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Carl. Are you fine, redoing it? Uh I am a bit concerned about the participants but maybe II flick through the sides very quickly. And then essentially, I'm sorry, if, if it wasn't live, none of the participants could have seen the initial parts. So it's just showing events starting soon for that month until now. Ok, great. Ok. So if you can see that'd be great. Thank you. No worries. Uh, hi, everyone. Um, I don't think you saw the start of the lecture. The basically on Z, um, I'm gonna, uh, just be going through structural heart disease. I won't be able to see the chart, unfortunately. Uh, just because of, uh, the nature of, er, this, er, er, um, software, but basically I'm gonna be doing structural heart disease and I think I'm the first cardio lecture. Um, so hopefully this isn't a too complicated way to start cardio. Let me just share my, um, my screen. It's the reason I, I'm doing structural heart disease. Uh sorry is, um, because first of all, I, I'm doing the cardio BSC at the moment. Um, so we've been doing conditions, um, and second, uh, because, um, I found it was one of the most difficult to do in second year. I don't think it was particularly done very well. Um, and, uh, uh, it was very complicated and I found that most people in my L year were trying to rote, learn everything rather than just try to understand and, and use that. Because if you try and rote learn everything, there's just way too much information and it becomes a very low yield. Even though this is a high yield topic, there are lots of questions on this, but if you spend way too much time just trying to memorize everything, um like l learn everything from memory becomes a very, like long process. So we try to understand it, it might make it a little bit better. Uh So these are the TYS I'm not really gonna go through them. This is how I like to structure my time, er, my lectures. So, starting with anatomy and function. This will be very quick, very easy. Um, but it's important that we just understand the basic content so that we can understand the disorder. And if we understand the disorder and the pathophysiology of that disorder, then we can understand the features and the management a lot better. So, very simple anatomy, we're gonna be focusing on the left side of the heart and looking at these valves, um, and the pulmonary veins in the aorta. Um Now, what's the function of the heart? Well, the function about those two functions. Um and this is something I learned again as I went through med school, which is that the heart can act as a battery or it can act as a pump and I battery, I mean the electrical circuit and my pump, I mean the myocardium er uh all the valves. Um So in terms of the heart acting as a battery, the myocardium is uh electric conductive, it allows electrical signals to be propagated throughout it and therefore allow it to do its other function which is pump and the pump and the blo uh and in terms of pump, uh the heart pumps blood around the body, very self explanatory. Basically, the reason why we try and separate the heart into these two functions is that basically every disorder can be uh put under an umbrella of one or the other. In terms of electrical circuit, we can have iron channelopathies. Um We have mineral deficiencies like potassium under the battery, but we also have pump conditions like heart failure, um cardiomyopathies, valvular dysfunctions, which is what I'm gonna go into. Uh So pump is basically mo mostly what we're gonna be focusing on a structural heart disease, a fair function of the heart in terms of its pump. So um as the name suggests, it encompasses a wide range of conditions that affect the actual structure of the heart. And we can broadly classify into congenital acquired, which is you can often do for many conditions. I'm gonna be looking at congenital first. It's looking at a SDS V SDS, coarctation of the alta P FO and electrology of Fallow. Um So let's start with the septal defects. So I'm gonna combine ASD and D SD atrial septal defect and septal defect into one. Basically what happens here is a wall can occur in the heart septum, either the atrial heart septum or the ventricular heart septum. And this allows blood to cross what's usually very well established, a left right divide. Uh It's important two reasons, pressure and oxygenation. So the left is much higher pressure because it needs to pump blood much further around the whole body as opposed to the pulmonary system, the right side of the heart, we just need to pump blood around the lungs and then back to the heart. So, if we get a hole in the heart wall, what happens is because the left side is high pressure, we get a left, right shunt, the blood is forced from the left to the right because of the pressures and we get a loss of oxygenation. Um We get a loss of volume which is both very important for body perfusion. Um The second problem. Uh um The second thing that can happen, which you might have heard about uh might be a bit confusing is basically the other way a right to left shunt. Um And what happens here is after a while of having a septal defect is um eventually the the pressure is almost equalized and they can even reverse. So you have the right side being high pressure and then you get a right to left shunt and this really causes uh bad cases of cyanosis. And often this um we need to do surgical intervention. However, having said that atrial septal defects can be very mild and you might have one your whole life without noticing. Um So it really depends on the size and the location of the sta defect. Um Tetraria fallow as the name suggests, uh Tetra being four has four key characteristics. One ventricular septal defect, two overriding aorta, three pulmonary stenosis and four right ventricular hypertrophy. So, I don't think is well understood is that the second one overriding aorta can actually cause numbers three and four. Um I'll just go through one by one first. So V defect is what we've just talked about. What's the thing in tetra fall or tof is um that it's very large and it actually means that er, and it's placed right by the left ventricular outflow tract, which is the tract which uh the blood flows down er to get out of the aorta through the aortic valve. It sits right next to the valve. So basically what happens is most of the blood actually ends up going down the aorta, both from the right side and the left side. So this results in very poorly oxygenated blood and bad body perfusion. 2nd, 2nd thing overriding aorta. This is basically where the uh aorta squashes the pulmonary artery and thereby stenosing it, which is number three. This stenosis means that there's pressure, a build up of pressure before and um, not so much pressure after. It's kind of like if you've got a tube, um, like a hose and you stick your, your hand over part of it, the pressure builds up er, before it and it's very uh the pressure after it is very weak. Um So this is what happens with uh your, your veins and arteries too when something is stenosed and we'll talk about this later when we talk about valve stenosis. So, arteries can be stenosed as, as here or, or veins. Um but also valves can be stenosed. And then finally, because it's stenos and because there's this pressure build up, the right ventricle needs to push more to get through the stenosis in the pulmonary artery. Um, to try and do this. The right ventricle gets bigger. It hypertrophies, the muscle gets bigger. Um And that's why we see right ventricle hyper and this is quite a a life threatening condition. So it often needs surgical intervention right above. Finally, coar of the aorta is basically er an aorta stenosis. Um not to be confused with the aortic valve stenosis. This is the stenosis of the actual artery. And again, there's increased pressure proximal to the narrowing and decreased pressure, distal to the narrowing. What this means clinically is that we see normal blood pressures, uh proximal to it or high blood pressures proximal to it. And this is basically all the arteries that come off the aortic arch. So, we've got the subclavian, you've got carotid arteries, um and basically the arteries that uh feed your arms and head. And after this, we've got a decreased uh pressure. So this could be uh the arteries in your legs. And what this means is that um uh you'll have lower pressures in your legs, but it also means that your legs are underdeveloped often uh in Children. So this is key to look out for. Um There's not really much in the lecture on these. Um And I think just understanding them is the best way to approach these uh in terms of questions for the exams as well. So we've just had a look at congenital structural heart diseases, which I think are fairly straightforward. Um And if you have any questions, by the way, unfortunately, I can't see the chat. Um So just pop them in and I'll, I'll go through them all at the end. Please ask anything. Um, more than happy to help. Um nw which I think is the place where most people struggled, at least in my year, um especially valvular dysfunction. Um So I think for this whole whole idea, it's important to understand what exactly we're talking about. So, as the name suggests, we're looking at a valve and we're looking at how it's not functioning well. So it can be the mitral aortic valve. Um But later, it can be applied to the tricuspid in the pulmonary and also closed or whether it's regurgitating and, and this is just quite key. Like I know this looks really simple. But I think if you have in your head, what is actually happening? Um.