of accumulate in these ventricles, and they will get plumpy big, right? So they're going to start filling up. So what's the problem with an increased backflow? So whenever you have this increased backflow, well, one thing here, let's actually do it like this. With an increase in the backflow into the left ventricle, where will it go? Well, I can't get out of the heart, so unfortunately, it'll start backing up and going into the lungs, and you'll start developing, oh my gosh, what a surprise, oh, pulmonary edema, right? So your pulmonary capillary wedge pressure will go up, and then what will happen here? You'll have pulmonary edema. I bet you guys don't know how this presents. Just kidding. Dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and maybe even acute respiratory failure if severe, right? So these are potential things that could occur because of that backflow.

All right, the other thing is whenever you have this increased backflow into the actual left ventricle, it does two weird things. All right, one is you increase your stroke volume. So imagine blood goes out of the heart and then a ton of it flows back in. When a ton of it flows back in, the ventricle will stretch. When it'll stretch, what is that called? Preload, right? You increase the preload. When you increase preload, what do you do to your stroke volume? Boom. So it'll increase the stroke volume. So this will increase preload, and we'll put here in like in parentheses, stroke volume. That'll then cause the heart to literally smash as much blood as it possibly can because it's going to get stretched. That'll then cause extreme bounding pulses. These pulses will be insane. And the membrane. All right, so you're going to have crazy bounding pulses. So during systole, you'll feel them. It's literally like a hammer is hitting, hitting your fingers. Then what happens is because of this, um, keep the colors the same. Look what I did here. I jacked all the colors up here, guys. So it should be an increase in preload here. And then this blue area here. A little bit of OCD there, sorry. But the other concept here is whenever I have this increased backflow during the actual diastolic process, what's really weird is imagine during systole, I push, just punch blood into my artery, boom, bounding pulse. So this would be during systole. During diastole, what happens? Well, generally the valve should close, and blood shouldn't come back into the heart. But in this disease, it will. So in diastole, a ton of blood is going to shoot back into the heart, and then the pulse will literally drop. And when that happens, what you're going to notice here is you're going to notice these like weird, like wide pulse pressure findings. So during diastole, I have this wide pulse pressure. We're going to put this wide pulse pressure, and this is particularly during diastole. The reason why I mention this is they use certain, um, there's all these like findings like you have the de Musset sign, you have the Corrigan's pulse or the water hammer pulse. There's all these interesting ones. The most important one, like finding here, is that it's going to present with what's called a water hammer pulse. This is one of the common features of the wide pulse pressure findings, and it's basically, if you palpate the actual radial artery, you'll feel these boom, these smashing pulses, but it'll just be pop, pom. It'll be a big pounding systole and it'll go completely flat during diastole. It's very, very intense, and that's usually associated with aortic regurgitation.

All right, that covers this one. So again, with aortic regurgitation, you'll notice shock. What do you notice pretty much out of all of these, though? Pulmonary edema. Right? Pulmonary edema could be a potential finding in all of these. AFib is a little bit more specific for mitral stenosis, right? But you can definitely see cardiogenic shock in aortic regurgitation and mitral regurgitation, especially if it's acute. The SAD features are really the big one that you'll pick up on aortic stenosis. But at least of this last one here.

So we talked about rheumatic fever being a very powerful trigger of mitral valve disease and aortic valve disease, mitral more so than aortic. And again, it was due to the Group A beta-hemolytic Streptococcus bacteria causing strep throat. Plasma cells reacted, produced antibodies. Antibodies then try to go and destroy the bacteria in the pharynx, but unfortunately produce autoantibodies that attack other tissue. And when they go and attack the tissue, they attack the joints, they attack the heart, they attack the skin and cause these weird nodules or red rash. And then they also like to damage the central nervous system. And I want you to remember the tissues that they attacked based upon this little, little trick here called Jones. And we're going to use the heart. We're going to use this like little corny symbol here. This is your Jones criteria. So first one is you're going to damage the joints. So these patients will have joint injury. You'll also damage their valves. And so they'll have valve damage. Which one more so? Mitral valve greater than aortic valve. They'll also have these weird bumps on their skin called nodules. And we say that this is called like, you have like the erythema nodosum. They'll have this other weird lesion here, these red lesions called erythema marginatum. So they'll have skin lesions like nodules, erythema marginatum. They'll also have these valvular disorders and joint pain. The last one is they love to have this kind of like autoantibodies lead to damage to the basal ganglia, which leads to Sydenham's chorea. What is chorea? Chorea, not the country. We're talking about the weird type of movement that they'll have. So they'll have this like weird kind of like jerky movement that they'll exhibit that's common in these patients. So if you have a patient who had strep throat, presents with joint pain, now valvular disorders, you hear a murmur on top of that, weird nodules, red rashes, and they have weird movements, think about rheumatic fever.

All right, my friends, that covers the valvular heart disease complications. Now what I need us to do is take a second and say, how can we differentiate these? Not just by complications, but also by the murmur evaluation. I think a patient has a valvular heart disease, one of the classic things is the patient presents with a murmur. We talked about this in the heart sounds and heart murmur lecture, but I want to quickly recap it so that you guys don't forget it. Some good spaced repetition. When I auscultate, I want to first know location, systolic versus diastolic or continuous. If I find the location and then I say, okay, this sounds like it's a systolic murmur, then I can automatically think of two particular ones on the left heart. I can think of a crescendo-decrescendo murmur that radiates to the carotids, that's aortic stenosis. If it's holosystolic and it's at the apex and radiates to the axilla, that's mitral regurgitation. Then if it's a diastolic murmur, okay, then I know I'm left with mitral stenosis and aortic regurgitation. So is it decrescendo? And if that is the case, it's aortic regurgitation. Even better, is it around like that left third intercostal space? That also helps. Next thing is, does it have an opening snap with a decrescendo rumble and is that at the apex? That supports mitral stenosis. So these are easy ways to go about that.

But maybe you're like, I'm still on the fence. Maybe there's some other murmurs that I'm not completely sure about. Do some accentuation maneuvers to increase or decrease the intensity to be even more confident in that. So then I say, okay, I'm going to change the position because I'm a little bit confused here. I'm going to have them lean forward. I know that that brings the aortic valve closer to the heart. That should increase the aortic murmurs. If I put them in left lateral decubitus, that brings the mitral valve closer to the heart. That's going to increase mitral murmurs. Then I'm going to have them increase kind of change their venous return. So I'm going to have them increase the venous return by squat or I do a passive leg raise. That brings lots of blood back to the heart. That should increase the intensity of all murmurs, right? The only exception to that is mitral valve prolapse and HCM. All right, so it increases all murmurs except for HCM and mitral valve prolapse. If I decrease the venous return, so I have them Valsalva or I have them stand, then it should decrease the intensity of all murmurs except for HCM and mitral valve prolapse. That's the concept there.

Then I go to the last thing, which is afterload. Now, if I increase the afterload, I have them squeeze some hand grips. What would that do to these systolic murmurs? Well, in this case, it would actually make it harder for blood to move out into this actual vicinity, out into the aorta. And so that should actually decrease the aortic stenosis murmur. The other thing is that it actually should increase the aortic regurgitation, the mitral regurgitation murmur. Why? Because if the afterload is high, the pressure in the aorta is high, so now blood will just flood back from the aorta into the left ventricle. So think about that. That's going to cause aortic regurgitation to be increased. Plus, you're going to have more volume in the left ventricle. So when the left ventricle contracts, it's going to push more blood back into the left atrium. So that's why MR and AR would be significantly increased. And then if I decrease the afterload, then I'm going to do what? I'm going to make the aortic stenosis murmur a lot louder. And then again, flip everything. Decrease the aortic regurg and mitral regurg murmur.

All right, that's the concept that I want you guys to understand with the heart murmur evaluation. Now, when a patient comes to you and they have a murmur, and you've auscultated, you've found, okay, it's here at this particular location, it's systolic or diastolic, it changes with this position or with this maneuver, and maybe they have some features that are suggestive of that type of valvular heart disease. The next thing is to obtain an echocardiogram and consider a cardiac cath. I wouldn't say that it's always needed. I would say an echo is going to be the first test of choice. What's nice about this is it'll definitely show you which valve is the problem and may even lead you into the cause of that valve problem. So if it's aortic stenosis, the problem is getting blood out of this left ventricle here into the aorta, and I'd be able to see that this valve would not be opening very well. So there's decreased blood flow across it, and then also usually left ventricular hypertrophy. Look at the thickness there.

All right, the next thing is I did aortic regurgitation. I'd be able to see that this blood flow that's going from the left ventricle up through the aorta, which you can't see from this window, is shooting right back into it. So there's a massive regurgitation jet back into the left ventricle. And also, I'd be able to see that this left ventricle is pretty dilated to accommodate for that large volume.

All right, with mitral stenosis, I'd be able to see again that there's a really difficult time in being able to get blood flow from the left atrium to the left ventricle, and this mitral valve orifice would be so tiny, and it wouldn't be allowing for me to get blood flow easily through here. Plus, left atrium should be big as a house, right?

Mitral regurgitation is, I would see, look at these valves. They're either defective, they're chewed up, the ventricles are dilated, or there's a papillary muscle rupture, and I'd be able to see the blood shooting back into from the left atrium, sorry, left ventricle to the left atrium during systole, and that's pretty common.

Now, what I did is, you could see in each one of these as we correlate again the echocardiogram with the cardiac catheterization, and this will show you the different levels of pulse pressures. So you'll be able to see the pulse pressures and where the different pressures in the atria and the ventricle change.

All right, now after we've done all of this, we've diagnostically come to the conclusion, hey, they have a valvular heart disease, and it is this, it is this one. The question is, could it have been because of rheumatic heart disease? And again, we have to think about that, especially in mitral stenosis. So if a patient has any of these major criteria, at least two of them, so any of the Jones: joint pain, cardiac valve, nodules, erythema marginatum, Sydenham's chorea. If they have two of these, you can make the diagnosis of rheumatic heart disease. If they don't have two of these, maybe they only have one of these, then you come over here to the minor criteria. Is there suggestion of fever, an increase in erythrocyte sedimentation rate, an increased PR interval, or polyarthritis? If there is one of these and at least two of these, then we can potentially say that the patient has what? Rheumatic heart disease. To add to the diagnosis, to make this even better, what about those antibodies that were actually causing these problems? Test them. Test them for the strep test to see if they had an infection there. Test them for the anti-DNase B and the anti-streptolysin antibodies. Okay, so again, two major or one major plus two minor, and you've met the criteria for rheumatic heart disease.

All right, we've determined the patient's valvular heart disease. If it's rheumatic or not. How do we treat them? This is super straightforward. You're not going to get hit with a lot of questions on this. But first, manage all heart failure symptoms. So again, we saw that aortic stenosis can cause diastolic, aortic regurgitation can cause systolic heart failure, mitral regurgitation can cause systolic heart failure, and mitral stenosis again, doesn't really cause a classic heart failure, but you'll notice that in these patients, they have specific features of heart failure. Treat that accordingly. If the patient does not improve, then you need to consider the potential for a surgical intervention. Aortic stenosis, we do what's called a TAVR, and we'll go through kind of like a vessel and we'll actually use a catheter and go up there and try to repair the actual aortic valve, or you can do it surgically. SAVR is a surgical, you open them up, open up their chest and do it. TAVR is usually preferred in all of these scenarios because it's less invasive. But you have to consider, is it severe aortic stenosis because the aortic valve surface area is super small? Are they really symptomatic despite management with medical therapy? And is their LVEF dropping? Because it really shouldn't, but if it starts dropping, that means that this is not going well and you need to start intervening.

Aortic regurgitation, same thing. Do they need a SAVR? Usually, this is always has to be repaired surgically. And again, is it acute heart failure? Is the primary indication? So in other words, that the, the valve just completely get ripped up and now they're in acute heart failure, you need to take these patients right away for surgery. Or do they have aortic regurgitation that's chronic, but they're not responding to medical therapy?

Mitral stenosis, same thing. We actually do what's called a balloon valvuloplasty, where you actually kind of like spread this sucker open a little bit, and that's usually if they have very severe mitral stenosis, so their mitral valve surface area is so, so tiny.

The last one is mitral regurgitation. This one's also mitral valve repair replacement. This is usually if they have acute heart failure or they're refractory to all the medical therapy. So again, I want you to remember, if they have aortic regurgitation or mitral regurgitation, and it's acute, that is an immediate indication for a replacement. All right, but again, for the aortic stenosis, a mitral stenosis depends upon the severity of the actual patient's disease.

All right, quick thing to add on here with mitral stenosis. I told you that it's the highest risk for atrial fibrillation. So therefore, they can pop emboli off, cause strokes. You need to consider that and determine the patient's CHA2DS2-VASc score and determine if they need anticoagulation. Usually, this is because it's a valvular AFib, it will require warfarin and wouldn't be best to treat with the DOAC. The other thing here is rheumatic fever. If any of these patients have these diseases because of rheumatic fever, you have to treat them with penicillin G, and they may be on that for a decent amount of time.

Last thing to discuss is if a patient gets a valve replacement, we put in a prosthetic valve, and this is either mechanical or it's bioprosthetic. Now, if they get a mechanical heart valve, these are highly thrombogenic, so you may have to put them on anticoagulation for the rest of their life. And again, because it's a mechanical valve, warfarin is the only thing that you can put them on. All right, and for that, you're aiming for an INR of 2.5 to 3.5. Remember that. What the problem is with the mechanical heart valve is again, they may need to be on lifelong anticoagulation. So they want them to be not too old because they're going to have a risk of bleeding. And again, these valves last a really long time, so you want them to also be younger because you want to give them a valve that's going to last a decent amount of time. If these valves do become damaged, it's usually the annular ring, so it's on the side where they're actually, like the adhesive, like that, where the surgical incisions are on the side of the valve, they start to become weak, and you can develop a leak on the side of the valve where it's actually kind of seated, and this can cause blood to regurgitate on the side of that, that new healthy valve. It's called a periannular leak, very classic from mechanical heart valves.

With bioprosthetic valves, these are not as highly thrombogenic, so you do not need to be on lifelong anticoagulation. The downside to this one is that the valve can actually get chewed away because it is bioprosthetic, and so it can actually get ripped away and eaten. And so what happens is, you can actually develop a leak right in the middle of the valve. So this is called a transvalvular regurgitation. If this happens, you want to be listening and saying, hey, do I hear a new murmur? That's one of the key features. If there is a new murmur that doesn't make sense to them, think about the prosthetic valve being dysfunctional. If that's not the thing that comes up on the vignette, think about weird things such as do they have any anemia, especially microangiopathic hemolytic anemia, or are they in acute heart failure? If any of these things present, you should start thinking about a prosthetic valve that's being dysfunctional, and then get an echocardiogram to determine which one of these valvular leaks it is.

All right, my friends, that covers valvular heart disease. I hope it made sense. I hope that you guys enjoyed it. And as always, until next time. [Music] Thank you.