Cram The Pance - S1E22 Heart Murmurs (Valvular Disorders)

Episode Date: May 8, 2021

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Okay, so moving on with cardiology, we're going to do Murmurs today. So Murmors is definitely important one that you need to know. I'm going to do my best to make this as brief as possible and really just stick to the stuff that you need to know for the exams as usual. As always, thank you so much for the comments, the likes. And if you haven't checked out my YouTube page, I always recommend that. I feel like you get a lot more information there. I have a lot more visuals and things like that.

So if you're on the go, these podcasts are great. But if you're at home and want a little bit more information, check out the YouTube channel under cram the pants on YouTube. Okay. So before we get started with murmurs and breaking down what you need to know for each individual one, I want to review a few key areas that will help you not only get the questions writing the exam, but help you in a real life. So first thing that I want to review is differentiating between systolic and diastolic murmurs and really just an easy way to memorize them for the exam that I came up with. So there are systolic and diastolic murmurs, obviously.

And remember, systolic murmurs occur between the S1 and S2 heart sounds. diastolic murmurs are going to occur after S2 between S2 and S1. Okay, so on the exam, how do you remember which is which? Really easy way that I came up with. If you just remember the sentence, you'll always know whether a murmur is systolic or diastolic. And again, this is for a test. This is an auscultating and figuring out that way, but on the exam, you'll never forget. So remember, Ms. Prarts died.

Miss Prarts died, and you'll always know which is which. So Ms. Prartz died is MS, M-S, M-R-R-R-T-S, and then died. And what that stands for, the MS stands for mitrostinosis. The PR and Prarts stands for pulmonary regurgitation, the AR stands for aortic regurgitation, and the T-S stands for tricuspid stenosis. So mitrostosis, pulmonary regurgitation, aortic regurgitation, tricuspet stenosis, and then died stands for die a stolic diastolic so miss prarts died mitralstinosis pulmonary regurge erotic regurge tricuspid stenosis died died diastolic so any one of those are all going to be diastolic murmurs if it's not in that sentence

it's going to be a systolic murmur so just remember miss prarts died and you'll always know died these are all diastolic murmurs if it's not in that sentence it's going to be a systolic murmur so really really easy way for you to remember, which is which when you have an exam. All right. So the second tip that I feel like is important for you to know is related to Venus return and its effect on the intensity of different murmurs, which is really important to help differentiate between the two. So all murmurs or almost all murmurs will increase when there's increased blood flowing back

to the body. So increase preload and some of the maneuvers that are going to increase your preload or Venus return to the heart are going to be squatting, leg raise, laying down, anything with gravity pulling it back to the body. to the body and maneuvers that will decrease venous return which will decrease your preload are going to be standing balsavum maneuver so anything that increases blood to the heart increases preload is going to make most murmurs louder and it makes sense you have more blood going through either a stonotic valve regurgitation whatever it is more blood is going to make the murmur louder

and then less blood decrease preload decrease venus return is going to make the murmur quieter and that's most except for two oddballs that you need to know. And those two oddballs that don't follow the rules are going to be mitral valve prolapse and hypertrophic cardiomyopathy. The way you can remember that is remember that the MVP hates conforming to the rules. The MVP hates conforming to the rules. And the rule, of course, is that murmurs should get louder with increased venous return and decrease in intensity with decreased venous return.

But the MVP hates conforming to these rules. So MVP obviously stands for mitralvents. while prolapse hates conforming stands for hypertrophic cardiomyopathy H.C. So it doesn't follow those rules. It hates conforming to the rules. And the murmur of hypertrophic cardiomyopathy decreases with increased venous return. And the click in MVP with increased venous return is delayed. And the murmur is also shorter and dilation. So instead of them going the opposite way, getting louder, longer in duration, increased venous return is actually going to decrease the murmur of hypertrophic cardiomyopathy, shortened the MVP.

murmur and then shorten the click of MVP. So remember, all murmurs are going to get louder with increased finesse return and softer with decreased venous return except for the two oddballs. And that's the MVP hates conforming to the rules. MVP mitral valve prolapse hates conforming. That's hypertrophic cardiomyopathy. All right. So that's the second tip.

One more thing that I want to go over that you should be familiar with before we break down each individual ones. So the third tip is that you have right side of murmurs. and you have left-sided murmurs. Right side of murmurs are going to sound almost exactly like left-sided murmurs. So tricuspid regurg is going to sound like mitral regurg, aortic stenosis like pulmonic stenosis. So how do you differentiate them?

So there's two ways. First is by location. These are obviously happening in different parts of the heart. So they're going to be heard best at different parts of the thorax. So for instance, aortic stenosis is going to be best heard at the right upper sternal border. While pulmonic stenosis, which will sound the same, it's going to be heard best at the left upper sternal border. So just kind of have to memorize these locations if you're going to use this method.

And then remember, they're not only going to be heard in these locations. They're going to be heard best. So a lot of times you can oscillate almost anywhere on the thorax and still hear them, but they'll be heard best in those locations. That's the first way you can differentiate right and left. But I feel like the easier way to differentiate is to remember that right-sided murmurs are going to increase with inspiration, increase in intensity, and left-sided murmurs decrease in intensity with left-sided murmurs.

And the way that I remember that is I remember that, I remember Rinspiration, rinspiration. So right side, increase with inspiration, Rinspiration, like R-I-N, increase inspiration, Rinspiration. And you can always remember actually what's going on, the patho. So when you take in a deep breath, it creates negative intertheracic pressure, it increases the venus return to the right side of the heart and increases the intensity of the murmurs. But on an exam, you just want to remember something easy. So just remember Rinspiration, right side, increase in inspiration. Rinspiration. I always remember that. And it helped me to remember.

So that's the main way to differentiate between the two. Okay, so now moving on to the actual murmurs, there's a few things that I'm not going to go over for not only the sake of saving you time, but I feel like it's not important enough. So I'm not going to go over the way to diagnose, because generally echo is going to be your best, least invasive test. So that's going to be the answer for almost all of these. Sometimes there's more invasive tests that are better,

but generally echoes how you diagnose these. And I'm only going to briefly touch on treatment, because in most cases, surgical repair is going to be your definitive option. There's really not a lot to test you on here. Most of the time, it's surgery. Sometimes there will be some meds that you can use as a bridge of surgery, help the symptoms. If there's something different, I'll point it out. But otherwise, diagnosis is generally going to be echo.

Treatment is generally going to be surgery, except for the fuel that I'll go over. And then the other thing I'm not going to go over either is the different maneuvers and how they alter the murmur. Because as you know, unless it's MVP or hypertrophic cardiomyopathy, you should just know. anything that's increasing venous return is going to increase this murmur. Anything that decreases venous return is going to decrease the murmur unless it's MVP or hypertrophic cardiomyopathy. So there's no point in going over that. I already gave you a way to remember that and you should know that.

So we shouldn't have to waste time on that. So, and then one last final note as far as your auscultation points. This is really just something to help you in your, your EORs and, you know, your Oskis and things like that. So if you ever forget when you're auscultating which point is where, remember that all patients eagerly take medicine. All patients eagerly take medicine. Well, that stands for all stands for aortic. So that's going to be, we'll start at the aortic, which is going to be the right upper sternal border at the right second intercostal. So all stands for aortic. Patience stands for pulmonic. You're moving now to the left. So pulmonic area is going to be the left upper sternal border at the left second intercostal space.

Eagerly is going to stand for your herbs point, third intercostal, just left of the sternal border. Take is going to stand to stand for tricuspid. That's around the fourth or the fifth intercostal, just left of the sternal border. And then finally, medicine stands for mitral, and that's going to be at the fifth intercostal at the mid-clavicular line. So remember, all patients eagerly take medicine. Start up at your aortic, aortic, pylmonic, herbs, tricuspid, mitral, all patients eagerly take medicine. In case you're auscultating in an oskete, and you forget, where am I excotating or where they ask me to. You just remember that. You can see it out loud in your head, and then you can remember where. All right, so let's get into the individual murmurs, and again, I'm going to try to really just focus on the things that you need to know for each and not waste your time with any of the extra.

So let's start with the most common valvular disease, the one you'll most likely be tested on, or you'll actually hear out there in clinicals listening to heart sounds. It's aortic stenosis. Or you can do what I did in clinicals, and when your preceptor asks you what murmur you hear and you have no idea, just say aortic stenosis and there's a pretty good chance that you'll be right. It's very common. It's the most common valvular disease. So, all right, aortic stenosis. Really simple. The aortic valve is narrowed for some reason. Blood's having trouble getting through the stenotic valve. That's what's going on. Now, why is that happening? So the etiology, there's two things you need to know. If they're young, it's going to be a congenital valve abnormality, like bicuspid valve. So under 70, young, relatively young. Congenital valve out of normality, think of a bicuspid valve. If they're older, over 70, think of calcification of the valve. It's really the only two you need to know. There are some other less common causes, rheumatic valve disease. It's just not as common as these. So just remember, if they're older, over 70, calcification of the valve. If they're young, think of a congenital valve abnormality like bicuspid valve.

Okay, that's etiology. Now, clinical manifestation. This one I'll kind of talk about a little bit because you're going to hear about this. So the triad you'll normally hear about it or you might be tested on with aortic stenosis is going to be angina, syncope, and heart failure. So ash, ash, ash. angiosynosynosyncope heart failure. It's important to note, though, that these symptoms are typically only seen in the end stages of aerok stenosis. And once these present, these patients normally only have about two to five years left of life without valve replacement. So you'll hear about it. You'll probably be tested on ash, angina syncopy and heart failure. But remember, if you do hear it in real life that these patients are kind of at the end of their life unless they get this valve replaced. So keep that in mind. That's probably the presentation you'll be tested on. But overall, the most common clinical manifestation is just like a decreased exercise tolerance dyspnea on exertion but definitely remember ash because that's what you'll get tested on

most likely now the murmur of aortic stenosis is a systolic remember this is not in what we went over the the mnemonic miss parts died so this is obviously not going to be diastolic it's going to be systolic so it's a systolic murmur so between s1 and s2 and it's going to be crescendo de crescendo. And what that means is the murmur starts shortly after the first heart sound, slowly increases, increases, increases, until it hits mid-sistoli, peaks at that point, and then slowly decreases, decreases, decreases,

and then ends just before the second heart sound. So louder, louder, louder, hits a peak, then softer, softer, softer. It's going to be best heard at the right upper sternal border. Of course, that's the aortic area. And then this is also really important. It radiates to the carotids. So you can actually oscillate the neck,

you can hear the murmur radiating to this to this region. One last thing that I want to mention on the physical exam that you should be familiar with is aortic stenosis can cause something called pulses parvis etardis. I may be pronouncing that wrong, but parvis in Latin stands for weakened and then Tardis stands for late. So the pulsing these individuals with the aerosinosis, it's going to be weak and it's going to occur late. And it makes sense because you have blood flowing through this stenotic valve. So the heart beats, but it has to push through the small valve, not as much as getting out,

which both delays the pulse and weakens it. So pulse, pulses, parvus, E, which is E.T. Tartis. So remember that weak and delayed pulse. Let's actually listen to the murmur. I'm going to try to do my best, so the quality is decent. Hopefully it'll be enough for you to listen to in the car. But let's listen to what aortic stenosis sounds like. Remember, again, cystocrychrchrchendo de crescendo.

Best heard of the right upper sternal border radiates to the karate. Let's take a listen more time. Okay, so hopefully that was enough for you to get an idea of what that's going to like remember that crescendo decrescendo murmur. Okay now as far as treatment really quickly surgery is going to be your only definitive way to fix the problem. You can do things as a bridge of surgery, intra-aortic balloon pumps, but ultimately surgery really is the only way to fix this for these problems. They need that valve replace. Okay, now moving on to aortic regurge. It's also known as aortic

insufficiency. So aortic regurge is an insufficiency with the aortic valve leaflets and due to this insufficiency they have trouble remaining the the valves, the leaflets have trouble remaining closed during diastole, which results in a portion of the blood leaking back from the aorta into the left ventricle, filling it up and overloading it. Now, the etiology, chronic and chronic aortic regurge, most common cause in developing countries is going to be rheumatic heart disease by far. Otherwise, it can be caused by calcifications, aortic root dilation. Marfan syndrome is another one, but overall in developing countries, it's going to be rheumatic heart disease. Now, if it's acute aortic regarge, you should be

thinking aortic dissection acute MI or endocarditis those are all causes acute causes of aortic regurgic clinical manifestations often these patients are going to be asymptomatic if it is severe they may develop angina dyspnea other symptoms of heart failure nothing really that specific okay now the physical exam remember this is the a r in miss prarts remember miss prarts PR A-R-T-S. This is the AR, meaning, remember she died, so this is a diastolic murmur. So, Ms. Prarts, died so we know aortic regurg is going to be a diastolic murmur. So it's diastolic decrescendo murmur. So it starts off louder, then it slowly decreases and tapers off from that initial peak. So high, then gradually low, low, low, low, and it's also described as a blowing or high-pitched

murmur. But remember, it's diastolic decrescendo murmur. Now, aortic regurgers, in addition to the murmur, it has a lot of different physical exam findings that you should be familiar with in case you get a question on one of these. Let's go over a few of what I feel like are the important ones. So the first thing is that patients with aortic regurge are going to have what's known as bounding pulses. So all that is, it's just a strong pulse. And the reason why these patients have these bounding or strong pulses is because they have a backflow from the erotic regurge, which in turn increases stroke volume. And this larger volume expelled during systole increases the strength of pulsation.

so you have this bounding strong pulses and it's just due to the extra volume that's coming out. And then there's a few other physical exam findings that you need to know as well in aortic regarge. And they're all due to the widened pulse pressure. So that's seen in these patients. So these patients have wide and pulse pressure. Remember pulse pressure again is the difference between systolic and diastolic blood pressure. So wide pulse pressure is normally greater than 60. So if a patient has a 120 systolic and 50 diastolic, that's going to be a 70 pulse pressure.

That would be a widened pulse pressure. Now, let's go over the first one. This one's known as Quinky's pulses. So Quinky's pulses is a capillary pulsation in the fingertips or nail beds. You're going to kind of see the heart beating. You're going to see this little pulsation in the fingertips or nail beds in the fingers. The way that I remember this is that Quinky is seen in the pinky. So you remember Quinky's pulses.

Quinky is seen in the pinky. You remember, okay, I remember that's in the pinky. So what does that mean? and you remember you have these pulsations in the fingers. So that's the first one you need to know. So Quinky's pulses. Quinky is seen in the pinky. Next one is something known as Corrigan or water hammer pulse.

Corrigan or water hammer pulse. This is a rapid rising pulse, which is forceful and strong, that rapidly collapses. So you can test this by palpating the radial pulse with the patient's arm at their side, then having them lift the arm while still palpating the pulse. And this is going to accentuate that water hammer pulse. So remember Corrigan. I remember Corrigan, raise the hand. Corrigan, raise the hand. Helps me remember the way you can actually test this in a physical exam. And now two other ones that I think you should know, because I do remember being asked these before, is Demuset sign.

This is, you'll have a patient sitting there. You can watch them. Their head actually bobs up and down. It occurs with each heartbeat. So their heads bobbing up and down. And another one similar to that is called Mueller's sign. But Mueller's sign, you look at the uvula and you actually see the systolic pulsation of the uvely. kind of bouncing up and down. So Demoset's head is bobbing up and down. Mueller's sign is going to be systolic pulsation of the uvula. Treatment surgical is going to be definitive. Nothing really to know here. You can't use medical management with afterload reducers like your ACEs, ARBs, Hydrolym, but generally just surgery. Really, they're not going to ask you on treatment for most of these

because like I said, it's pretty similar across the board. Okay, so let's actually take a listen to that murmur of aortic regurg. So let's listen so you can get an idea. Okay, so here we go. Try to make that a little bit louder. All right, I'm trying my best. Hopefully you're able to hear that, but it's kind of hard on the podcast. So that was aortic regurgers. All right. Let's move on to mitral regurgitation. So this is going to be a valvular disorder where there's abnormalities in any part of the mitral valve apparatus. So that includes the leaflets, papillary muscles, corday tendene, and because of this abnormality, you have this result in retrograde blood flow from the left ventricle back into the left ventricle back into the

the left atrium and it's going to lead to increased pressure in the atrium also dilation of the atrium which will cause some other problems we'll go over in a minute now as far as the etiologies degenerative mitral valve disease like mvp that's a really big MVP it's going to be the most common cause in the u.s. for mitral regurgitation so remember mitral regurg you should be thinking mitral valve prolapse and that's a degenerative mitral valve disease and most common cause in the u.s. in other developing countries rheumatic heart disease is actually going to be one of the more common causes for mitral regarge, but here in the United States, think of MVP, developing countries, think rheumatic heart disease.

Now, there are some other less common causes like infective endocarditis. Some meds actually like ergodamines that are in migraine meds, that are the migraine meds, Bromocryptine and Capargoaline, which are both meds used in hyperprolactinemia, can actually cause this as well, but much less common, so I wouldn't really focus on those. Now, clinical manifestations, again, dyspneas, common. hypertension is also positive, possible. But what I think you should be familiar with here is the fact that these patients can actually develop aphib. And it's due to the atrial dilation that these patients have.

It predisposes them to aphib. And any condition that dilates or enlarges the atrium, like mitral regurg, mitral stenosis, whatever the condition is, there's dilation of the atrium. You should know that these patients are going to be at a higher risk for aphib because of the stretching of the atrium, which leads to multiple reent. circuits that can coexist as well as fibrosis, which can also cause conduction abnormality. So remember, mitral regurge, aphib. That's kind of different than what we've gone over before. So I feel like I should point that one out.

Now, physical exam, the classic murmur for mitral regurge is going to be a hollow systolic murmur. That's best heard at the apex. So apex, bottom of the heart, and that's at the mitral area. So you remember, apex, bottom of the heart, and mitral area. And what hollow systolic means is that the murmur has the same intensity through. throughout systole. There's no peak, there's no decrease, there's no increase. It's just regular, flat, rigid. The intensity does not vary. And the way that I always remembered that, and hopefully this works for you, because I never forgot this, is that mitral regurge, MR, mitral regurge stands for mostly regular or mostly rigid. Since it's hollow systolic, it's rigid across the

board. It's regular. It doesn't peak. There's no valleys. It's rigid. It's mostly rigid, mostly regular. So I remember MR stands for mostly regular, mostly rigid, and that's a hollow systolic murmur. So I felt like that always helped me remember it. And then one other important thing about mitral regurge is that this murmur can radiate. And when it does, it radiates to the axilla. So in addition, I remember that this is a mostly regular or mostly rigid murmur. You should also remember it mostly radiates. So radiates mainly to the axilla. So let's actually listen to that murmur of mitral regurge. Okay.

All right. So hopefully you're able to hear that. Again, I apologize if they're not coming out too well, but I tried my best to try to get it so you're able to hear them and get an idea. If not, you know, there's always ways to check it out online. All right, let's move on to, well, I guess the last thing to mention with mitral regurg treatment, surgery is definitive, and you can use symptomatic control with afterload reduces. So, mitral stenosis.

So mitral stenosis is an obstruction of blood flow across the, mitral valve from the left atrium to the left ventricle. It's due to a narrowed mitral orifice. And due to the stonotic valve and mechanical obstruction, you're going to have increased pressure in the left atrium, which is going to back up into the pulmonary vascular, eventually can back up all the way to the right side of the heart leading the heart failure. Now, etiologies, as far as etiology is for mitral stenosis, remember this rheumatic heart disease, rheumatic heart disease, rheumatic heart disease. That's what you should be knowing for, that's what you should know for mitralinosis. It's the most common cause of mitral stenosis. So again,

heart disease. Remember that. It can also be caused from calcifications. It can be congenital. Just remember rheumatic heart disease. That's what you should focus on because that's the most common cause and that's what they're going to ask you. Now, as far as clinical manifestations, this condition actually has some high yield clinical manifestations that I feel like you should need to know. Unlike the other ones that were kind of nonspecific. This one has a few that you should be familiar with that are kind of different than what we've seen in the past. So one, like I went over before, you can develop a fib. And that's due to the increased pressure and size of the atrium. So that one is just like in mitral regards.

But the one you really need to know, and the one I absolutely remember getting asked, I think in school at some point, is that this can cause hoarseness, which is the one I got. It can also cause something called mitral phases. So these are the things that they like to make exam questions from, for whatever reason.

So let's start with the hoarseness. So why would mitral stenosis lead to hoarseness? Well, as the left atrium enlarges in mitral stenosis, as it gets bigger, which it often can in mitral stenosis and pretty large and dilated. It can actually compress the nearby recurrent laryngeal nerve, which can cause hoarseness in these patients. So they may actually have hoarseness on presentation,

and it's probably the last thing you think of, but it's possible that it can be from mitral stenosis. Now, the other clinical manifestation, something known as mitral phases, I never know if I'm saying this right, but mitral faces, F-A-C-I-E-S. I've also heard it's called fasces or facies, I don't know, mitral faces, which really only happens when these patients develop severe mitral stenosis. But it can cause, mitral stenosis can cause pulmonary hypertension, diminished cardiac output.

And when this happens, these patients get this cutaneous vasodilation. And they basically just have these rosy cheeks. They have this pinkish hue in their cheeks and just a rash over their cheeks and just looks like rosy cheeks. And it's from severe cases of mitral stenosis. So if you do see this in a patient that has mitralstinosis, it's pretty severe. It's not going to be in mild cases. So remember, mitrophases and hoarseness can be seen in patients with mitralstinosis. Those are important to know, although maybe not that common.

They can definitely ask you those questions. You need to be familiar with them. Okay, so on physical exam, what's the murmur sound like in mitral stenosis? Well, we know it's diastolic because remember, miss MS. Prartz died, so MS. mitralstinosis, so it's diastolic murmur. It's going to be a rumbling murmur, and it's best heard at the apex of the heart, again, the mitral area during auscultation. Now, so again, diastolic murmur, rumbling murmur, best heard at the apex of the mitral area.

Now, the other thing that's really important is that this murmur has an opening snap. And the way, and this is due to the mitral valve being forcefully open due to the high pressure. And the way that I remember opening snap is I remember mitralstronosis MS, opening snap OS. I remember Microsoft MS is the operator. system OS. So that makes me remember mitral stenosis opening snap. Remember Microsoft MS. Operating system OS. So remember Microsoft is your operating system MSOS, mitral stenosis, opening snap. Pretty good way to remember it. Hopefully that'll help you. Now treatment, this one's a little bit different because normally in younger patients, they try to do a percutaneous balloon valvuloplasty.

and just because I'm going to mention this a couple of times, percutaneous balloon valvuloplasty is basically just what it sounds like. It's they introduced this deflated small balloons guided by a catheter into the stononic valve, and they inflate it. They blow up this balloon over the valve to open it up and just kind of loosen the stenosis, and that's what that is. So in these patients, normally it's going to be percutaneous balloon valvuloplasty over a valve replacement, which is another option, but normally not the first line.

So again, you know, just remember those couple things that are a little bit. bit different. And then let's listen to the murmur of mitral stenosis. Okay, here we go. One more time. Okay, so that was mitral stenosis. Now let's move on to mitral valve prolapse. So mytile valve prolapse is when the two valve flaps of the mitral valve don't close properly. Instead of closing, having this nice flush point where they're both kind of close together and pinch together, they bulge or prolapse up into the left atrium. So not down. They're actually prolapsing up into the left atrium. There's a slight predominance in younger women, and often what you'll see in a vignette is a young woman that presents with anxiety, chest pain, palpitations, other associated autonomic dysfunction.

So remember that because that's likely what the vignette will look like. A younger woman with anxiety, and it's related to the mitral valve prolapse, which I'll go over in a few minutes. Also remember that mitral valve prolapse is going to be the most common cause of mitral regurgurge in the U.S., which we went over before. Now, etiologies, you're going to have primary and secondary. MVP. So primary is when there's a degenerative disease present. It's known as mixomatose degeneration, but there's no associated connective tissue disease that's causing it. So that's primary. So you have some degenerative disease, but no associated connective tissue disease. Now, secondary MVP, you have a connective tissue disease present. And the one that you really should know,

the one that you'll hear about the most, is going to be Marfan syndrome. And that's a big one. You'll also hear about Ehlers Stanlos, but Marfan is really the one. you'll most commonly be asked about. So those are etiology's clinical manifestations. More often than that, these patients are actually going to be asymptomatic, but you do need to be familiar with those autonomic dysfunction symptoms I went over. So these symptoms are sometimes known as MVP syndrome, and it consists of anxiety, palpitations, dizziness.

So that can be seen in these patients, and there's a good chance that you have a question on it, but it's also important to note, and I try to always give you, like the most up to date data, that in real life, the validity of MVP syndrome is actually questioned. The studies that initially conducted it where they came out with these ideas about MVP syndrome were actually flawed and now they're kind of going back on it. So they don't know how high the chances are that this is going to be seen in a patient or how often it is, but you'll still probably see it on a vignia. Just know that it may not be as common as they first thought.

Okay, so now on the two things that you need to know for the sculptory findings in a patient with MVP, there's two things you need to focus on. So first, this is the big one, a mid to late systolic ejection click. That's huge. Don't forget that. It's probably the most important thing to know about MVP. It has a mid to late systolic ejection click. And it's from the snapping of the mitralcorde when the valve prolapses into the atrium.

So you hear this mid to late systolic ejection click. there's a good chance that you're also going to hear the murmur of mitral regurge, which remember what I talked about previously, it's very common in MVP, so you may also hear mitral regurge. But don't forget about the mid to late systolic ejection click. And then the second thing, as we went over in the beginning, this is the only time I'll go over this because otherwise you know the rules. MVP is not following the rules.

So remember MVP hates conforming to the rules. So in a patient like this, if they have increased venous return, It's going to make the, in most patients, normally, increased venous return will make the murmur louder or last longer. Decrease makes the murmur softer or shorter. And MVP, it's the opposite. So remember, MVP is going to have the opposite effect of those normal maneuvers and other murmurs. So increase preload, like raising the leg, when there's more blood into the heart, is actually going to decrease the amount of prolapse. It's going to shorten the length of the murmur and cause the click to be delayed and happen later.

and then decreased preload, like standing, Volsava, which makes the left ventricle smaller, makes the valve prolapse even further. And it's actually going to cause the murmur duration to increase and cause the click to happen earlier. So that's what decreased preload. So just remember, it's the opposite on those maneuvers. Now treatment, asymptomatic patients are just going to be reassurance. And this is going to be the treatment for most patients. You're only going to have surgery as an option in patients who develop severe mitral regurge

along with the MVP. So generally, it's just going to be reassurance and observing these patients. Beta blockers can be used for some of those autonomic symptoms that I went over before. Okay. So that is mitral valve prolapse, and let's listen to that murmur. Okay. You can actually hear that click. Okay, so that is mitral valve prolapse.

Okay. So now let's move on to the right side of the heart. So those are all the left side in murmurs. I'm going to keep these more brief. because there's not a lot to know compared to the left side of murmurs, and they overlap with the left side of murmurs. So pulmonic stenosis is going to sound just like aortic stenosis. So I'd suggest just know the left side of murmurs really well, and then you'll know the right-sided one, since they're similar. They're only going to, the only difference really is based on the location like I went over before,

and that they're going to increase with inspiration. Remember, Rinspiration. They're just not tested on as frequently, but obviously let's go over the things you do need to know. So the first one is going to be pulmonic stenosis. And with all the pulmonic disorders, whether pulmonic stenosis or pulmonic regurge, you should be thinking congenital. So all of these pulmonic disorders are going to be very common in children. So pulmonic stenosis, it's an outflow obstruction of the right ventricle, and it's due to a stenotic pulmonary valve. And it's seen in about 7% of children with congenital heart disease.

So it can be an isolated lesion, but it's also associated. with tetralogy of philoh, congenital rubella syndrome, and nunan syndrome. So those are some of the associated conditions. Now clinical manifestations, many patients are going to be asymptomatic, but they can't experience mild exertional dyspnea and other symptoms of right heart failure. Okay, now the actual murmur on physical exam is going to be mid-sistolic ejection, crescendo de crescendo, at the left upper sternal border, the pulmonic area. Now, does that sound familiar? should sound familiar because it's the same description outside of the area of aortic stenosis. So pulmonic stenosis is the same mid-sostolic ejection crescendo decrescendo.

That's going to be heard at the left upper sternal border. So that's the only difference there. It can also radiate to the neck. So remember, this all sounds very familiar with its left-sided cousin aortic stenosis. But remember, this is a right-sided murmur. So rinspiration, it increases with inspiration rather than decreasing left, like the left-side murmur. So that's what's going to help you differentiate that in the location. So treatment, mild disease, you're just going to observe, and then moderate or severe disease. It's going to be

a balloon valuoloplasty. And I'm sorry I don't really have any good murmur sounds for the right-sided ones, but you're not going to hear about these as often. So it's not as important, but I'm sure you can find some if you do look for it. Okay, so that's pulmonary stenosis. Let's go on to pulmonary regurg. This is another condition that's commonly congenital. It can be seen alongside Tetralgia endocarditis rheumatic heart disease and these patients are going to have back flow from the pulmonary artery back into the right ventricle which in more severe cases can lead to right-sided heart failure so clinical manifestations normally asymptomatic unless it's severe then they can develop

symptoms of right-sided heart failure so physical exam just like its cousin aortic regurg this is going to be a diastolic decrescendo murmur the murmur though is going to be best heard at the left upper sternal border at the pulmonic area again and remember this murmur like all right side of murmurs were inspiration it's going to increase with inspiration rather than the left side decreasing and then also be familiar because sometimes the person making the exam likes to trick you you read the vignette and you'd be like oh I know this one is pulmonary regurge and you look at the answers and pulmonary regurge isn't

there but something called Graham steel murmur will be so this is another way of describing the murmur you hear in pulmonary regurge so Graham steel murmur may be used as a replacement name for pulmonary regurgent. So the murmur of pulmonary regurgitation is known as Graham Steele murmur as well. And you can remember that because Graham Steele, like the man of steel, is a superhero, and he protects the realm. So pulmonary regurge, Graham Steele, so PR, Pulmonary Regurge, Graham Steele, Protector of the Realm, PR. I don't know, that's not great, but it worked for me when I was in school. So remember that Graham Steele, Man of Steel. as a superhero protector of the realm PR.

Okay, so treatment generally for these patients for pulmonary regurg is just going to be observation or treat the underlying cause of its tetralogy of low endocarditis, etc. Okay, now tricuspid stenosis, we're almost there. We're running towards the end here. Tricuspid stenosis, it's pretty rare. It's usually going to be found alongside either tricuspid regurge or other volvular lesions. You're not normally going to find this as an isolated lesion. And it's basically just a stenotic tricurge.

Cricuspid valve due to some underlying condition and it's going to lead to blood backing up into the right atrium, eventually leading to right atrial dilation or enlargement, and potentially, if it's left untreated, you can have right-sided heart failure. Now, as far as etiology, just remember rheumatic heart disease. It's going to be the most common cause of tricuspid sinosis. There are some iatrogenic causes like from radiation therapy, fibrosis, from endocardial pacemaker leads, but really just focus on rheumatic heart disease for tricuspid sinosis. Now, clinical manifestations, again, really kind of nonspecific, fatigue dyspnea. And remember, this isn't going to be an isolate allusions. You're going to have symptoms not only from tricuspid stenosis, but potentially mitral and aorta valve disease. So overall clinical manifestations are too nonspecic to really be tested on.

Now, in the physical exam, the murmur of tricuspid stenosis, like all the right side of murmurs are going to sound very similar with the left side of cousin. So what did mitral stenosis sound like? Remember, MS is OS. So it's going to be a diastolic murmur. It's the TS in Miss Prarts. And then also remember, like in mitral stenosis, it has an opening snap. So the MS is OS. Same in tricuspid stenosis.

So there's going to be an opening snap. It just normally occurs a little later than what we heard in mitral stenosis. So again, remember the other differences, that's going to be best heard in this case in the tricuspid area, which is around the fourth intercostal space, just lateral to the xiphoid. and then also it's going to increase with inspiration, rinspiration. Treatment surgery is going to be definitive. Medications can also be used to decrease right atrial overload like diuretics. Okay, so tricuspid regurg, this is going to be the last one.

Trichusper regurgs back flow of blood into the right atrium during systolee, and only severe cases can really cause any problems like right-sided heart failure. Most patients aren't going to have any hemodynamic consequences from tricuspid regurgents. It's normally pretty well tolerated. And tricuspid regurge, and like some of the other right side of murmurs, it's actually really common. And a small degree of tricuspid regurge is actually seen in about 70% of adults. So that's a pretty common thing to have. And again, like I said, most patients are going to be asymptomatic.

So it may be an incidental finding on an echo if they were looking for something else. Now, Etiologies, Epstein's anomaly is going to be the most common congenital heart disease that causes this. condition can also be seen in infective endocarditis, Marfan syndrome. There are some iatrogenic causes like from pacemaker leads or even when they're doing an endomyocardial biopsy. This can happen. But just remember really that Epstein's anomaly. That's going to be one of the more common ones. Now clinical manifestations, like I said before, most patients are going to be asymptomatic. And really, I wouldn't waste your time on this. Like most of them, the clinical manifestations, there are of course severe cases where they may have some nonspecific symptoms of dyspnea.

exercise and tolerance but again you know really don't waste your time with clinical manifestations now physical exam again remember your left side of murmur and you can figure out the right so mitral regurge which was mostly regular or mostly rigid meaning a hollow systolic murmur same thing here so this is going to be a hollow systolic murmur just like your mitral regurge so you'll remember the only difference again I keep saying this but remember like all right side of murmurs this is going to increase in intensity with inspiration and it's going to be heard best at the tricuspid area, just lateral to the zyphoid.

And another difference, two, between this and mitral regurge that is, unlike in mitral regurgers, this murmur doesn't generally radiate. So that's another thing that's different. Treatment, again, is going to be surgical, definitive, and severe cases, and then diuretics for any fluid overload. Okay, so those were the murmurs. Let's do five quick questions. I know this was another long one, and then we'll wrap this up.

Okay, so question number one, name all of. the diastolic murmurs. So name all of the diastolic murmurs. All right. So hopefully you remember, Ms. Prarts died. So MSP-R-A-R-T-S died, and that stands for mitral stenosis, pulmonary regurg, aortic regurge, tricuspit stenosis, and then, of course, die, diastolic. So those are all your diastolic murmurs, matril stonosis, pulmonary regurge, erotic regurg, and tricusped stenosis. All right. Second question. Describe the murmur of aortic stenosis. So, just describe the murmur of aortic stenosis. It's going to be a systolic murmur, crescendo de crescendo, and it's going to radiate to the carotids. And of course, remember, that's best heard at the

aortic area, which is the right upper sternal border at the second intercostal space. All right, third question, what is the most common cause of mitral regurge in the U.S.? Most common cause of mitral regurge in the U.S. is going to be mitral valve prolapse. Mitral valve prolapse is going to be the most common cause of mitral regurge in the U.S. Fourth question, describe Quinky's pulses. So Quinky's pulses, remember, quinky is seen in the pinky. It's a capillary pulsation in the fingertips or nail beds seen in aortic regurgitation. Last question, what is the most common cause of mitral stenosis? Most common cause of mitralstinosis is going to be rheumatic heart disease. That's going to be the most common cause of mitrostonosis. All right, so you got

through that one. That is murmurs. Thank you, as always. I say it. single time you'll get so sick of hearing it, but I do really appreciate everything, the comments, the likes. It means so much to me, and it means so much that you guys are, you know, seeing improvements maybe in your exams or this is helping you on your exams. And as always, good luck on your pants, your panery, your EORs, and good luck in PA school. And thank you for listening to the podcast.