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Hello. Can you hear me or see me now? I'm sorry, just say yes in the chat if you can? Perfect. Ok, fine, thankfully. Ok, I got it to work now. Um, let me perfect. Thank you. Let me just share my screen. Um, and um, Zen Xeno, is it ok? If you just let me know in the chat, if people can see my screen as well, can I see it? Yes. Yeah. Yeah, perfect. Ok, let's make a start. Um, because I know we have been a bit delayed. So, um, welcome to the first session on um, er, in um, Mi Minor Bleeps final series. And er, this one is the first of our cardiology series and this is gonna be about a valvular disease and the reason why I picked this topic is, er, because it's good for written exams and also it's really, really helpful for us you findings as well. Um, or now the exam is called CPS A which is the same thing. Um, so what we thought of is just to focus on this, uh in this lecture and what we're gonna talk about is the basics of valve function. Um, how the kind of sounds they produce when they're functioning normally and they're moving onto pathologies in both the left and right sided heart valves because usually the right sided heart valves are very commonly missed. Um, and they're not really talked about. However, even in my ask you just as a personal story, I actually got someone with tricuspid regurgitation. So I think it is really important to maybe just gloss over. Um, and then we'll just delve into the management of common heart valve pathologies. Um most commonly the left sided ones because they're usually the ones um that leave people more prone to systemic complications. So for example, such as syncope, um and then right at the end, we've just got some exam style MC Qs, hopefully that will get the clogs working after um some heavy heavy content. OK? Um So enjoy the lecture. Um And if there's any questions, er Zenna will highlight them um and um stop me after each slide and we can er answer any questions that may come up. Alright. Um And last, but not least um right at the end, we've got a feedback form as well. Um It's really, really important just as this is our first session as well just to let us know how it, how you think it went and what we can improve so we can make our next session even better than this one. OK. So let's make a start. So er by the way, My name is Doctor Ali Bhi. Um, and er, this is Doctor, er Zenor Kami as well. So we're both, um, cardiology leads for, er, mind the bleep. Um, and also I'm one of the final year leads as well. Um, so if you have any other questions as well, um, I can pop my email, um, on the chat as well at the end, er, for any inquiries or anything like that. Ok. So, um, in this slide just to quickly gloss over just the gross anatomy of the heart, I'm pretty sure most of you are probably final year, but we might have also some doctors, um, and also maybe some, er, preclinical students as well. So it could just be a bit useful just to uh go over this quite briefly. Um, so we've got two types of valves. Um, they're split into atrioventricular valves and semilunar valves. Now, it's quite self explanatory. The atrioventricular valves are the valves which um, connect or they're in between the atria and the ventricles on each side, both the left and right side. Um, and then we also have the semilunar valves, which are the valves that basically connect from the ventricles to um, the er, systemic vessels that can either be the pulmonary artery on the right hand side of the heart which goes to the lungs or it can be the aorta which goes to the um, systemic system, so to speak. And um, supplies all kinds of organs that are not the lungs, basically. Um as the uh blood has already been oxidated by the lungs and it goes um to the rest of the body. So, uh the two times the atrial ventricular valves that we got are the mitral valve and the tricuspid valve. Um So the mitral valve is on the left hand side and the tricuspid valve is on the right hand side. Um, so the mitral valve is, er, has two cusps and the tricuspid, as you can see, tri has three cusps, that's kind of the way to identify them as well. Um, now, uh what they do is, as I've kind of said, they control the blood flow between the atrium and the ventricles. And, and the interesting thing about these two valves that makes them unique is the fact that they have these things called chordae tendinae, er, which are basically little strands of, er, tendon essentially. And they connect to these, these things called papillary muscles, which are in the ventricles. And the reason why they have this is basically, it helps to er, angle um the valves downwards to help close the uh the valves. And the reason why that's important is because during systole, which when the ventricles are contracting, um it helps to keep the valves completely shut. And without that called a 1010 tendency, the systole will then end up, er, resulting in displacement or prolapse of the valves into the atrium. And that has a high risk of backflow of blood into the atrium. And therefore, it's not going to um the rest of the systems in terms of the rest the organs, which is the lungs, the brain, et cetera. So you have ineffective flow. So that's why they're really, really important. And when they burst or when, for example, there's any kind of pathology in either the chord tendon or the papillary muscles, um that can cause some very deleterious effects that we'll talk about later in terms of valvular pathologies. Uh then the other valves that we've got the semilunar valves and these valves just consist of the aortic and the pulmonary valve and again, quite self explanatory, they connect to um the aorta and the pulmonary artery respectively. Uh And what that does is just control the blood flow from er, between the heart and also the extra myocardial organs um including the lungs. And as I said, the brain, um the gastrointestinal tract, et cetera. Ok. And so hopefully, that makes sense. So as I said, guys, we're just gonna cover the quick basics and then we're gonna go into the pathology. So, so, so it all makes sense to everyone. Um So, on this slide, um it just shows the cardiac cycle. So we've got four stages and er the reason why I wanted to highlight this is because it's important to know um how the valves move and when they open, when they close the kind of sounds that they make, er, because that will also be important in terms of understanding what happens when stuff goes wrong with the valves and how we can discern that. So, um, what we have is we have the first stage which is mid to late ventricular diastole. And that's basically just when uh blood enters the atria and it goes into the right hand side and obviously the left hand side through um the various veins. Er, and then what you've got is when the atrial pressure starts to rise, it forces the atrial ventricular valves open. So we can see here the atrial atrial ventricular valves open. So that's a late diastole, ok. Um And that's when the ventricles are uh completely relaxed at this particular time and they're just filling from the atria and you have the atrial ventricular valves, as we said, that connect between the two chambers, um they open and they allow the blood to rush through. And right at the end, you've got something called the atrial kick, um which is basically where the atria contracts right at the end of um it basically expelling all the blood that's in it. Um And that is synonymous with the P wave that we see on the ECG as well. Um So when you see the P wave, all that means is that is the atrial quick, so that there's a atrial contraction right at the end of mid diastole and this precedes er, systole and precedes the contraction. And then what we've got is something called isovolumetric contraction. That's the second stage. Isovolumetric just means that the volumes in er, all the chambers stay the same and the volumes in the vessels also stay the same. There's no change in the volumes. But what starts to happen is essentially, um, you have basically naught point, naught, two to naught point naught three seconds of the ventricle, basically building up sufficient pressure to then push um the semilunar valves open. Right? And that is what er isovolumetric contraction is. It's just these couple or couple milliseconds essentially um that needs to build up er pressure for the contraction before the contraction can occur and for blood to then completely expel out the ventricles and to er the organs. Um And as this occurs, what happens is ventricular pressure exceeds the atrial pressure that forces also the atrioventricular valves er from above to shut as well. So that is really important in preventing any backflow of blood into the atria at this particular time. And what this is synonymous with is when you've got the and seminula valves um opening and also the atrial ventricular valves closing at this particular time. And as you can see on this graph on the right, um this is what this is showing um when you've got that you have the lub sound. So you know, you have the lub dub sound in the heart, the lub sound is synonymous with the semi, with the atrial ventricular valves closing, sorry. Um, and also you've got the seminar valves opening at the same time. Um, and then blood just flows out the heart to the systemic system. You've got the lungs and also the coronary circulation as well just to supply the heart with some blood too. Ok. Um, and the fraction of blood, er, that is expelled is known as enddiastolic volume, um, which is quite important because when it comes to calculating the, the stroke volume, and then we look at valvular pathologies and how we analyze them. That's what we look at. Ok. Um And then what we have after is mid to late ventricular systole. Um And what happens here is basically the ventricles are emptying at this point um as we've talked about and they're emptying and emptying and emptying until the pressure in the ventricles becomes lower than the pressure in the vessels. Either be it the pulmonary vessel or the aorta. And what happens then is then eventually the semilunar valves close shut because what happens is that blood that's in the aorta. Um And that's in the pulmonary arteries. What they do is they, they backflow because of gravity, right, they're gravity dependent. So when they backflow, they cause the shutting of the valves. Um and that's usually when the pressure is high enough and then last, but not least, um once they shut, that causes the dub sound, which is also known as an S two sounds. So you've got the S one and S two. And this is synonymous um, the ventricular relaxation with uh the T wave on the ECG. Um And, um, then we just restart again and it restarts a cycle. So hopefully, that makes sense in terms of when the valves open and close. Um And we're gonna delve deeper into why that's important next. So, um, I think what's important is just to go over quickly. Um, just the various sounds that we have in the heart and again, what's normal and what's not normal. So, we talked about S one and two and this happens usually during the entirety of the systolic phase, you have S one at the start S two, at the end, right? That's when the valves open. Er, that's when the valve, sorry, er, close, um in preparation for the ventricles to eject blood and then valves close later on, um to basically signify, er, no more blood being expelled from the ventricles, right? So that's normal. Ok. Er, and that's usually during systole. Um, and then you've got the abnormal, which is, um, usually always during diastole is abnormal, um in terms of valvular um sounds, but also during cysto, we do have some pathological sounds. Um And examples of this, er, can be, er, for example, um when you have, let's say an S3, er, an S3 and S four sound. So these kind of sounds and they come about usually during, er, heart failure, right. So, uh when you have heart failure, you can either have a dilated ventricle or a hypertrophic ventricle, right? I don't know whether this is starting to make sense to you guys or you're starting to remember your heart failure management. Um, but when you have the S3 and four sounds, um so usually the S3 sound is right at the start of diastole. Um, and that's usually, er, basically when, um, there is a dilated and compliant ventricle, that's what we call it and it produces a sound that, um, apparently sounds like Kentucky, I've never heard it in real life. That's apparently what it sounds like. And then also, uh, you've got the S four sound which is towards the end of diastole and right next to the start of systole. Um, and basically that's the sound of the atrial contraction hitting a non compliant ventricle. So that's right at the end of, um, the, er, diastolic phase um at the late diastolic phase and, er, that causes a sound that apparently sounds like Tennessee. So these are just two pathological sounds to know about. Um, but also you've got some valvular sounds as well. Um, and that's what this top, this lecture is about. So I guess that's what's important. Um, so what you have is, er, for example, um, when, er, you have during systole, er, if you have, er, pathologies in the aorta, such as aortic stenosis, for example. Er, so aortic stenosis can cause a systolic murmur. Um also in diastole, er, you have murmurs, such aortic regurgitation. So, er, right at the start of diastole, you have a murmur, er, because the there's backflow of blood uh from the aorta. Um, once the ventricles inject the blood into it, there's a backflow of blood back out, back, out of it into the ventricles. Um, so that's one way to kind of classify murmurs. Um just by whether it's a systolic phase or diastolic phase, and we'll go into that in a little bit as well. Um And number two, the other way to kind of classify it within, within respects to timing is the abruptness of the murmur. So the murmur can be um called early or mid or late or pan pan, meaning that the murmur occurs throughout the entirety of either Sicily or diastole. And then you've got early. So for example, early ones, as I said, is aortic regurgitation. Um and also potentially mitral regurgitation depending on how severe it is as well. Um You've also got middle, mid, mid ones. So for example, aortic stenosis that usually peaks in the middle as a crescendo, dec crescendo murmur. And we'll talk about what that means later on and you also have late murmurs um that can also occur and we'll also talk about some examples of that and then you've got this, this er image in the bottom corner, er, which kind of discusses just what we talked about and how murmurs can be classified and divided. Um, another way er to classify murmurs is by pitch and by grading. Um so pitch can be classified as high, medium or low pitch and then grading grading is just loudness. Um So pitch is basically just relating to frequency and grading is relating to how loud the murmur actually sounds. Um And in terms of the pitch, what what is, what determines how high the pitch is and how loud the murmur is, is mainly the pressure gradient across the valve. So for example, if you've got some some level of stenosis, right. So um aortic stenosis, for instance, the there's a quite high pressure gradient across the valve because obviously, you've got a stenos valve which means it's more closed than normal even when it's supposed to be as open as it as it can. Um there's still a bit of um close closings of it, er so to speak. And therefore, because of this, it can create a high pitch cos obviously, there's a high gradient er from behind the valve er in term er in comparison to in front of the valve. Ok. So hopefully that makes sense. And in terms of the grading, it's the same kind of thing, it also depends on um the er pressure gradient across the valve, but also it's dependent on the flow of blood across the valve. So the amount of blood that's flowing across the valve essentially. And that is determined by the enddiastolic volume in the ventricle and how much blood the ventricle is basically pumping out. Ok. Um And there's six grades we don't need to go into, into this, into too much detail. But if you wanna, if you wanna know in your own time, um grade four is probably the most significant one just because that's when uh there's a palpable thrill, which means that when you touch the patient on their chest over the valve, you can actually feel the murmur. Um and past grade four, there are thrills with um all of them. And uh another way to classify murmurs is also by the shape. So I mentioned crescendo, dec crescendo. Um and what that means and um essentially er what this is describing when we say shape of the murmur, it basically just describes er the fact that there's changes in the intensity of the murmur across the cardiac er cycle, right? Um So, for example, um in aortic stenosis, we'll take that as an example. Again, there's something called crescendo decrescendo. And the reason for that is because we at the start of ventricular contraction, right? There's quite a loud sound, right? Because it, there's blood flowing through a stenos valve, right, and therefore flowing through uh less of a gap right in the valve. But as the valve starts to open and open a bit more, which it struggles to throughout Sicily, but it opens eventually depending on how severe the the stenosis is. It has a decrescendo phase, meaning that it becomes a bit quieter. So it has a loud and then quiet phase and this is occurring um throughout the cardiac cycle. Um So that's why I say it's really dependent on what stage of the cardiac cycle it's in. Um And that's another way to classify the murmurs as well. And we just have a diagram here on the right base, just explaining um how the sound um, is in terms of the peaks and the troughs and the, er, and the sound and last, but not least, um, we can classify murmurs by their location. And, um, one important thing to note here is, you know, we all, we all probably know, er, the fact that, you know, we, we listen to the right, upper sternal edge, left, upper sternal edge and the lower left sternal edge and then the apex, right. Um, we know where we've already probably done cardio cardiovascular examinations before and we know where to listen to. But the important thing with this slide is really knowing as well, um where the murmur radiates because the location where murmurs are best heard are not always across the valvular location. Um, and a lot of the time as well just to bear in mind cos you can see uh the picture of the heart here. Um, and the surface anatomy, you can see that the valves where we listen to and where we auscultate isn't necessarily where the valve is. It's where it projects, however, where we listen to is where it projects most right, but it can radiate to other areas and that's important to know. Um because a lot of murmurs for, for example, cross over in terms of where they radiate and that's where imaging is really important to understand what valvular pathology. there actually is because it can be very difficult to diagnose this just off an examination. Um And uh the good thing is we have just this er other image just on the right hand side er on, well, on your left hand side, I guess. Um and er this other image on the corner on the upper corner and this is basically describes where the murmurs radiate and where we can best hear them. So, for example, in aortic stenosis, uh the murmur can radiate to the carotids. Er and that's because the blood flow is towards the carotids from the AAA uh AORTA, sorry. Um So that's just something to nose as well. Um So it's not just about where the valves are, it's about where the sound radiates to and that's really important um because it can help with auscultation and uh last but not least um the way to really know that is by understanding the cardiac cycle and the direction that the blood is flowing in. So, um I think Astro's going all over all of that. Um It's a good idea to start going over some pathology. So, let's start with tricuspid stenosis. Um So this is one of the right um heart um valve pathologies. Um and this is in the valve that is connecting um the right atrium to the right ventricle. And now the main risk factor for this um is a quite rare er valve pathology. Um but it usually comes about from patients who have a history of acute rheumatic fever. Um And we have just a diagram on the top corner that just um explains um the main signs and symptoms of acute rheumatic fever. So, we have a major, minor criteria and uh the five main things um to really look for in patients is if they have any polyarthritis, um if they have any carditis. So, for example, any chest pain that is not um indicative of a, a myocardial infarction or a heart attack or anything like that. Um And it's more of like an inflammatory um myocardial pain. Um Also you get some nodules um usually over the extensor surfaces and it's something called erythema marginatus, which is basically is a painless rash um that is migratory and it appears as pinkish red macules with very, very defined borders as well. Hence the name marginatus, which means margins, er, and then last, but not least you've got sinning chia um which is just essentially uh when you've got um uncoordinated jerky movements. And that's just because um, an autoimmune attack on the basal ganglia. Um, that, you know, if you guys probably had basal ganglia before in Parkinson's, um, it's the same thing. Um, and it attacks that and that causes uncoordinated movements. Um, so that's something to look out for, for patients with, um, a history of tricuspid stenosis. Um, and the associations, um, it's most commonly associated with mitral stenosis actually. So, usually if you have tricuspid stenosis, you more than likely have uh tricuspid stenosis as well. Um And the findings on examination, usually what we hear is we hear um some, something called a middiastolic rumble and that's on the lower left sternal border. So we osculate on the lower left sternal border. That's where the er tricuspid valve radiates to right in terms of its sound. Um And we hear a middiastolic murmur and the reason why it's middiastolic um is because usually, um you know, you, we have no sound during diastole in terms of uh the valve opening, however, because it's a stenosed valve, um we do get a sound and instead of the sound happening right at the beginning of di ay, it takes a bit of time for the valve to actually open and therefore we have it in the middle of diastole, hence a middiastolic rumble and it's usually low frequency because of two things. Number one, the blood flow is quite low in the right heart. Um compared to the blood flow in the left heart just because of pressure differences. Um and also, um because of the fact that it's through um a um it's for a valve on the right hand side in terms of the fact that it's not, it's from the, to the ventricles, not from the ventricles outwards. So the pressure from the atria as well itself in general, both like left and right um isn't too high, so it's not pumping um blood at really, really high pressure. So we don't get that high frequency murmur that we usually hear and that is usually heard best with the belt of the stethoscope. So anything which is a low frequency murmur, we usually use the bell of the stethoscope to hear it. Um And the thing that we see is something called um Rivera er Carvalho sign. Um And basically that just means that the murmurs louder on inspiration. And the reason for that is just because during inspiration, we have a higher venous return to the right heart and therefore more blood and therefore, er more blood going through the valve and therefore a louder murmur. It's as simple as that and the way we investigate murmurs um in general, er, but also for tricho stenosis. Um but you'll see this as a recurring theme throughout is that we use echocardiography and echocardiography is usually the gold standard for diagnosing um any valvular pathology. And there's two types we either use um trans um transthoracic er, which is TTE or we use transesophageal and transthoracic can be good and it's usually the first line, what we do, what we do is we can see it use basically echocardiogram outside of the body. Um However, T OE which is transesophageal is just when there's a camera that's put down um or instead of a camera actually like an ultrasound kind of machine essentially and it's put er down into through the esophagus. And you can basically visualize the valves a lot better and it's usually used in patients who have a very large body habit, habits as well and it's actually something to bear in mind. Um And one other investigation er, that we can use is a JVP graft and the JVP graft just visualizes um the jugular venous er pressure um and er the movements within the er jugular vein. Um And the, the reason why that's important, especially for this is just the fact that usually hear what we see is an elevated JVP in a prominent a wave and an A wave is usually a synonymous atrial contraction. And the reason why it's prominent is because the atrial contracting against a closed stenotic valve. Ok. Um And that therefore increases the pressure and causes a backflow into the er jugular veins and that causes like kind of pulsation there. And then last but not least the couple of complications we have is uh right heart failure. Um that is in tricuspid um stenosis and also we also have atrial fibrillation. Uh and the reason why for atrial fibrillation is just because the atria are getting wider and wider. Um because obviously, there's more and more blood that's collecting in the atria. Um and that kind of change in the heart's uh morphology uh can result in atrial fibrillation cos it just messes with the electrical fibers in the heart. So hopefully that makes sense and then move on to er tricuspid regurgitation. So, uh tricuspid regurgitation. Um again, one of the main risk factors is um acute rheumatic fever. Um and it was very, very similar to tricuspid um stenosis, essentially um similar risk factors um and the findings on examination. However, the main difference is the fact that it's a systolic murmur and we call it a hollow systolic murmur, meaning it occurs throughout the whole of systole. Um And again, we hear it at the lower left sternal border. So that's the main theme with the Tricuspid valve. It's usually uh all the pathologies are heard in the lower left sternal border. Um the loudest um and the reason for this holosystolic murmur, the reason why it comes throughout the whole of systole is because throughout the whole of cyst, the ventricles are contracting right. And when the ventricles contract blood usually is supposed to go through either the pulmonary artery or the aorta. But because of this kind of dodgy valve instead of hitting a closed valve. Right. What's happening is it's hitting a valve that's quite leaky. Right. And when it's hitting a valve that's quite leaky, there's some level of backflow into the atria during systole. And that's why we have something called a holosystolic murmur, meaning it occurs throughout the whole of systole and where it can radiate to is the upper area of the precordium, meaning the upper area of the chest. And the reason why is because as the ventricles pump upwards, um, and it goes through the tricuspid valve, er, in a upwards manner, um, it can radiate er, in terms of the sound, um, also upwards as well, um, to the upper areas of the chest and again, um, we also, so I see the Rivera Carvalho sign here as well, um, because again, higher venous return, er, in inspiration and therefore more blood there, more blood going into the ventricles, er, from the atria, er, on the right hand side and therefore more blood being pumped, er, back into, er, the, er, atria via the Tricuspid valve that's leaky as well. Um, and in terms of the investigations, again, as I said, we use echocardiography for all of them. So that's gonna be the main theme throughout. Um, and, uh, the other thing that we can also use is a JVP graph again. However, the sign here is that we see something called a, uh CV sign. Um, and er, the CV sign that we see is basically just a physical finding wherein the visible pulsation of the jugular vein can be seen can be seen as synonymous with a giant V wave and that compounds with ac wave of ventricular contraction. Um And the reason for that is basically, um you have the fact that um with the er wave that's occurring here, essentially when the valve is closed, the atrioventricular valve usually drinks Sicily um and the ventricle is pumping usually against it as there's no valve to pump against. As the valve is very leaky. The blood that's pumping from the ventricle. Instead, pump pumps through the leaky tricuspid valve and goes all the way into the jugular vein and that causes that kind of pulsation that we see um on the JVP graft and that's called the LCI sign. And in terms of the complications, it is very much the same. Um The only thing that's different from tricuspid stenosis is the risk of uh heart failure is much higher in tricuspid regurgitation as you have a volume overload um in the ventricle itself. Um So that means that the ventricle becomes er dysfunctional here straight away and that can lead to blood collecting there and then going all the way into the systemic system and back backflow all the way to the liver. And that can cause advanced liver disease as well due to that excess of congestion and it can cause a kind of pressure atrophy on the liver. Now, in terms of uh the pulmonary valves, um there's pulmonary regurgitation and stenosis as well. Uh pulmonary regurgitation is very, very rare. So there's no point really talking about it. Uh pulmonary stenosis. On the other hand, it can be important because it's one of the causes of cyanotic babies. Um and it's most commonly a a congenital uh condition. Um hence the fact that it does cause um cyanosis in kids and this is where it becomes very significant. Um because obviously, when you have a cyanotic baby, you have a high, high risk of death. Um and the findings on examination, um usually when you find out the baby comes out, you wouldn't really examine them straight away. Um you'd go to the management protocol but um just for the purpose of teaching or just go through the examination and the findings. So you, you find a crescendo, decrescendo systolic murmur and that's on the upper left sternal edge, right? And that's where we hear the pulmonary uh artery and the pulmonary valves. Um and the crescendo decrescendo is just because there's some level of stenosis. So, as I said, so at the start, um basically the blood is flowing through, er, from the ventricles, er, into the pulmonary aorta um into the pulmonary artery, sorry, and it's flowing at um quite a high rate and it's going through a stenotic valve that isn't fully opened. Er, so the picture is quite high. Er, but then obviously, as the valve starts to open throughout this, even though it takes, it takes its time to open eventually. Um, it just becomes fully opened and therefore, uh the sound becomes less and less and less. So it becomes decrescendo. Um and the murmur can radiate to the left clavicle. And again, the reason why is we talked about it in tricuspid regurgitation, then pulmonary stenosis, um the blood is obviously flowing from down to up from the ventricles into the pulmonary artery. And er, that sound can therefore radiate upwards and that goes all the way to the clavicle in terms of investigations. Again, we just do echocardiography. Uh There's no JVP findings on this because the JVP findings are usually on the tricuspid valve. Um and in terms of the management, er, we usually, er, it's very simple, we usually just give a prostaglandin. Um And the reason for that is because it, it allows for a patent um PDA. Um and what that does is it promotes blood flow to the peripheral tissues. And as a pulmonary stenosis can reduce the blood flow into the lungs and back into the left heart and therefore reduce the blood flow in general, reduce the cardiac output and that can cause hemodynamic instability. So, if you have a patent ductus arteriosis, then that allows some blood to flow from the, from uh the pulmonary artery er, into er, the aorta. Um and uh that will allow some level of blood flow to systemic symptom and therefore the baby to be oxygenated. Um, and usually the, er, management in terms of just a long term management for this kind of patient. Um, or, uh, you know, as soon as we've given prostaglandin is we usually do a percutaneous balloon, pulmonary valvuloplasty. And what that means is basically, we just uh put a balloon, um, all the way feed, feed it all the way into the heart, er, near to the valve itself and then inflate the balloon and that balloon will completely open a stenotic valve. Now, we can move on to the left side and this is where it gets interesting. Um because usually this is what you'll probably see on the wards um in terms of uh mitral stenosis. So, um as we talked about before, it was the same as same thing as tricuspid stenosis, pulmonary stenosis, same kind of thing. The valve isn't opening properly, that's what it means. Um And it's usually characterized in mitral stenosis, specifically, it characterizes thickened mitral valve leaflets and fused leaflet tips. Um and also some calcification as well. And the calcification is really important because that's usually the one of the main causes. Um is we have something called annular calcification of the annulus of the valve. Um and we call it um m ac related disease and that's the name of it. Um And usually what that means, as I said, it's just a nonrheumatic build up of calcium um in the mitral annulus. And, but the important thing to know is that the orifice, which means the center of the valve is usually left unscathed. And this is important because when it comes to the management, it becomes quite difficult. Um because we can't just open a balloon, simply, it's quite difficult to do that, right. Um In terms of clinical features, the main clinical features, breathlessness and that's because when we have mitral stenosis, the blood isn't flowing in from the atria, on the left hand side into the left ventricle. So therefore, blood collects in the left atria and starts the backflow into the lungs. Um and that causes pulmonary edema and therefore some breathlessness. Um and obviously, it can result in right heart failure as well, cos it can cause pulmonary hypertension. Cos obviously, you've got high BP in the lungs now. Um and in the pulmonary artery, um because obviously the blood is flowing backwards from the um from the mitral valve and obviously the er atria um on the left hand side and that can cause pulmonary hypertension, therefore, result eventually in some right heart failure as well. And that can lead to some systemic symptoms from right heart failure too. Um and it has some various other symptoms um such as for example, very flushed cheeks and also a hoarse voice as well, that's called cardio vocal syndrome. Um So that is important to know and that's just because the left atrium, er it lies in very, very close proximity to the recurrent laryngeal nerve uh in terms of findings on examination, uh what we hear is we hear a very low frequency. And again, that's because it's in the um atria, it's an atrial sound, what, what is, what we call it. Um And er, therefore we have a low frequency uh opening snap, um which is when the valve opens and it's followed by a decrescendo, crescendo, er diastolic rumble. Um And the reason why it goes from decrescendo to crescendo um is it's quite interesting. It's because um apparently from, from, well, from my notes though, when I was actually doing research on it, cos I kind of didn't really understand it too well. Um It says that basically there is um it struggles to open er, during the mid, late er diastolic phase, right? And there's a rumble through a narrow valve. Um but this is during passive ventricular filling. So when the ventricle is filling passively, there's usually quite a soft sound and then it becomes louder as there's that active filling phase, which as we said is synonymous with the P wave. And that's when the H is contracting against the valve and that's when it becomes louder. Um So hopefully, that kind of makes sense. We have a decrescendo crescendo, which is the opposite of the uh pulmonary stenosis that we saw. Um Another thing that we might see is a loud s one sound and that's just because the closing of a stenotic valve can cause a loud sound. Uh and also we can see some in, we can hear some inspiratory crackles. Uh and the reason for that is just because of uh some level of pulmonary edema that can occur uh in these patients. Er, and that can contribute to some breathlessness. Uh in terms of your investigations. Again, an echocardiogram, we can also do a chest X ray just to see the heart failure in terms of the pulmonary edema and any other symptoms uh associated with that. Uh And in terms of the management, er, the management is for pregnant people. Um usually, uh we just use diuretics and er, the reason for uh diuretic use is basically just to offload, er, the patients um, and just to reduce er, any kind of congestion, er, within the, um, within the lungs, er, for non pregnant patients. Now, this is where it gets interesting. Again, we use diuretics but if it's caused by rheumatic heart disease, which means that usually the orifice itself, which is the center of the valve is affected, then we can use a balloon to open the valve. However, if it's because of calcification and therefore calcification on the outside of the valve, a balloon is not gonna really gonna help because the valve is gonna remain closed with or without the balloon. Er, cos the balloon is gonna try and I inflate and the valve, it will just become very resistant to any opening at all and we call it, er, balloon resistant essentially. Er, but usually if, if it is due to rheumatic disease, um, when, when we do initiate this kind of protocol of doing a valve replacement or anything like that, um, usually it's, if they're severely, severely symptomatic and they have a gradient across the valve of more than five. and also a valve area of less than 1.5. Um And obviously that goes in line with the fact that it's a stenosis, which obviously means there's a higher pressure gradient across the valve and a lower valve area. Ok. And in terms of the complications, it's the same as before. The only main complication I want to talk about with this is stroke and stroke is can be very, very common if untreated. Um And the reason for that er is because of the fact that there's flow stasis because of the fact that atrial fibrillation is very common here, right. So we already have some level of stasis within the heart, right? But also on top of that, uh we also have loss of the mechanical propulsion from uh from er the fibrillating atria essentially. So basically, you, you have flow states already because of the fact that the valve stenos and then you have the fact that atrial fibrillation is also occurring, meaning that it's also not pumping correctly into the ventricles. So it's kind of a double whammy really, uh in terms of having um, stasis of blood and that can obviously lead to a clot and that can eventually, er, that clot can then eventually be circulated all the way up to the brain and cause a stroke. And the next one is mitral regurgitation. Um, and, er, in mitral regurgitation, um, usually, er, the main risk factors are uh mitral valve prolapse. And what that is is basically just when the valve is already a bit dodgy, it's not really leaky yet, right? Um But it's not, let's just say, as rigid as it can be, right? And uh this kind of valve is usually what develops into mitral regurgitation is it becomes just fully fledged. Um nonfunctional, essentially, um Other risk factors can be infective endocarditis, which is uh basically just an infection um that uh that can uh affect the endocardium, but obviously, the endocardium lines, the valves as well. So when you have an infection of the endocardium, that can also affect the uh the valves. And uh once the valves are affected, then that can cause uh all kinds of a valvular pathology such as stenosis or regurgitation. Um and in terms of the other causes, um we also have uh rheumatic heart disease as well and um a myocardial infarction can also affect these patients. Er, the reason being is that a myocardial infarction, what it can do is it can, er, basically affect, you know, the, remember the ch tendinae that we talked about in the papillary muscles because the, my, a myocardial infarction usually affects the musculature of the heart. It can affect these little papillary muscles that connect to these tendons that hold the valves in place. And therefore, when these are affected, what can happen is, uh, the valves don't open and close the way that they should. Um, so that's also just something to, er, bear in mind here as well. Uh Now, in terms of the findings on er, examination, uh we have a um high frequency, er, holosystolic, er, murmur here and again, similar to tricuspid regurgitation. That's because um the blood flow is occurring from the ventricles, er to the um aorta, right. Um But obviously we have a dodgy valve, er, on the left side as well. And so some of the blood flow is also going through this dodgy valve. Um, and that's what causes that kind of sound throughout the whole of systole as well. Um And the main thing, er, to also know is it's heard loudest at the apex and that's where all the mitral valve, uh pathologies are heard the loudest. Um and it can radiate to uh either the left axilla or all the upper areas of the Precordium. And that's again, just because of the direction of radiation of flow. Um and usually what we get is a diminished SS one sound. Uh The reason why we get a diminish s one sound is because we have regurgitation of the valve. Therefore, the valve is not closing properly and therefore, we don't get that characteristic love sound that we hear. Usually. Um at the start of, er, systole in terms of investigations. Again, echocardiogram, you guys are probably gonna get tired of me saying that. Um, but I just want to drill it into your head. Um, and then when we uh move on to the management, if it's acute mitral regurgitation, we always employ immediate surgical intervention. And by acute, what I mean is uh patients who present usually with acute onset of shortness of breath and symptoms of congestive heart failure, right? Um And obviously with known uh mitral regurgitation, these kind of patients are the ones who need surgical intervention because it shows some level of decompensation of the heart, right? And it shows that it is an acute decompensation because usually what happens when it's a chronic mitral regurgitation, it's progressive, right? Um What can happen is the the heart remodels and it gets used to it. So it starts becoming more dilated, it starts um getting used to the fact that there's more blood in the heart and it makes do essentially and therefore the cardiac output can stay relatively similar in acute mitral regurgitation. However, the heart isn't used to it. So there's no time for any compensation and therefore, when you have some acute mitral regurgitation straight away because the heart's not big enough, it hasn't compensated, it hasn't dilated. Um The heart starts filling uh with the blood and it cannot pump it out right. Um And because obviously it starts filling and filling and filling, it starts overwhelming the heart and therefore there's backflow into the atria and then there's backflow of blood all the way into the pulmonary system. And therefore you get some pulmonary congestion. Um and this can cause uh pulmonary edema. Um and also uh in some cases, some er pleural diffusions as well if it goes all the way to the right heart. Um So that's what, you know, one of the, one of the main things to really consider is in acute mitral regurgitation, we manage immediately, um especially if the patients are obviously fit for surgery as well. Um in terms of chronic mitral regurgitation, we can do surgical intervention, but that really depends on certain factors. So, for example, uh the patients usually, er if they're symptomatic, then we do surgical intervention. However, if they're, if they're asymptomatic, they have to tick certain criteria. Either the fact that their ejection fraction is less than 60% or their left ventricular systolic diameter is more than 40 millimeters. Um which obviously shows basically that one of the criteria has to be some level of dilation of the heart to show how severe the mitral regurgitation is. Um And how essentially how much the heart is compensating for this mitral regurgitation. Um And for secondary mitral regurgitation, which basically mitral regurgitation due to causes such as a heart attack or anything like that. Um Usually the management is dependent on the course. So we try and treat the course. So if someone, for example, has a heart attack, um we obviously try and relieve them of that heart attack. Um And obviously, if someone has infective endocarditis, we try and treat the underlying cause. Uh in terms of the main complications, obviously, as we said, um cardiogenic shock can be one of them when the heart um acutely cannot pump blood to the rest of the body. Um because it gets overwhelmed due to its volume overload, uh also congestive heart failure, as we said, and something called flash pulmonary edema, which again, um the heart cannot compensate acutely, blood er therefore collects in the pulmonary system um from the ventricles atria and then goes all the way to the pulmonary system. And then what that does is it pushes blood into the alveoli because there's high pressure in the pulmonary system and this can cause pulmonary edema and therefore resulting in marked breathlessness. Uh Now we move on to the extremely interesting ones. Um cos these are the ones you're probably most likely going to be tested on er in your exam and this is aortic stenosis. Um Now, aortic stenosis, um what it means is it, it, it just means calcific aortic disease and it usually represents a spectrum er ranging from aortic sclerosis uh which is basically just leaflet thickening, right. So, er, the thickening of the leaflets of the aorta, right? But without any obstruction. So you don't really get any symptoms from it. And um you don't really see even much on an echocardiogram either, right? There's not really much to see. Um, but this can develop into aortic stenosis. So, from sclerosis to stenosis. Um and um usually what precipitates is kind of aortic sclerosis developing in the first place. Um One of them can be a bicuspid um aortic valve. Um And the reason why I wanted to just note this er specifically is that um bicuspid aortic valve is usually congenital. So, so people are born with it and um what this can cause it can cause an abnormal blood flow across the valve. Cos instead of two leaflets of the valve, we have three and um this abnormal blood flow can cause damage to the endocardium li lining the valve. And therefore this damage can then result in thickening of the valve and therefore, stenosis, other causes are usually uh metabolic syndrome. Uh so basically hyperlipidemia, um hypertension smoking, uh chronic kidney disease and a rheumatic heart disease. But rheumatic heart disease is, is much rarer. Usually it's the kind of metabolic syndrome and all these kind of risk factors of um weirdly of a heart attack as well. So, they're kind of synonymous with that. Um And uh you've also got a bicuspid aortic valve that can cause it. Um And last, but not least one other thing that's just missing from this slide is that you can also get an infective endocarditis causing aortic stenosis as well. It's a bit rarer but it can happen in terms of clinical feature of aortic stenosis. Um It's quite important to note that it can very much present like a heart attack. Ok. And that's because um what it can result in is something called a type two myocardial infarction. I'm just gonna explain that in just a little bit, but I just want to just talk about the clinical features. It usually presents as a triad of three things. Angina, dyspnea, meaning breathlessness and syncope right. Now. In terms of, you know, people might ask why, why, why is it, why does it cause these three symptoms? So let's go from the start angina in terms of what it calls angina, we have um the fact that you know the er ventricles on the right, on the left side, they pump into the aorta and in the aorta, what we have is we have the two coronary vessels dividing and going in and supplying the heart. So if blood isn't going through this valve properly and therefore not going to the coronary arteries properly, what happens you get ischemia, right? And uh this ischemia is what can cause this angina er that patients can get a second thing, aortic stenosis, aortic stenosis, right. What can happen is you have a high afterload, right? Because obviously the stenosis is causing um essentially a very high pressure that the ventricle has to pump against. So to compensate for this. So the ventricle tries to uh pump more blood out and therefore increased cardiac output. The ventricle starts to hypertrophy, meaning there's more muscle cells collecting and dividing uh to create a stronger heart muscle. However, when this happens, there's obviously more musculature to supply, right. So there's a higher oxygen demand of the heart and this can also cause some ischemia and therefore can cause some uh pain as well. Uh in terms of breathlessness, um why would it cause breathlessness? Uh That's usually just because of the fact that there's an inability of the left ventricle to meet the mental metabolic er demands. That's number one. So we can go into a metabolic acidosis because the cardiac heart is not high enough and this can cause some level of compensatory hyperventilation, right. That's number one, but number two is the fact that there becomes some diastolic dysfunction as well because this hypertrophy, heart muscle eventually becomes dilated, right? As these uh compensatory uh cardiac uh tissue ends up dying because it's, it's only, it's only a temporary cardiac tissue, right? Er for a temporary cause it's not supposed to be a long term fix, right? And it therefore becomes more dilated and more dilated. And then what happens is it cannot pump blood properly uh because there's not enough heart muscles, right? And therefore the blood backs up into the atria and then therefore backs up into the pulmonary system again. Uh and therefore you get this breathlessness last but not least we get syncope reason being is that um the heart is again pumping against a sonos valve and therefore less blood going er into the systemic system and therefore less blood going to the brain. And that can cause syncope in terms of the findings. Uh we have quite a few. So uh number one, we have a ejection murmur. So that's when the valve opens, we have a murmur straight away, then also it carries on and we have a crescendo, decrescendo systolic murmur. Um and that's again similar to pulmonary stenosis. That's because er, as the valve is very narrow at the beginning of er systole and it's trying to open, er, there's very, very high pressure flow through the valve and it becomes lower and lower pressure as the valve begins to open. And this is usually lo loudest at the right upper sternal edge instead of the left like in pulmonary stenosis. And that can radiate to the carotid again because of the direction of blood flow that's radiating. Uh what we can also get is uh we get a soft S two sound. Now, this is really important because on the wards, when you're examining patients or even in Aussies, um usually you can hear an S one and S two sound the S two sound, however, that becomes less and less loud as the aortic stenosis gets worse. And that's because as the aortic stenosis gets worse, the valve because it becomes so, so stenosed that it hardly even closes and it basically very, very much struggles to close. And when it does close, it doesn't have that characteristic click because it's very, very much stenosed. Um I'm not gonna talk about the splitting sounds because you're not gonna find that on examination, it is very, very rare. Um But one other thing you might see is an S four sound and that's because of the hypertrophic heart that we talked about and it's a noncompliant ventricle. And therefore, when the atrial contracts against a noncompliant ventricle to uh push blood into it and it strikes a noncompliant ventricle, it causes an S four sound. And that's right at the end of the A when the atrial contracts, um in terms of the investigations, again, echocardiogram. Um but also interestingly here, an E CG can be helpful as well and that's because an E CG can show some left ventricular hypertrophy and that's just seen by very, very large er airwaves, um, usually across all the lateral leads that point to the left side. In terms of complications, we can get acute heart failure and also we can get some, uh well, for very, very unfortunate patients who are usually more on the symptomatic side, we can get sudden death and that's just because of the fact that um we get brain death and also uh what's it called, er, cardiac death, er, at the same time or going through a cardiac arrest essentially because of the lack of blood flow. Um and therefore, uh you know, um you can kind of call it hypovolemia, which is one of the features of cardiac arrest, er, because of the lack of blood through the, through the coronaries. And uh just this image on the right. Er, this just shows um the kind of stages that the heart goes through in terms of its morphology um throughout aortic stenosis uh as it worsens in terms of the management of aortic stenosis. And I think this is the most important, probably slide out of all of them because er for the written exams, especially, er, cos I've seen this tested many, many times throughout all my years at university. This question came up and, and it's really important to know um the indications of when we, when we intervene and when we don't intervene. So, uh if a patient comes in and they have aortic stenosis known um and they come in with some hemodynamic instability, meaning that they have a low BP, some angina uh or maybe they might come s come in syncopic. Um Usually, what we'll do is we'll do balloon valvuloplasty immediately. Uh And that's similar to what we talked about, you know, with the percutaneous balloon valvuloplasty and pulmonary stenosis, same, same principles. You wanna balloon the valve open. Ok. That's the main thing we need to do to save these patients and increase the cardiac output straight away. Uh, if the patients are clinically asymptomatic and they have an ejection fraction, less than 50% we can also valve, replace them as well. Ok. And uh we can usually use surgical uh aortic valve replacement or uh we can use something called, um, I think it's ran transcutaneous um, aortic um, valve replacement. Um, and usually what that does, er, or trans catheter, sorry, not trans er, yeah, transcatheter, aortic valve replacement. Er, and that's basically just inserting a valve using a catheter. So it's not an open surgery. Essentially. Er, we basically put in a catheter through femoral access and we feed the valve all the way into the heart. Ok. Er, if they're clinically asymptomatic, um, and they have severe A s or they have an elevated BNP or they have an abnormal exercise test or there's just rapid progression in their a er, aortic stenosis. Then we can also do um, uh what's it called a valve replacement. However, usually we go for the surgical route rather than the trans er catheter route. And if they're clinically symptomatic and they have severe A s um, then usually we do valve replacement, but the type of valve replacement really depends on the age. So, if patients are usually on the younger side, we actually opt for surgical. Er, and the reason for surgical is because there's less likely, um, that there's less of a chance that we need to replace the valve in the future. However, if we do trans catheter, there's more, more of a likelihood that we're going to have to replace the valve. That's what we usually do on older patients because usually in eight year olds and over their life expectancy isn't gonna be more than 10 years or so. Um And therefore the, the risk of having to replace the valve in the future is probably gonna be quite low. Um So we just usually just go for the transcatheter, but for the younger patients, we go for the surgical um method and hopefully that makes sense. Just 11 thing that I just wanted to note as well. Um just in terms of, sorry, just one second. Um just in terms of what we consider uh severe, er because a lot of people might say what is severe aortic stenosis. So when do we intervene? Cos a lot of these um criteria say severe A s right. Uh And in terms of uh what we call er severe aortic stenosis, it's usually usually when uh the velocity uh across the valve is uh four um or when we have uh the valve area is less than one millimeter squared. So that's usually when we intervene in aortic stenosis when it's a chronic aortic stenosis. However, as I said, when it's acute and patients are hemodynamic unstable, everything kind of just goes out the window essentially. And, um, we just, you know, uh we just treat er accordingly basically and we try and just do, do push a balloon and, um, just to treat the patients. Um. Oh, sorry, 11 last thing as well. Uh just in terms of, er, with aortic stenosis, um, when we, er, call it severe, um, I just made a mistake there. It's actually 55 per second uh in terms of the velocity, uh not four. and in terms of the gradient across the valve as well, that's one other thing that we look at and usually if it's more than or equal to uh 60 in terms of the gradient across the valve, uh then usually we intervene as well. Ok. So hopefully that makes sense. Um And last, but not least in terms of the valvular pathologies, we have aortic regurgitation. Er and this is just the opposite of stenosis. So, instead of uh the blood struggling, well, struggling to push blood out of the valve, er, the blood actually comes back through the valve and into the ventricles once it's pumped out. Um and it's usually during the diastolic phase, cos obviously during the systolic phase, that's where we're pumping, but out of the ventricles during the diastolic phase instead of staying in the aorta and going into the sy systemic system, er it back flows all the way into the ventricles again and that's what creates, er, this sound that's characteristic of aortic regurg, which is known as an early diastolic sound and it's a decrescendo murmur, er, because there's no active pumping of this blood, it's just blood, er, simply back flowing from the aorta, back into the, er, ventricles. So the sound gets quieter and quieter, um as the blood flows through cos obviously, there's less and less blood that's flowing through as time goes on. Um, and it's usually heard again at the up right sternal edge. Um However, it radiates to the mid left sternal edge and that's because the blood is traveling downwards. Um So therefore, er, the sound radiates downwards with it as well. Um, we have a few signs, er, on examination, we have the musset sign, which means that you get a, a characteristic head bop with aortic regurgitation. We also have tube sign, which is where you hear this kind of, er, bullet noise, this kind of flashing noise, I guess, er, through the femoral arteries if you want to auscultate. That, er, and one other thing is we get a bounding pulse that I'm sure you've seen on cardiovascular examinations as well, which where we just lift the arm up very briskly and feel the pulse while we're doing it and we feel a bounding sensation. Ok. Uh In terms of clinical features, the main clinical feature of aortic regurgitation is breathlessness and that's because um similar to mitral regurgitation, uh the blood can collect in the heart, it can cause some level of volume overload and eventually can back up into the lungs and cause pulmonary congestion and therefore breathlessness. In terms of the investigations we do, uh we usually do an echocardiogram that confirms the diagnosis. Uh we can uh check an E CG as well. It might show some pathologies on an E CG er very rare though usually. Um and also uh we can do a chest X and actually look just to visualize the pulmonary congestion. Uh in terms of the complications, er the main complication is heart failure. Uh and that's usually due to volume overload, not due to pressure. Um So we usually get a dilated uh cardiac phenomenon. Um And in terms of the management of a aortic regurgitation um with acute aortic regurgitation, usually these patients obviously again, similar to acute mitral regurgitation. Um we usually have uh blood that er collects in the heart. Um and there's a volume overload. Uh However, uh instead of um you know, in mitral regurgitation, the kind of management that we talked about and also in acute um aortic um stenosis usually here, what we do is we give them some inotropic support and some vasodilators. And we usually use vasodilators that is to reduce the afterload that the heart is pumping against. And we use some inotropic agents just to increase the contractility of the heart to help the heart contract and therefore increase the cardiac output and supply the rest of the organs and to make sure there's no organ failure. Uh in terms of chronic aortic regurgitation, usually er the indications depend on what we see on the right. So what we see on the right, we see what the meaning of severe aortic regurgitation is. And usually we only treat in the in cases where there's severe aortic regurgitation And obviously, if they're a surgical candidate as well, um in terms of the parameters of what we consider severe um the width of the um the jet, which basically just means that um essentially the the damage of the blood flow basically. Um so obviously, the higher the blood flow through the aortic through the aortic valve, that obviously means that there's more regurgitation, therefore, the more severe the aortic regurgitation, um also, er we can look at the regurgitant volume itself. Um So, not just the width but the volume er that's actually going back into the heart. And that can also estimate how bad the regurgitation is. Uh also the fraction. Um And er yeah, so the, these are basically just the main er parameters er to really look for uh when it comes to uh aortic regurgitation. Uh and what we consider sever and therefore, when we intervene, um it's less important to know this than with aortic stenosis. Um but these slides can be very helpful in just uh knowing just the rough kind of parameters and indications for it and that's it. So, in terms of any uh questions, let me know in the chat. However, er for now we can move on to the MC QS. Um So I'll let you guys read the first question. So a 21 year old patient is found to have an irregularly irregular pulse and a middiastolic murmur and auscultation. What is the best strategy for anticoagulation in this particular patient? So, this is a bit of atrial fibrillation, uh kind of management as well. Um Cos I want to throw that in there too. Um So I'll let you guys ponder that. Oh, sorry, one second, I'll let you guys ponder that for a minute and uh Zel can tell me uh some of the answer in the chat. No, I'll wait for about 10 responses. We're at five so far. Yeah, that's fine. We'll let people, we'll let people take their time. All right, we'll wait for a couple more responses and then we'll go through. OK. Should we go ahead? Absolutely. So there's a great split between all answers A to e but by a small margin, the most popular answer is E is E OK. That's interesting. Fine. Um OK, so we'll, we'll probably need to go through a bit of a more thorough explanation on this then. So the answer is actually a the patient should be commenced on Warfarin. Um And the reason for that is in the guidelines, any patient with valvular disease and concurrent atrial fibrillation should be started on Warfarin. Um And that's just what the studies show the, er, the most efficacious er, anticoagulant, er, for patients with valvular disease. And af is warfarin. Now, usually if there wasn't a valvular disease and it was just af um what I would say is, er, the doac um option is the correct one. However, um we don't really know, we don't know the gender of the patient. Usually, usually the chad Vas score is based on the patient's gender as well in terms of the scoring. So, um we, we wouldn't really be able to discern whether a do that can be commenced or not based on that patient's particular Chad VSC score. Um So that's one reason why that can't be correct, but also just in general um just the fact that Warfarin is more efficacious than Doac in valvular disease. Er So hopefully that makes sense and that's why obviously c uh C wouldn't be uh one of the options as well. Um because number one, they didn't even calculate chad Vas score. Er, but number two, just because the patient is young, it doesn't mean that they don't need um any er cover for a stroke. Um And in terms of whether the Warfarin should be commenced or not, if the Chad VSC score is too or higher. Um usually in any patient with valvular disease, we don't even use a Chad VSC score. Um, we just go straight away to um prescribing uh warfarin if they've got concurrent, er, valvular disease and af because the risk of stroke is so high. Er, and that's what I tried to mention, er, before as well and what I tried to hit home. Uh, but hopefully that makes sense for you guys and if there's any questions about that, then please a ask it in the chat next question. Uh a 78 year old patient with a ejection systolic murmur radiating to the carotid presents your clinic on examination. You expect the apex be to be where I'll let you guys have another minute to answer this. So uh yeah, Zen or if we can just upload the next gear. Perfect. Yeah, thank you. We've got 11 responses. The most popular answer is D with 54% of people choosing that. OK. Again, inter OK. How about, how about we do this? Can someone one brave person um maybe just message in the chat why they put D cos I'd like to get it cos the, the answer isn't d just just so you guys know um the answer is er in fact, b um but I just kind of wanna know where your guys' mind is at. So if, if someone could just maybe put in the chat, um I'll give you 20 seconds, 2030 seconds just to maybe pop why you put D down. Um just So I understand where, where, where you guys are coming from. So I can explain um the, what's called the rationale behind the answer a bit better. Is any brave person volunteered then? Or, or? No, not as of yet? Ok. That's fine. We'll wait another 10 seconds. If not, I'll just go through the answer. That's ok. OK. I'm, as I'm assuming we're not gonna get an answer. That's OK. That's fine. Um So the reason why it's big, um usually it's mini very minimally displaced because it's hypertrophic, usually in a hypertrophic heart in cos it's a aortic stenosis, by the way, this is the uh valvular pathology that it's describing. Remember what we talked about about the fact that aortic stenosis is usually a hypertrophic heart. Um usually in a, in a hypertrophic heart, it doesn't become hypertrophic uh from the outside. It actually becomes hypertrophic on the inner part of the heart um on the kind of endocardial uh aspect of it. Um So the myocardium kind of builds up um more and more um internally essentially. So it doesn't get bigger on the outside. So that's why er the apex beat isn't actually displaced really. Um And it's a very pressure loaded heart and that's because of the stenosis. That's what he's trying to kind of describe here. Um Usually, if it was volume loaded that, that is more of a aortic regurgitation type picture where it becomes volume loaded. And therefore we have a displacement of the apex beat. Uh So hopefully, that kind of makes sense. Uh If anyone has any questions about that again, I'm more than happy to answer it. Uh Question three. What is the most likely E CG finding in a patient with severe aortic stenosis? I mean, to be honest, we talked about this. So I think um I think that this is quite, yeah, this could be a quite simple. And by the way, I just saw some of the chat as well. I saw that Hussein said due to left ventricular hypertrophy. Yeah, you're correct, by the way. Um That's what I was explaining before. Yeah, sorry. I only just saw that. Um and what I uh AA said um as well. Um the hypertrophy of the um er muscle er maybe would be to maybe be be to the left. Oh OK. Fine. Yeah. So yeah, as I, as I tried to explain, so the hypertrophy is usually internally not externally. So the heart actually doesn't really get bigger. Um the heart um only becomes more hypertrophy internal. Hopefully that makes sense. Um So just for the third question, we've got eight responses. Let's get a couple more. Um And uh then we can go for go through the answer. You haven't got any other guesses in terms of the E CG findings and aortic stenosis. That's fine. That's OK. Uh We can press ahead. So um it's left ventricle hypertrophy and we talked about that. Um Usually we get really, really ma marked really big er, R waves um in the lateral leads. So V six V five, and lead one are usually, er, the main, er lateral er leads. Er, and these are the ones that really show these huge, huge r waves in patients with left ventricular hypertrophy. Uh question four. So, er, we have a 46 year old female with a history of HEP C and intravenous drug abuse. Uh She presents into ad with fevers, dry gauze confusion and acute shortness of breath. Her vitals are as follows. Uh what we have is we have a chest X ray as well and it shows a diffuse pulmonary edema. So that part's already done for you. That part's already been interpreted and we have an echocardiography that shows a vegetation on the noncoronary cusp of the aortic valve. Um So the third cusp of the aortic valve and um this was severe aortic regurgitation. Um Although awaiting surgery, the patient is admitted onto the cardiology ICU, which intervention is the most appropriate. Next step. Is it a uh nitro pero? Is it B adenosine? Is it C nor epinephrine? Is it D furosemide or is it e amiodarone? I'll give you guys um two minutes chance of this cos it is quite a difficult one and we'll try and get as many response as we can. What kind of answers are we getting? We've got four. So, far, to be honest, it's a bit of a tough one. We got any more. Ok, we got seven, let's maybe just wait 1015 more seconds. Ok, we've got nine responses. I'm happy with that. Er, D is what most people said. Ok, I can see why. Let me, ok, let me explain this. So, um, we can see that this patient is presenting quite acutely, right? They have quite an acute shortness of breath and we can tell that they have some level of reation, quite severe. Remember what we said about patients who present acutely with severe er valvular pathology, um especially with aortic regurgitation, we usually start them off. The number one thing. The first line is we start them off with inotropes um and also with vasodilators. So, um nitros is actually a vasodilator that we use. Um And usually what that, what it does its mechanism of action is it increases the amount of nitric oxide and that can cause vasodilation, reducing the afterload in the heart and therefore increasing the cardiac output. So that would usually be the most appropriate first line intervention in terms of what we would use after. For obviously, for the fluid overload, we would use furosemide. That is correct. That would be the second line thing that we would use in terms of once the um hemodynamic instability is corrected, we would then go for the furosemide. But the first line thing is nitro pers, which is a type of vasodilator or uh also a venodilator as well. Does that all make sense to you guys? If not, again, I'm more than happy to answer in the chat, but just let me know. And last but not least, we have a 78 year old male is admitted to ICU with chest pain, shortness of breath and respiratory distress requiring urgent intubation. The chest radiograph again shows pulmonary edema worse in the lo lower lung lobes. Um His vital signs are as follows. Um and the patient's electrocardiogram demonstrates ST elevation in the 23 and AV F. So, in line with an inferior M I with reciprocal changes in lead one and A VL on physical examination. He has a systolic murmur. Um bilateral crackles on lung auscultation and cold and clammy extremities. The cardiac enzymes however, are pending. What interventions should be considered? Is it a er an intra aortic balloon pump? Is it b norepinephrine? Is it C inhalation or epoprostenol? Is it er D er Mione or is it E referred to a PCI laboratory? Uh PCI being percutaneous intervention, coronary intervention. Sorry. What do you guys think? What kind of answers are we getting on this? Ok. We got a nice split. Good. We'll just wait for another minute. Cos this is quite a difficult one. It's quite a long one. And I think in a, in a real, in a real life exam, this will take you guys probably more than 30 seconds. What do we think? Ok. Ok. So a split between A&E and someone for be as well. Um, ok. II can see why you think e and to be honest, e wouldn't be ok. So the interesting thing is it was actually an M CQ on, er, my exam, er, for finals. Um, the answer was actually a, um, but E II think to be, I put e in the exam so I actually got this wrong. That's why uh I even chose this question to begin with. Um Now, although it presents as an M I, right, um with, you know, er S elevation E 23 and A VF er and usually, you know, it's a, it's ast elevation M I, which means that usually we go for a PCI, right? Um Obviously, if it's within 12 hours and within 120 minutes of presenting in the hospital, um The only thing I would say that makes me more inclined to go for an intra aortic balloon pump is the fact that the underlying cause is aortic stenosis cos that can result in the chest pain that can result in the reduced flow in the coronary arteries that can result in a type two myocardial infarction. And therefore, it can result in the ST elevation that we're seeing here, right? Um And also it can resolve with all the other kind of things uh that we're seeing and usually a PCI laboratory. What does a PCI do? You're putting a balloon into the coronary artery, cos there's a clot there, right? But if we're looking at this cause, what is the cause of this M I? Is it because of a clot or is it more because of lack of blood flow? So, if there's a lack of blood flow, putting a balloon in the coronary artery is not gonna do anything. What the main thing we wanna do is we wanna rectify, um, the fact that, you know, we have um, a stenosis, we, we have um, low blood flow through the coronary arteries and that's because of the stenotic valve. So, what we wanna do is we wanna use an intraaortic balloon pump to rectify that first improve the flow through the coronary arteries and us usually through that uh that will cause a reversal in this kind of. Mm I picture. So hopefully that makes sense. Er, if anyone has any questions about that again, feel free to answer, feel free to ask, er, in the chat, if not. Um, that concludes the end of the session. Um Thank you all for listening. Um, we're giving out uh obviously attendance certificates for all of you as well. Um So please fill in the feedback forms to get the, er, attendance certificates and we'll send it to you. Um, and you can just use the QR code that's here. Um Let us know what you thought of the session. Um, obviously sorry about the mishap at the beginning. Um but hopefully the entirety of the session um as a whole, you found it really, really um interesting and engaging. Um So just let us know um how you found it. Uh And so we can approve for the next time, er, cos we have our next cardiology session uh next month. Um and it will be um surrounding heart failure. So, er, anyone interested in that and I think it could be useful for both your exams and also for Os as well. Um Then please join and hopefully you found it um really interesting and helpful. So, thank you. Um Oh, this is sorry, there's just a few questions on the chat. Let me just answer it. So, um Havre said um so is the M I essentially secondary? Yes, that's what we call it. A type two M I so secondary M I, it's not because of a blood clot in the coronary arteries. Is this session recorded? Yes, the session is live, it is recorded and it will be uploaded onto metal. Um Hopefully, you know, that's a good sign. It means you're interested enough to, you know, go through the lecture again and actually, um you know, kind of pick apart what I was saying. Um But yeah, hopefully you guys thought that it was really engaging and good and interesting. And if you have any other questions, um I'm, you know, if you wanna ask, I'm more than happy to put, put my email in um into the chat and you guys can ask me any questions regarding the lecture. Um But just let me know if you, if you require any contact details. And I'm more than happy to, to um to oblige, that's fine. But um if not, then um thank you all for attending and um look out for the next cardiology session. Um When is the next date? Um ok, so, um yeah, there we go. So Zen, I'll put it in the chat. So the next cardiology session is on the 13th of January. So look out for that. Um And hopefully we'll see all of you there and more. Um and no worries. Um Ashok, I'm more than happy to give a lecture and the next and the next time it will be Zen or that'll be given the lecture as well. Um And I can assure you it will be a very, very interesting and informative lecture at all. So, yeah, thank you all for your time. I'll leave the QR code actually just up there just for another couple of minutes, uh just for you guys to access and then um we can close the we up. Yeah, unfortunately the same, we had to go through everything very, very quickly. Um, cos valvular disease is such a big topic. I didn't want to leave you guys for about four or five hours, um talking about the same topic. But um I assure your heart failure will be a bit more speedy. Um and a bit less uh how do I say it a bit less rapid? Um But a bit more of a um how do I say a, a shorter lecture, hopefully? Ok, I think by now everyone should have um completed the QR code, um completed the feedback. Sorry. So, um yeah, thank you all for attending. Um And as I said, we'll see you um after the New Year. So all of you have a good Christmas and have a good year uh New Year and we'll see you all soon. Thank you.