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OK, I think we are now that I think so too. Ok, good evening everyone. Can you just let us know if you can hear us please? You can just drop a message in the chat. Oh, so just to check, do we need to record this as well or is it so it should automatically record? Ok, because it's live. Yeah. What? OK. We just wait for someone to apply to let let us know we can. So if someone could just respond in the chat, please just to let us know that you can hear us. Ok, then we will get started or you can react to a Hersh's message. Ok. Ok. Someone can someone in this one? Amazing. OK. Good, good. I'll stop sharing. Mhm. Ok. Hang on. Ok. Can you see that? Yes, perfect. OK. So welcome everyone to our teaching session on murmurs just to introduce ourselves. So I'm Emma, I'm 1/5 year medical student and my name is Harish, also 1/5 year medical student. We are both at UCL and yeah, like I said, we're gonna be talking about murmurs today. Ok. So just a quick introduction to teaching things. So we do weekly tutorials that's accessible to everyone. Um It's made by medical students for medical students and we are everything that we do is reviewed by doctors just to make sure that what we say is accurate. Um and just a quick reminder to follow us on medal if you haven't already. So today what we're going to be covering is the different types of murmurs that there are how they present and be associated symptoms, how we can investigate murmurs and how we can treat and manage patients with murmurs. So just as an introduction, what are murmurs, murmurs are basically just blood flow that you can hear and to simplify it specifically to valvular murmurs. There's two main causes which is either stenosis, which means a narrowing of the valve or regurgitation, which is where blood flows in the opposite direction to where it's meant to so backwards through the valve. Um So just to remind you of the four valves, um we have starting on the right side of the heart, blood flowing through the tricuspid valve and then into the pulmonary valve and then from the lungs, going to the left side of the heart through the mitral valve and then the aortic valve out to the rest of the body. Now, all of the valves can be affected by either stenosis or regurgitation. Um The main valves that are really important to be aware of are the left sided valves. So the mitral valve and the aortic valve and we'll go into a bit more detail on that throughout the session. So again, a, a sort of cover of um cardiac physiology. Um just thinking about which valves are closed during systole. So when the heart is contracting, we want the mitral valve and the tricuspid valve to be closed, so that blood doesn't go backwards into the wrong side. So we want blood to go during systole, we want to go, we want blood flow to go either to the body or to the lungs. And then therefore, during diastole, we want the aortic and the pulmonary valves to be closed, which means while the heart is relaxing, we want that blood flow that has gone through to the heart or the sorry to the lungs or the rest of the body. We don't want that to then flow backwards into the heart. And so that helps us to understand a bit about which types of murmurs are caused by which pathology. So, if we think about systolic murmurs, so, murmurs that occur during the systolic phase of the cardiac cycle, um it's caused by either stenosis or valves that are meant to be opened during systole, which are the aortic valve and the pulmonary valve or regurgitation of valves that are meant to be closed during systole. So the mitral valve or the tricuspid valve, the same works. Therefore, for diastolic murmurs. So, diastolic murmurs are caused by either stenosis. So narrowing of the valves during diastole, which are the mitral and tricuspid valves or regurgitation of valves that are meant to be closed during diastole, which are the aortic and the pulmonary valve. Amazing. So, before we kind of get into the murmurs and how they present, I'd just like to talk a little bit about how you examine murmurs in your cardiovascular exam. So, a lot of you, I'm sure have done many cardiovascular exams or you're quite new to it. And this is something which takes a lot of practice. And the biggest advice we can say is just to listen to as many hearts as possible, whether that's in Ed, whether that's on the ward or GP wherever it is, the only way you get confident with understanding is just by repetition. OK. So the first thing we wanna talk about is so how, where and when are you gonna listen, assess murmurs and that is when you're listening to your heart sounds. So you take your stethoscope and you're putting it on the chest around the heart to listen. So, first of all, where do you listen in the first place if we could get the next slide? Mhm Amazing. So we've got four regions. And um just to let make sure you guys are aware, this is primarily for adults, for Children and especially neonatal babies and things, things are slightly different cos obviously, they're a lot smaller. Uh this is particularly focused towards adults. We have four different areas. So we have the aortic area which is in your right side of your chest by the sternal border. And it's in the second intercostal space, the pulmonary area which is on the left sternal border, second intercostal space, tricusp which is slightly further down fourth intercostal space again on that left sternal border and then the mitral area, which is your fifth intercostal space in the kind of midclavicular line on your left side. Ok. So those four areas are really the most common areas are going to hear murmurs and you may also feel a palpable thrill. So a thrill is basically a a vibration which has been caused by the murmur and you can feel it when you just feel across the chest like that with the ulnar border of your hand. And just so you guys are aware in reality, you know, these areas on exactly defined in those exact places and sometimes your aortic ones may drift across. But as for the vast majority, those are the best areas to listen to. Ok. So yeah, a place to meet. That's a good way. So a place to meet. It's a good little uh mic you can use if you struggle to remember things. Um So we've got a question. So what is the difference between a heave and a thrill? So a throw, like we said is the kind of palpable murmur. So it's a vibration that has been caused by that murmur and you can feel it with the ulnar board of your hand. A heave on the other hand, is a sign of ventricular hypertrophy. And so this is might have been caused by the murmur or it might just be like heart failure or something. And, and that's when your, your heart is beating so hard because of all that extra muscle that your hand is basically going up like this. Um Yeah, and that's caused by hypertrophy. Ok. So the next thing with murmurs is as Emma uh mentioned earlier, there's, we have systolic murmurs and we have diastolic murmurs. And when you're examining, you, you have to be able to kind of understand which is your systolic murmurs, which your diastolic murmurs. And we do this by listening to the heart sounds. So our normal heart sounds, we have S one and S two. So S one is the closure of your A B valves. So that's the end of diastole start of systole, whereas your S two is your closure of the um aortic and pulmonary valves. So S one mitral and tricuspid are closing. S two aortic and pulmonary are closing. And then sometimes you'll hear these things of S3 and S four and these are kind of extra noises um during diastole caused by either rapid filling or turbulent blood flow. Sometimes these aren't always pathological and it can be quite just normal and sometimes these are caused because of murmurs which we'll get on to slightly later. So S one S two is that kind of lob dub that you're, um, I'm sure all of you are familiar with. And when you're examining, to identify the difference, you should palpate the carotid artery. And when you're listening, it's good practice to palpate the carotid artery whilst you're listening. So you can match them up as to, is this a systolic one or a diastolic murmur? And always remember if you're gonna palpate the carotid artery, please always listen in case you want, you want to identify if there's any Bruits present, which could uh signify carotid stenosis because the last thing you want to do is dislodge a stenosis and then risk a stroke or some kind of er cerebrovascular event. Ok. Um I hope that all makes sense like I mentioned in the chat, please drop us any questions you have at any point. And, ok, so now we're gonna talk about how do you exacerbate murmurs and make them a bit more better for you easier for you to listen to. So our first one is an acronym called Ryle. Some of you may have come across this before and what this um is to do with. So Ryle. So first R and I so right sided murmurs, which is exacerbated by inspiration. Now for a long time, I really got confused by this thinking that right sided meant the right sided like, you know, your aortic region or your pulmonary region because it's the right side of the chest. But no, in in reality, what it means is right side of the heart so that it can, it's commonly confused. So just make sure you remember that right sided murmurs. So it's the right side of the heart. So that's your Pulmonary and Tricuspid. And these are exacerbated by inspiration. And this is because you have increased venous blood flow to the right side of the heart by the vena cava. And you have kind of some pooling in the pulmonary vessels and reduced blood flow to the left side and the same goes for the opposite side. So le so left sided murmurs. So your aortic and mitral, these are exacerbated by um expiration. So that is completely typed wrong on the sides, but it's exacerbated by ex um expiration and this is because of increased venous blood flow to the left side of the heart. Ok. And now we have some further maneuvers that we can do. So the first one we think about is turning the patient to their left side. So you'll have the, you'll have a stethoscope in the mitral area. So, like we said, midclavicular line, fifth intercostal space, and you ask the patient to roll over to their left side. And what this does is it brings a mitral valve closer to the chest wall. So you can hear it a bit louder. And similarly, you can also listen up towards the axilla so kind of towards your armpit region. And this is because mitral regurgitation radiates to the axilla. Um and then another one is listening to the carotids. And this is because aortic stenosis, it radiates to the carotids. And the reason you kind of, if you think about that one is because your aorta, one of the first vessels, it kind of leans towards your carotid artery, right. So it radiates to the carotids and then the last one is sitting the patient forward. So asking them to lean forward and again, it's bringing that aortic valve closer to the chest wall and that exacerbates aortic regurgitation. And yeah, so the one more thing is kind of grading murmurs. Um This is something that you kind of get taught and it's takes a bit of like, you know, you just have to kind of go over it a lot of times to remember things, but it's a way to see how severe this murmur is. So one being, you know, it's very slight, you might not even notice it and then it all the way leading to six being, it's extremely loud and you can probably hear it without touching the chest wall. Um like you would just see them and you can probably hear their heart beating and you can hear that murmur. But like I said, it's very, very rare. Ok. Ok. So we'll start with the systolic murmurs. Um So of the systolic murmurs, aortic stenosis is the most common type of murmur. Um and so, aortic stenosis just means the narrowing of the aortic valve. Um there are different causes for aortic stenosis. So, the most common by far is just degenerative disease. So you see it in older patients, um it can be age related. Often the patients have um multiple comorbidities like hypertension or coronary artery disease. Um One of the other not necessarily causes but predisposing factors of aortic stenosis is a bicuspid aortic valve which you can see on the right hand side, um where the aortic valve which is normally meant to have three leaflets, um just only has two because of the patient's anatomy and because their blood flow will be not normal. It might, it, it predisposes those patients to having abnormal calcification of the aortic valve. We also have some less common causes. Um So, particularly in Europe and in the western world, rheumatic fever is quite rare. Um However, in less developed countries, it is very much, still a disease that exists and very much causes aortic stenosis. Um but often also has a sort of a mix of aortic stenosis and aortic regurgitation. Um then radiation therapy, especially in the chest. So, previous cancer can predispose patients to aortic stenosis and a condition called infective endocarditis, which we'll go into a bit more detail in later. So, what is aortic stenosis? It's a narrowing of the aortic orifice or the, the hole that the blood needs to go through. Um And as I mentioned, it's caused by calcification and atherosclerosis. So, the same process, this or similar disease process that happens in the veins and arteries as we age and that leads to the valve leaflets being stiff and not very mobile. Um And the fibrosis causing leaflet thickening, which ultimately leads to left ventricular outflow tract obstruction. So, blood struggles to leave the left ventricle. Um And so you've got this high pressure gradient between the left ventricle, which is trying to push all of the blood out and the aorta which is not receiving as much blood as it wants to receive. And so you end up getting concentric hypertrophy or thickening of the left ventricular wall. Um and you also end up getting diastolic dysfunction. So where the heart struggles to relax properly and that together leads to heart failure. And so you've got, when you in sort of late stage disease, heart failure and ischemia go together um simply because you've got a thickened heart wall, um which needs more oxygen because you've got more muscle to supply. But you, at the same time, you've also got less blood leaving through the aorta and less blood going into the coronary arteries. And so overall, you've got a heart muscle that is not being sufficient, sufficiently oxygenated. So how aortic stenosis presents is with a triad. So we'll start with dyspnea or short shortness of breath. It's often the first symptom that patients uh, present with, um, and it's often first noticed during exercise. So when people are doing strenuous exercise, um, but there is a scale or what we call the nyha class, um, of dyspnea, which is where, um, you can see there's a sort of range of whether symptoms present with any physical activity or whether they present at rest. Um And the, the shortness of breath is caused by the diastolic dysfunction. So that's um what I mentioned before where the heart can't create enough cardiac output to supply the rest of the body. Uh part of our triad is also angina. Um So that's again where I mentioned before in the pathophysiology, where you've got um your, your heart requiring more oxygen than it did before and often with additional coronary artery disease and this reduced perfusion of the coronary arteries. Um You then end up getting symptoms of angina. So chest pain on exertion and syncope or fainting, um you might also get presyncope, so sort of feeling lightheaded. Um And again, it's often first noticed on exercise um which occurs because of hypotension, so low BP, um and that low blood, the low BP is caused by exercise, induced vasodilation. So your blood vessels um becoming wide and therefore reducing BP. Um And as I mentioned before, this inability to increase cardiac output enough, often these patients will also have arrhythmias at the same time. Um But not necessarily. So, as I mentioned, severe aortic stenosis will also present with heart failure, which has um your typical symptoms of um paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion and pulmonary edema or lower limb edema. On examination. You also find a what we call a harsh ejection systolic murmur. Um So as you can see in the picture, um looking at not figure number a, you've got two nice separate heart sounds um with nothing in between. Whereas in aortic stenosis, there's kind of a blurring of the two heart sounds in the, in the systolic section. Um And it kind of they also call it a crescendo, decrescendo. So as you can see in the picture, it gets louder and then it gets quieter throughout the systole and you have nothing during diastole. So it's silent during diastole. Um And as mentioned before the murmur, um can radiate to the carotid. So you can hear this murmur while you're listening to the carotid pulse. It also has an association called Galardin phenomenon, which is where um the murmur sounds almost musical. It's got high pitches um rather than just the normal heart sounds that we hear. Um And as mentioned with the maneuvers that we can use to exacerbate. Um aortic stenosis is loudest when you're sitting forward and during exploration and I'll try and play this audio clip. Can you hear it? Yeah, we can have that. Yeah. So just for clarification, this is a normal heart sound. You've got two very separate heartbeats. Yeah. Whereas this is what aortic stenosis sounds like. So, can you hear it's difficult to tell the difference between the first and the second heart sound? And there's um you can hear a murmur in between the systolic part, but during the diastolic part, there's silence. I hope that makes sense. This is mainly for reference if you want to come back for this as well. So other signs that you might hear during aortic stenosis or other signs that you might notice um pick up on examination are what we call pulses, pelvis Tardis, which means a slow rising and low volume carotid pulse on palpation. Um but sometimes, especially in elderly patients, you might not be able to feel this um because their vessels might be stiff anyways. Um And in terms of the second heart sound, often it can be soft or absent, which is um it kind of coincides with the blurring of the 1st and 2nd heart sound. Um And what we call reverse splitting. So where normally the aortic valve is meant to close ever so slightly before the pulmonary valve. Um But in aortic stenosis, what happens is the pulmonary valve ends up closing slightly before the aortic valve because there's this blood that the left ventricle is trying to squeeze out. And other features that might come up in exams, usually more in sort of SBA settings. Um uh So you might have a narrow pulse pressure. So, um in, um, in looking at the BP, I'm pretty sure it's looking at BP. You've got, um, your systolic and your diastolic, the figures will be closer than in a normal patient. Um, a heaving apex beat or a systolic thrill which coincides with the, um, left ventricular hypertrophy and of palpable thrill and as I mentioned before, signs of heart failure. So, does anyone want to write in the chart any initial investigations that we might consider in patients where we're suspecting aortic stenosis? No, if you can check the chat for me because I can't see it. Yeah, I'll keep an eye on it. Thank you. So, these are just initial investigations if you're, let's say you're an A&E and you don't have too many resources, which, which investigations would we consider doing? Yeah. So we've got a couple of you were saying ECG bloods and echo fantastic. That's exactly what I would do. Um So an eg we're getting more specialists there. So an ECG is a fantastic starting point for any patients that we're considering a cardiac pathology in. Um and that's first of all to rule out any arrhythmias that patients might have. Um but it might show us other signs as well. So in aortic stenosis, um if there is left ventricular hypertrophy or left ventricular strain, we might be able to see that on ECG, which you can see with the sort of really dramatic. Um QR S complex is here um we might consider a chest X ray. If a patient is presenting on aortic stenosis, you might not be able to see very much. Potentially, if they have pulmonary edema, you might be able to see that or heart failure, you might be able to see those signs. Um And an echo. So often we start with what's called a transthoracic echo. So just looking through the chest, um and there are different measure measurements that will be taken. Um These are just some words that I wanted to introduce you to because they do come up in sbs occasionally. Um so something called transvalvular velocity, which is the speed at which the blood is flowing through the valve, um mean and peak pressure gradient. So what I mentioned before about this pressure gradient between the left ventricle and the aorta, um they might measure the difference between those. Um and that can tell us a bit about the severity of the aortic stenosis. Um They also might measure the aortic valve area. So the effectively the size of the aortic valve. Um and because we know in aortic stenosis, if there's a narrowing of the valve, the aortic valve area would also be reduced in aortic stenosis. And then we might also measure things just to see the degree of um problems in the rest of the heart. So, left ventricular ejection fraction, which shows us how much blood the heart, the the left ventricle is able to pump out into the aorta and we might look at the left ventricular wall thickness as well to see if there's any hypertrophy. And then there are some more specialist tests that we might do. So. Something in aortic stenosis that is often commonly done is called exercise stress testing. Um, and as most of the symptoms in aortic stenosis begin to present with um symptoms on exercise. It's a really good way of telling whether patients who are normally asymptomatic because they might not be exercising much in their daily lives, whether they actually are symptomatic. Um We also do other things. So, Dobutamine stress echo, which kind of mimics the, the dobutamine mimics exercising. So it puts your heart under stress and then we can do an echo while, while we're doing that. And that can again tell uh maybe more um it, it can tell us a little bit more nuanced differences in aortic stenosis. We then also do blood tests. So one of the common blood tests we'll do in aortic stenosis is BNP or NT pro BNP, which looks at the degree of heart failure, um and can also help innate symptomatic patients to tell whether they need to be um they need to have treatment or not. And finally, this is much more specialist, might not be done on every patient, but a cardiac MRI might be done in more specialist centers um to look at how much fibrosis there is in the heart and then there are some investigations that have to be done before, um, before patients are treated. Um, so they'll, the patients will often have a coronary angiogram to see if there's any coronary disease as well. Um As I mentioned before, often these patients have multiple comorbidities. Um We next also do something called a transesophageal echo. So instead of looking at the um part through the chest wall, instead this echo is done through the esophagus and it gets a more detailed view of the heart. But of course, we don't want to do this in patients who don't need it because it is more invasive. Um and then something called a multi slice CT. Um So the CT, the specialist CT scan um that might be done in patients. So we have our first SBA um I'm going to read it out and then I'd like you to just write what you think the right answer is in the chat, please. Um So we have a 59 year old man who presents to the outpatient clinic with symptoms of angina exertional dyspnea and fatigue. Additionally, he has experienced several episodes of syncope in the past month. He has a background of type two diabetes, mellitis and hypertension on examination. He has a grade three ejection systolic murmur with radiation to the carotids. What is the most appropriate definitive management for this patient based on the likely diagnosis? Yeah. So this should come up on a poll in on your screen. So please answer on the poll and we'll go through it on this in a moment. Ok, let's give it about 30 more seconds. Ok. So you've had some varied responses. 50 50% of you have gone for a surgical replacement with mechanical valve. Uh, 12% of you have gone for both balloon, valvuloplasty and ta and then the rest of you have gone for bioprosthetic valve. Ok. So echocardiogram is, is not popular. No, not at all. Ok. I'm I'm glad to hear that. That sounds like most of you have got the right answer. Um So the most appropriate answer is c using a mechanical valve and I'll go on to explain why. So we have quite limited treatment options for aortic stenosis. Unfortunately, um looking at the definitive management, which is what the question asks. We have two main options, either surgical valve replacement or transcatheter valve replacement. And the only difference is surgical valve replacement is with a open heart surgery and transcatheter valve replacement is using a catheter that goes through the femoral artery and into the heart. Um I'll talk briefly about the differences. Um So surgical aortic valve replacement is effectively the gold or was the gold standard for a very long time and is considered particularly appropriate in younger patients, transcatheter aortic valve replacement or TV. Um has only quite recently become an option for patients and currently is only licensed in patients above 75 occasionally 70 years old. Um And that's just because we don't know how long these valves can actually stay in patients. Um I'll also quickly mention so we, the question talked about bioprosthetic and mechanical valves. So on the left side of the screen, you can see a mechanical valve, um it's just a effectively a metal valve. Um And that is favored in patients who are younger simply because we know that it lasts the longest. The problem is, as it says on the screen, patients with mechanical valves need lifelong anticoagulation specifically with Warfarin. Um And that's because the valves have an increased risk of clotting. And Warfarin is the only medication that can get the blood thin enough to prevent clots forming. We then in the middle of the screen have the m prosthetic valve, which is, there are different types but usually made from either pig or cow um valves. Um And we know that they can last quite a few years, but especially in patients who are younger. So like a 59 year old patient from the question, um it probably isn't going to last until the end of his life. And so he would, if we were to implant a bioprosthetic valve, he would have to have a second surgery at some point. And ideally, we'd like to prevent that from happening. And finally, on the right hand side of the screen, you can see a tay. So this is um a catheter that's been inserted and the valve is then effectively pushes the native valve out of the way and puts a new valve in place. We've got a question. Um Just about what age do we mean by young patients? That's a good question. So typically aortic stenosis, you're right. It affects all the patients. Um What we talk about with young patients with aortic stenosis, I mean, some patients, especially if they've got rheumatic fever and infective endocarditis can be as young as their twenties or thirties and that of course, would be considered young. Um but even patients in their sixties and early seventies are considered young because most patients who have aortic stenosis are, you know, getting on into their later seventies, eighties and nineties. Um So that's kind of the cut off. There's no official cut off, but approximately early seventies is where we would consider the cut off for young and old patients. Another question about why not option A and I think we're getting on to that in a minute. What was option? A? We'll, we'll get onto that in a bit um in terms of indications for the definitive management, um patients as soon as they're symptomatic should be treated. And I've got a graph in the top which shows you as soon as uh so this shows you the kind of um progression through the disease. So patients who have aortic stenosis as long as they're asymptomatic, you know, have a very good survival. And we know that as soon as they become symptomatic, the life expectancy is between two and five years. Um, depending on which symptom is the predominant symptom. And so, if we leave patients who are, as who are symptomatic untreated, we know that their survival is very limited and that's why symptoms, the onset of symptoms is really important. That's why we have those investigations to try and exacerbate the symptoms to see whether they do need treatment or not. Um, we also know that symptomatic patients have a really high risk of sudden cardiac death which is quite unpredictable. Um However, we also know that if they have really severe comorbidities and are really, really symptomatic, possibly from other pathology, giving them something like open heart surgery might not be the best option for them. We also know that severe aortic stenosis. So, um as measured on the te, which you know, the, the um different values that I mentioned before, if we can measure that they have severe aortic stenosis, that's another indication for management. And we have other indications such as um reduced left ventricular ejection fraction or if they happen to be undergoing other cardiac surgery, you might be able to sort of fit in an additional aortic valve replacement as well. We then have palliative management and that's for patients who are too unwell to undergo either surgical aortic valve replacement, which is the gold standard or to TV, which is currently indicated for the older population. So, if they're so unwell, but are symptomatic with aortic stenosis, we can consider something called percutaneous balloon valvotomy, um which is similar to the TV, in the sense that it's again a a percutaneous or transcatheter approach. Um But all it does is it opens up the native aortic valve. So you're not actually implanting a new valve, you're just opening up the existing valve. And the problem with that is it's not as good, it's not as effective as a surgical valve replacement or at and in our 59 year old who has some symptoms but is otherwise pretty fit and well, we would want to give him the definitive management rather than just a a palliative treatment option. And then we also have some important considerations um for conservative management in either mild or asymptomatic aortic stenosis um or in patients who are so unwell that they can't even undergo the percutaneous balloon ult toy. Um and that includes regular monitoring. So either six monthly or yearly, depending on the situation, um managing the hypertension to reduce further disease progression, um maintaining sinus rhythm to again reduce their symptoms from other things like arrhythmias and treating any heart failure if they have any. Um just to sort of clarify on the SBA. So as we know, our patient is symptomatic, just giving a just giving him echo surveillance isn't enough. We do need to treat him also. It's not a definitive management which is what the question is asking for. Again, the balloon valvotomy is a, um, a palliative management. Exactly. So, it's, it's not what the question is asking. And then the other two, so, using the bioprosthetic valve, given that our patient is only 59 years old, we would prefer to give him a long term measure. And because he only has effectively type two diabetes and hypertension, he's fit and well enough to undergo open heart surgery. And that's why number C is the correct answer. Ok. So we'll quickly talk about mitral regurgitation as well. Given that it's the second most common heart murmur that patients might present with. And there are again, different causes for mitral regurgitation. They're somewhat similar but still different to the causes of aortic stenosis with the most common cause in the western world being infective endocarditis. Um And that's because the mitral valve is the most likely valve to be affected if the valve was previously normal. Um And the reason why infective endocarditis can cause mitral regurgitation is because vegetations which occur in infective endocarditis can prevent the valve from closing properly. Um But also we know that if the valve is abnormal before it's more likely to be affected by infective endocarditis. So we'll talk a bit about what is infective endocarditis. So it's an infection of the inner surface of the heart and usually includes any of the valves or one of the valves. There are certain risk factors that are important to be aware of. So, being older and being male are risk factors. Being an intravenous drug user is a massive risk factor. And that's because you're in injecting potentially bacteria directly into your bloodstream, which can lead straight to the heart. Um And because you're injecting bacteria into the bloodstream, which goes into the venous circulation, it's most likely to cause tricuspid valve problems, specifically tricuspid regurgitation. Um just because that's the first valve that it affects. And similarly, any. So, iatrogenic causes uh include IV lines, hemodialysis and any dental or surgical procedures because it's the same mechanism where we're introducing bacteria into the bloodstream and they can then get effectively stuck on the heart and cause an infection. And then you can ii if patients have any existing structural heart disease. So that includes any of the valvular problems, but also things like congenital heart disease or if they have an existing prosthesis. So, if they've had previous heart surgery in the past, this can predispose patients to infective endocarditis, some important um causative organisms to be aware of. This is a very common SBA question in exams is so the the most common overall is Staphylococcus aureus. Um And that's because it's associated with any kind of healthcare infective endocarditis as well as intravenous drug users. Um And that's because we have staphylococcus aureus commonly on the skin and so you're introducing it into the bloodstream, it can cause pathology. Um We also have something called viridans group streptococcus and that can cause most commonly community acquired infective endocarditis. So, in your sort of 80 year old patient who's unexpectedly presenting with infective endocarditis, they're most likely to have vine group streptococcus and then something that's very specific. But these are key words for exams. Um the the bacteria, streptococci bovis is very specifically associated with ulcerative colon cancer. So, if a patient is noted to have infective endocarditis that's caused by streptococcus bovis, they need to be investigated for bowel cancer. And then finally, very specifically, we've got the has organisms. Um You don't need to know the names of each individual, but it's an an acronym for um five different types of organisms. So, how does infective endocarditis present? Well, there are kind of different ways it can present, it can pre present very acutely with acute sudden heart failure, it can present subacutely. So, not quite as suddenly, but still within the matter of days or weeks. And then you can have a chronic presentation over months. Annoyingly. Infective endocarditis is very nonspecific and has all of the very nonspecific signs and symptoms, fever, weight loss, uh myalgia. But now my question goes to you, does anyone know any of the specific signs that are specific to infective endocarditis that we might find on examination if you'd like to write them in the, in the chat? And these might include signs that you find elsewhere on the body? Not necessarily just on a, on auscultation of the heart. Any ideas, guys, just give me a couple of seconds. Mhm. I think people are feeling a bit shy today. No, it's ok. Thank you. Should, should we move on if no one? Yeah, I think so. Yeah. Ok. So we have some very specific signs. They're quite uncommon but if you find them, they can be almost diagnostic of infective endocarditis and these include splinter hemorrhages. So these are sort of lines, um red lines in the nails. Um We also have jane ray lesions and Osler's nodes which are um so Osler's nodes are painful lesions. Jane ray lesions are not painful lesions. It's sort of red little bumps on the hands and Roth spots, which are again, these um small hemorrhages in the back of the eyes. So, in, in the retina, um infective endocarditis might present with right sided heart failure, particularly in tricuspid regurgitation and you might have all of the associated signs and symptoms. So, peripheral edema pulsatile, hepatomegaly and raised JVP, but it might present with left ventricular failure if infective endocarditis is presenting with mitral regurgitation, and then you would get pulmonary edema dyspnea, shortness of breath and a cough with a pink, a pink or frothy sputum. And then you've got some complications that can in fact be the initial presentation of infective endocarditis, which includes either pulmonary septic emboli. So, where a little embolism forms in the lungs. And that's particularly associated with right sided. So, tricuspid um infective endocarditis or you might get an embolic stroke. Um if an embolism dislodges and goes to the brain and that's particularly in left sided disease. So similar, uh no, not similar. So some investigations that we would do in infective endocarditis is blood cultures and they are diagnostic. So if, if a bacterium is found to be in the blood, um that's quite, it's diagnostic of infective endocarditis. But we would also then do um an echo either att or then moving on to a to e um if we're suspecting, you know, if we can hear a murmur, if we're suspecting valve um pathology in terms of managing infective endocarditis, antibiotics are the mainstay treatment. Um And that depends on the likely organism. That's why it's so important to know what is most common, what's most likely in which situation because that will guide our empirical antibiotic treatment before our blood cultures come back. Um If there is a source of infection, things like lines or catheters, we would remove that. And if there's any signs of heart failure or valve dysfunction, we'll go to valve surgery and um depending on which valve is affected in what way, um that will determine which surgery is most appropriate. So, moving on to other causes of mitral regurgitation, um Coronary artery disease or myocardial infarction can cause mitral regurgitation. Um And that's because the papillary muscles which um hold the mitral valve leaflets in place can be affected or can rupture and that can then cause mitral regurgitation. And there are some other rarer c uh causes of mitral regurgitation that are less relevant. So, how does it present? Well, most patients are actually asymptomatic and often patients won't need treatment if they are asymptomatic. But there are symptoms that can be caused by either left ventricular heart failure or arrhythmias that they might get, particularly if um their left atrium dilates, they're much more likely to um develop atrial fibrillation and pulmonary hypertension. So, high BP in the lungs, specifically, um, mitral regurgitation also presents with a systolic murmur, but it's a pan systolic murmur. It's often in, um, sort of in SBA S. It's noted as blowing or whistling. Um, it's best heard at the apex of the heart. And as Harish mentioned, it radiates to the axilla. You might have a quiet S one and in severe mitral regurgitation, you might have a split S two. Um, so I will try and play the audio. No. Right. Ok. Ok. So you can possibly hear that S one is slightly quieter. Um, but the main thing is it's not as harsh in, as the aortic stenosis murmur, it's much softer and it goes throughout Sicily, we then have a silent diastole, but throughout the whole of Sicily, you can hear this soft m so investigations, these ones are similar to the aortic stenosis investigations and that includes the ecg that we mentioned where you might have a broad P wave, um also known as P metrial, which is where the atria enlarge they dilate. Um and that's because the blood is flowing backwards into the atria. And so they just dilate to accompany more blood or to not accompany to um because there is more blood they need to dilate. Um and on an E CG that would present with a broad P wave um on a chest X ray, you might see an enlarged heart. So, cardiomegaly again, due to this atrial enlargement and um doing an echo, the TTE would be our initial investigation, the te would be our gold standard. So that's the diagnostic investigation to manage. Again, there's not particularly much we can do in mitral regurgitation in patients who present acutely, we can give them different medications to stabilize them, which might include nitrates, um diuretics, positive inotropes to increase their BP and something called an intra arterial balloon pump, which again increases cardiac output in patients presenting with heart failure, you would treat them as you would treat any heart failure. So, ace inhibitors, beta blockers, spironolactone, and then we've got our surgery which again is the definitive management and in mitral regurgitation, it's not quite as closely linked with the symptomatic or asymptomatic disease. Um But if there's an acute or if there's severe disease, we would want to treat that. Um the difference in mitral regurgitation or mitral disease in, in general is the mitral valve can actually be repaired, especially depending on the cause. Um we can repair the mitral valve without needing to replace it entirely, which is not really possible on the aortic valve. I also briefly mention congenital heart disease just because there are quite a lot of congenital heart disease has associated murmurs. Uh You don't need to know this in too much detail, but it's particularly useful for SBA S in exams. Um So starting with tetralogy of follow, um we have four features. Hence, it's a tetralogy, we have a ventricular septal defect. So, uh but what's important to notice is the ventricular septal defect into Trelegy fallow doesn't cause a murmur. We have right ventricular hypertrophy, which again doesn't cause a murmur, um an overriding aorta. So an aorta that kind of sits in between the right and the left ventricle. And again, that doesn't cause a murmur, but we have right ventricular outflow tract obstruction and that effectively acts as pulmonary stenosis in itself. Often patients also have a secondary associated pulmonary stenosis and going back to what we mentioned right at the beginning, if there's a stenosis of valves that are meant to be opened during systole, which includes the pulmonary valve that will then lead to a systolic murmur. And so tetralogy, a fellow um often has a an ejection systolic murmur. Um something for exams to to note is t challenge of fall will usually in exams at least present with what they call tet spells. So these are cyanotic spells, um, that are usually worse when or usually occur while the, um, child is feeding or while they're distressed while they're crying. Um, so it's important challenge of fallow always presents at least in exams, always presents in a cyanotic way. So you'll, um, have a effectively what's called a blue baby. The second type of congenital heart disease is con coarctation of the aorta. And that's effectively just a narrowing of the aorta. So you can see that in the picture up here and you can think of it similar to aortic stenosis. But instead of um the in terms of the murmur, it's aortic stenosis with a slight delay because the blood has to move through the aortic valve through the first bit of the aorta and then to the part with the coarctation. And that's why it presents with a mid systolic murmur, coaptation of the aorta. Also notably on exams presents with or in fact, in reality as well, presents with reduced or difficult to feel femoral pulses and what's called rib notching on chest X ray, which is where the ribs um kind of don't follow a nice smooth line but instead have slight indents in them. Then looking at atrial septal defect, we have increased blood that flows through the pulmonary valve. So because the blood is moving from the left atrium into the right atrium into the right ventricle and then through the pulmonary valve, we've got more blood that needs to flow through this pulmonary valve. And because there's increased blood flow, it effectively works in the same way as pulmonary stenosis, which is why again, we have an ejection systolic murmur. And in ventricular septal defect, we have blood flowing from the left ventricle into the right ventricle and that happens throughout systole, which is why we've got a pan systolic murmur, systolic murmur throughout systole. Um, what's interesting to note in ventricular septal defect is a louder murmur is associated with a smaller defect. And that's because we have a smaller hole where lots of blood needs to get through and that causes a louder sound. Ok. So moving on to our SBA we've got a three week old child brought into the emergency department. His mother reports that he was initially well, but over the last few days, she's noticed that he's become significantly more breathless and is particularly breathless, pale and sweaty when feeding, he was born at time with no complications on examination. His growth chart shows poor growth and he is tachypneic and using his accessory muscles to breathe on auscultation. He has a pan systolic murmur at his lower left sternal edge and a loud P two. Which of the following is the likely cause of this presentation. Again, there should be a poll for you to answer. Yeah, I just starting to get some responses in now. Perfect. Ok. So just wait for 30 more seconds just to get a couple more responses. Ok. So we've got a couple of people who have gone for to Trelegy of fallot. Um, 56%. 0, no. Well, it's 5050 50% of you have gone for to Treg of Fall and the other 50 have gone for BSD V ST. Ok. So the correct answer is A VSD and I'll explain briefly why. So, tetralogy of Fall, um presents with an ejection systolic murmur rather than a pan systolic murmur. And as I mentioned before, it has the cyanotic or text spells. Um And this, this child is presenting um with instead with shortness of breath and being pale and sweaty but no cyanosis, no blue baby. And so it's not a challenge. Your fellow um coarctation of the AORTA has a mid systolic murmur and as I said, they would mention reduced femoral pulses. Um mitral regurgitation is a pan systolic murmur as well, but it doesn't have a loud P two ventricular septal defect is correct because it's a pansystolic murmur um in the tricuspid area which it mentions here, lower left edge has allowed P two and heart failure symptoms. So that's the breathlessness, the pallor sweatiness and then finally, an atrial septal defect again has an ejection systolic murmur rather than a pan systolic murmur. Ok. Amazing. So we're gonna move on and talk about diastolic murmurs in a second. But just before we get started, I'm gonna send a feedback form. Um So if you could please fill this in for Emma and then I will send it again and if you could refill it for myself. Ok, so I'll send that and please do fill it in at some point. Um And ok, so we're gonna talk about diastolic murmurs and like we mentioned at the start, uh the diastolic murmurs are murmurs that happen during diastole if we can get the next slide, please. Mhm. Ok. So first of all, what is actually happening during diastole? Well, so diastole starts with the closure of the aortic and pulmonary valves, which is so the end of systole and a big part of this and throughout all of um diastole is ventricular diastole. So the ventricles are quite relaxed and the whole point of diastole is to fill these ventricles with blood and start increasing the pressure to then um go into Sicily and put uh send that throughout the body. So it starts off with the majority being atrial diastole and this is filling of the atria from with blood, from the um IVC or S VC or for the right side of the heart and the left side of the heart, the pulmonary vein. And as this blood is now filling, um the mitral valves and trichosis valves will then open blood will now start flowing into the ventricles. And then we have atrial cysto where we have contraction of the atria to push that blood into the ventricles and this will start to increase the pressure in those ventricles. Um to, you know, get that pressure building, especially on the left side of the heart to then have enough pressure to uh send it around the heart. And it ends with closure of the mitral and tricuspid valves. Ok. So where do we think we can get murmurs in diastole? So there's a, there are two points. So if you like uh we have on the slide, so it's these two points of closure of the aortic or pulmonary valves and opening of the mitral or tricuspid valves. So, if it's closure, like we said, at the start, if it's something to do with closure, it's gonna cause regurgitation and if it's to do with opening, it's gonna cause stenosis. So, first of all, let's talk about the diastolic murmurs, like we said. So, closure leading to aortic and pulmonary regurgitation and opening causing mitral or tricuspid stenosis. Ok. So, first, let's talk about aortic regurgitation. So this is a backflow of blood from the aorta into the left ventricle and this is because of some kind of leaky aortic valve and this is caused by either disease to the aortic valve or something to do with the aortic root itself. So, it's some kind of dilation. And so what are the different causes? Um So let's first look at the normal aortic valve on the left and in aortic regurgitation, you can see that these valves aren't fully closed, which is gonna let leak blood pass through. And on the right side, we can see about the kind of aortic valve and specifically looking at the aortic root. As you can see, this is quite normal and the valve stays closed. However, on the very right side, you can see that the dilation of the aortic root is pulling those valve leaflets apart which makes it more leaky. Ok. So we've got a table here and this is kind of going through some of the causes of um aortic regurgitation in both the chronic and acute presentation. So let's first take acutely. So, like Emma mentioned earlier, infective endocarditis. And though this isn't particularly commonly found in the aortic valve, it is possible and it is something to be aware of and this is affecting the valve itself and then we have aortic dissection, affecting the aortic root. Now, aortic dissection is a um you know, it is a major emergency and we'll get on, get onto that slightly later and this is something you have to notice and get treatment for very quickly. Otherwise, it can cause very serious um harm and and can cause death to the patient. And now, chronically, if we look at first the aortic valve, um rheumatic fever, and this is a very common cause and it commonly causes a different murmur which we go on to slightly later, but it can cause aortic valve regurgitation. And then calcific valve disease, connective tissue diseases such as rheumatoid arthritis and and SL E and bypass by aortic valve, bicuspid aortic valve, which I'm gonna get onto in the next slide also can affect the aortic root. Same with something like ankylosing, spondylitis, hypertension, uh tertiary syphilis. And also you kind of like collagen and disorders like marfans and DAOs. So let's talk about bicuspid aortic valve. So your aortic valve when you're born usually has three leaf, three leaflets in some patients, two of these leaflets can fuse together during future development. And this is often inherited and it results in the valve consisting only of two leaflets and the consequence of this is it causes narrowing or narrowing or stenosis or it can also cause leaking or enlargement of the aorta. And over time, this can lead to left ventricular hypertrophy and heart failure um because of overworking and can cause downstream aortic aneurysms. And a big risk factor is the increased risk of aortic dissection. And though this is often asymptomatic, you can get some of those like heart failure signs like um Evan mentioned earlier. So kind of chest pain, fatigue, shortness of breath, pallor and sometimes arrhythmias as well. And it's important to monitor dental hygiene here because of that risk of infective endocarditis. Ok. So, looking at the pathophysiology of some of the other causes. So a big factor like we've been mentioning is age and comorbidities, atherosclerosis and calcifications of the valves leads to them not being able to, they're less mobile and therefore they can stay used open but causing regurgitation, connective tissue disease. This can cause fibrosis and thickening of the valves in the bases. So, for example, in Marfans, um we have anti fibrillin one which causes dilation of the aortic root. And as I'm sure many of you are aware of this is a very big risk factor for aortic dissection. And it's something that if a patient, especially a patient comes into ad and they say they have chest pain, this is something you have to have to rule out as soon as possible. And then Alexander Syndrome. So, this is a collagen. Um it's a defect in the collagen synthesis. So this kind of reduces that strength of the aorta um and increases the viability and fragility causing that dilation. S similar with hypertension, increased stress on the valve leaflets leads to dilation of the aortic root and syphilis. The tertiary syphilis causes syphilitic aortitis, which is again, inflammation, weakening of the aortic root causing dilation. So what features may we present with? Um again, it's similar to the kind of like heart failure features. So it it could be things like chest pain, edema, shortness of breath, palpitations, syncope, or presyncope and irregular heartbeats. Um and these are, they can be quite common. So I'm gonna put up a poll now and if you guys could take a go at this. So a 57 year old patient has come into the emergency department with severe ch central chest pain. He describes the pain as a tearing sensation and feels that it radiates to the back. When you take BP measurements from both sides. What are you most likely to see? So if you guys could take a go at this, please, so just give it around 30 seconds. Yeah. Ok. So we have a few responses in which is good. So 75% of you have gone for C to the left side with a BP of 100 and 10/70 the right side with a BP of 80/60 a couple of you have gone for B with a left side of BP of 200/1 20 a right sided BP of 100 and 70/100 and 10. Now, in fact, the right answer here is actually b so this is a very classic presentation of aortic dissection, this tearing chest pain radiating to the back. It's a very, very classic presentation of aortic dissection. And I can understand why some of you may have gone for C because of that 80/60. And you're thinking, oh, if the, you know they're hypotensive, they're kind of in shock. And that's the kind of picture you might be thinking about and you would be right. However, in aortic dissection, what's actually happening is you get this variation between BP of both arms and you usually see greater than 20 mL millimeters of mercury variation. So if you can see MB, that you have 200 100 and 70 it's usually higher BP instead of lower. Um And that's why it's B over C though C does have that variation as well. It's usually seen with higher blood pressures. Ok. I hope that makes sense. And one more question here. So I'm gonna start this next poll. So a 57 year old patient, so similar, same patient. What investigation is diagnostic of this condition? So we've said that it's a aortic dissection. So what do you think is the um diagnostic investigation? The and I apologize for my spelling because some of it is not the greatest on the policy. Ok. So just wait for a few answers. Mhm OK. Amazing. So all of you have gone for a ct of the chest abdomen and pelvis and you all would be correct. So the answer is D and this would be diagnostic af and you'd see a false lumen which is the diagnostic of aortic dissection. And if we just go through the other one, so a chest X ray, this may show a widened mediastinum, but it is not diagnostic and you know that could be because of a number of other things, an abdominal ultrasound. This is something which would be really useful if it's an abdominal or aortic aneurysm. Um but in this case, obviously, we're looking more at the chest, an MRI of the thorax. Yeah, this would not be considered at all when you were to go through this, you know, you're risking safety to the patient and transesophageal echocardiogram. And this is actually second line for patients who might be too unstable to undergo a CT scan. Um but yeah, in this case, first line diagnostic would definitely be ct of the chest abdomen and pelvis. Ok. So what are the features of aortic regurgitation? So this is an early diastolic murmur and this is because you can hear the blood rushing in from the aorta immediately at the start of the diastole and it's increased by this hand grip maneuver. Um which is something I didn't mention earlier, cos it's a bit more niche, but it's something that you can do. So it's basically getting the patient to make a fist almost similar to what you get them to do when you're trying to get blood flowing for venipuncture. And what this is doing is increasing the afterload of the heart, increasing the work of the heart and therefore, it's increasing the inte intensity of that murmur. So it's a bit louder when you go to hear it and, and if possible, could you play the sound? Yeah, not try. No. Yeah. So hope you guys can hear this. Thank you. So if II hope you could hear that day, it was very early as soon as that dub came along, you could hear the murmur and this is um and its characteristic, this high pitched and blowing murmur as well, er, which I hope you guys are able to hear. Um So Emma to answer your question, no, this isn't the machinery one and that will come on to slightly later um afterwards. And what you're thinking of is more of a inherited congenital thing, but we'll get onto that. So a couple of other features you see in aortic regurgitation is first of all, a collapsing pulse, also known as the water hammer or Corrigan pulse. And what you're doing here is you're palpating both the radial and the brachial artery and you're just gonna, as you're palpating both, you're gonna rapidly raise the arm and you're gonna feel the kind of that blood um kind of falling away. You can feel it just like collapsing. And so what's happening is in severe aortic regurgitation because you have so much blood reentering the heart, your arterial tree is actually quite empty. And so when you raise the arm like that, you're kind of feeling that blood draining back into the heart and that's what's causing that kind of collapsing feeling that you might feel. Ok. And so the next one is a wide pulse pressure. And similarly because blood is coming back into the heart, you have a really high systolic pressure, uh which is to maintain perfusion. And because of that regurgitation, the diastolic pressure will get reduced. So you see quite a wide pulse pressure. Ok. And then finally, a couple of these er other signs which are, you know, you have to have quite severe or regurgitation. Um So first is the Quik. So this is pulsation of the nail beds and then demos, which is a kind of rhythmic bopping, bobbing of the head in synchrony with your heartbeat. And again, this is because you can, that strong pulse is causing your head to just like bob along. OK. So how do we investigate aortic regurgitation? So similar to the murmurs that Emma talked about earlier, we're gonna be doing echocardiography. Um And the you're gonna see that kind of blood coming back into the heart and on the right, you can kind of see it slightly but you're not expected to interpret an echocardiogram. So do not worry, especially at the undergraduate level, post graduate level is a bit different, but at our undergraduate level, this is not, I expected for you to understand. OK. And management. So first of all, we're gonna always do you kind of like um I if we're worried about things like heart failure, obviously, you're gonna try and improve any modifiable risk factors. So, you know, smoking cessation, diet and exercise, and then we have our medical management like beta blockers, ace inhibitors, aldosterone antagonists diuretics for acute exacerbations. And always importantly to remember is your vaccinations. So, annual influenza vaccines, one of pneumococcal vaccines monitoring that dental hygiene that we talked about earlier as well. Ok. And then the surgical management. So this is your kind of definitive management of aortic valve of of aortic regurgitation. And it's gonna be aortic valve replacement. And this is indicated in either symptomatic patients with severe aortic regurgitation or asymptomatic patients with severe aortic regurgitation who have that kind of left ventricular systolic dysfunction. And it'll be similar to what we mentioned earlier with kind of like the mechanical valve, bioprosthetic valve. But I'm not gonna regurgitate that now and then our next diastolic murmur. So, mitral stenosis. So what's going on here is obstruction of blood flow across the mitral valve um from the left atrium to the left ventricle. And this leads to increased pressure within the left atrium, pulmonary vasculature and also the right side of the heart. And until proven otherwise, this is almost always caused by rheumatic fever. There are very few other causes which are all very, very rare. So, mitral stenosis, if your patient has mitral stenosis, there is a good chance they've had rheumatic fever. So, what is rheumatic fever? You might ask? So this is an immunological reaction 2 to 4 weeks after a streptococci streptococcus pyogenes infection. And so just a bit about the pathophysiology. So you kind of have this activation of your innate immune system which leads to antigen presentation to your T cells and then the B cells then produce your IgG IgM antibodies and also activation of the CD four plus T cells and you kind of get this cross reactive immune response. Um And we also have so strep Powergen itself, it has a cell will contain an M protein. This is a virulent virulent fracture factor, which is highly antigenic and antibodies against this M protein cross react with myosin and the smooth muscle of arteries. Ok. So I this is all quite complex and it, it can might be a bit difficult to understand, but don't need to worry about it too much. It's just to kind of age your understanding. So this kind of immunological response leads to clinical features of rheumatic fever. And so these include um so you have your razor, rising streptococcal antibodies, positive throat swab or rapid group, a strep antigen test, um erythema marginatus. So this is kind of a rash along your um legs, polyarthritis. So, you know, joint pains, valvulitis. So, specifically mitral stenosis on blood, you might see a raised ES RCR P. Um you'll have pyrexia arthralgia and maybe a prolonged pr interval as well. And we manage this with oral penicillin B um which is uh like phenoxybenzyl methyl penicillin, uh nsaids and also just treating the some of the compli complications. Ok. So mitral stenosis itself, how does it present and what are its features? So you have dyspnea. So, increased left atrial pressure will increase um the pul the pressure within the pulmonary venous system. So you get pulmonary venous hypertension, which might cause you to be quite short of breath. You might get hemoptysis and this is that classic pink frothy sputum that some of you may have heard of. And what's happening here is you get hemorrhage secondary to thin walled and dilated bronchial veins and these might um rupture and you might cause you to cough up this pink frothy sputum. You might get atrial fibrillation. And as you can imagine, if there's increased pressure in that left atrium, it's gonna enlarge and you're gonna get turbulent blood flow and it's gonna kind of throw off your electrical system and your heart and you also get mala flush. So this is kind of causing it's, it's because of CO2 retention and vasodilation of the arterioles in your cheeks. So you see this kind of like flushing on around your cheeks um to known as malar flush. OK. And other features. So this one is a mid to late diastolic murmur and it is best heard in expiration and it's character, this kind of rumbling sound. So Emma, if you could, could you please play the clip first? No? Ok. Ok. Ok. So I think this one's a bit harder to hear. So, um I'll put the II, put the website in the chat earlier and you, I'll put it on again. Um But it's, yeah, so you hear this kind of loud s one and an opening snap and what's happening here is because it's the nose and it's quite narrowed. It's that increased pressure to a point where the valves then just flick open, which is, that's snapping if that makes sense. Um, ok. And you get this low volume pulse because the pressure is just not the same. And sometimes you have very severe mitral stenosis and this is characterized by a longer murmur and the opening snap is almost right next to S two. So it's kind of like almost really difficult to, to differentiate between them. So how do we want to investigate this? Well, we may, we may do a chest X ray to show the kind of left atrial enlargement. So this white dotted line you can see is the enlarged left atrium, whereas the blue one is the kind of hard border itself. And again, we always, we're gonna go back to our echocardiography and we're gonna see a very tight mitral valve with a smaller cross sectional area, but this is always gonna be done by our specialist. How do we treat it? Well, we're always gonna treat our symptoms first. So, atrial fibrillation and most of you, I'm sure will be aware that for atrial fibrillation, one of the biggest things we're gonna give is dua to, you know, reduce our stroke risk and clot risk. However, for mitral stenosis, we typically prefer to give warfarin um because it's proven to be better in asymptomatic patients, you're gonna monitor them with regular echocardiograms and with symptomatic patients, we're gonna consider things like percutaneous mitral balloon, valvotomy. However, like we mentioned before with the aortic um balloon valvotomy, this is more of a temporary measure just to open the m the valve up and then we have our mitral surgery. So first thing is a commissurotomy and what's this is, is kind of sniffing some of these leaflets and opening them up so that um blood can flow. And then of course, definitively a valve replacement. Um And again, if we're using a mechanical valve here, we wanna, the patient will have to be on warfarin for the rest of their life. And in this case, their target inr will be about three or 3.5. And I can't remember which one. Ok. So now we're gonna talk about some of the other murmurs. Ok. So, first of all, we have a Graham steel murmur. So this is a pulmonary regurgitation. It's early diastolic, um high pitched and blowing in character. And then we have an Austin bled murmur. So, an Austin Flint murmur is a mid to late diastolic and this is significant of severe aortic regurgitation. So this one actually can get quite confused um with mitral stenosis because they sound similar. But in this case, it's actually really, really severe um AOA regurgitation. And then finally, we have a continuous machine like murmur. So Emma this is what you were talking about earlier. So this is actually a patent ductus arteriosus. So, a PDA um in fetal development is a connection between the aorta and the pulmonary vein. And typically this closes off within a couple of days of life. Sometimes this doesn't close and you get a pit and ducts, arteriosis typically seen in newborn babies. And we treat this with indomethacin and Ibuprofen or paracetamol and this helps close it. However, sometimes we actually try and keep these open using prostaglandin E one. And what this is for is in patients with cyanotic congenital heart disease. So something like um transposition of the great arteries, for example. And this is because this is the only way of maintaining your systemic and portal circulate uh systemic or pulmonary circulations and getting oxygenation to the whole body. Ok. And you also have this thing called innocent murmurs. So these are typically heard in Children. So there's two kind of types, there's like a venous hums which is just turbulent blood flow um within the great veins. And you hear this kind of blowing noise underneath the clavicles and you have a stills murmur as well. So it's quite low pitch sound um at the lower left sternal edge, but these are completely innocent in the sense that they cause no symptoms. There's um it sometimes varies between standing and sitting. There's no added sounds or thrills, there's no diastolic component and usually there's no radiation either. Ok. Ok. So this is a website that we've been using to kind of show off all of our heart sounds in this presentation. So I will link, I will put the link back in the chat again or please refer to the slides which will be available on the metal page afterwards. And these heart sounds are really good for you to kind of hear and listen to and they show off the murmurs really well. And a reminder, like we said at the start of the presentation, the best way to get more comfortable and more confident with um understanding murmurs is to just listen to as many as possible. And importantly, l listen to as many normal hearts as possible so that it's more obvious when it's abnormal. Ok. So thank you for watching. We really appreciate you all coming along and I've dropped the feedback form again in the chart. So please please do fill this in. It gives us a lot of important information that we can improve on for future teachings. You need to stop sharing. So it will stay on for a couple of minutes. So please drop any questions you have. But otherwise, yeah, thank you for coming. Absolutely. If there's anything else that we can clarify or anything that you're confused about, we're happy to answer. Oh, thank you. Thank you. Thank you all for coming as well. Just a note on the website, they have a really, um they've actually got quite a lot of different members. We only picked out some of the three important ones, but they've got loads of different mas that you could listen to. Um, the, the website is, um, Harish is just linked in the chat. You see? Ok. You know this? Ok. So should II will stop.