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Yes, I'm anyone started? Hello, everyone. Um Just gonna check quickly. Can everyone hear me if anyone can just pop in a message on the chat function, please? Yeah, perfect. Hello everyone. So my name is Hasna Con and I'm a finally a medical student soon. I mean, right now in Fy Zero place in Belfast and I'm also the present of the Child Health Society. So today we're gonna start our first topic being pediatric cardiology and the speaker for this evening, Salle Cooker and F I Zero placed in Enniskillen currently. So if you do have any questions, please post it on to the chat function just down below and we'll try to answer it as soon as possible. And towards the very end, we're also going to send in a link, um which helps you gain a certificate essentially. So you need to stay throughout the entire event for the certificate if that's ok. So just gonna hand it on to sell. All right now. Hello guys, uh, listeners that I'm F Y zero, placing Enniskillen. So I'm gonna be talking to you guys about pediatric cardiology today. Um I've just, is that, is that Phil Screen or is it? Yeah. I think, I think it's fine if, if everyone can just click on the full screen button, I think it's fine. Yeah. Okay. Um, should I start? Yeah. Okay. So today guys, we're gonna be talking about pediatric cardiology, high heel topics for the exams, dividing it into cyanotic heart disease, non signing up cyanotic heart disease, infectious diseases and then some buzzwords and genetic associations, which are probably important for exams as well. So, we're gonna start off with the cyanotic heart disease is, it's very commonly known as the five teas. So, tetralogy of fallot, tricuspid atresia, truncus, arteriosus transposition of great vessels in total anomalous pulmonary venous drainage. The two have highlighted are tetralogy of fallot and transposition of great wrestles because they tend to be most commonly looked at for exams. Um, looking at the general manager one second. Sorry. Um, I don't think the slides are changing. Are they not seeing you? Mhm. Uh huh. Yes. Yeah. It's working now. Yeah, it's working now. Is it feel full? Which, which side, uh, cyanotic heart disease? Is it feel full screen or? Yeah, that's fine. Yeah. So, yeah, I said to you the five different types of cyanotic heart disease. So, the general management of a cyanotic child, um, of the sign on a baby in particular is quite important. So for life and for exams which generally presents is they'll say to you, you have a baby who's breathing very, very rapidly elevated respiratory rate, patient will have a central cyanosis. Um One thing I just want to draw your attention to is not on the slide. But I mentioned the central cyanosis here. If you've seen an exam question or you're outside in real life, you see a peripheral cyanosis. If you see cyanosis of maybe the fingers of the toes, this is actually quite normal in the initial stages of of life. And this is because due to vasal motor changes that you experience within the smooth muscle of the vascular tissues. So if you see peripheral cyanosis, it can sometimes be normal. And this is known as a crow cyanosis. But if you see central cyanosis, it's always pathological and this is when the general management of cyanotic baby should be sort of initiated. So the ABC approaches, you know, looking at the airway, the breathing circulation, you know, that's, that's the standard stuff. But um when we see a cyanotic child, we do two things. We can do something called the nitrogen washout test. I've not mentioned it here, but it's essentially you want to give the baby high flow oxygen at 100% 15 liters for 10 minutes. And then you want to do an A B G and check for the arterial concentration of the blood. If the arterial concentration of the blood is very, very low. It indicates that the patient has a cyanotic heart disease and it's a duck dependent condition. If the patient's oxygen saturations improved, then that you find, then you can investigate why that happened. But generally, if, if for example, purposes, when they ask you and give you a lot of options of what you want to do, first line, you want to give them prostaglandins. So I've written there, maintain concurrent flow between, maintain concurrent flow. So what prostaglandins will do such as a lot Christodoulou in the 5 to 29 g per kilogram, per minute to minute, they maintain the patency of the doctors arteriosclerosis. And that's the first sign as I've highlighted there. So one thing I've written below that is what is the normal closure. What is the normal physiology of dot closure? So what happens is when we give birth? Um So when, so generally what happens is the placenta, secretes, prostaglandins, okay. Prostaglandins, uh endogenous prostaglandins that are secreted from the placenta. Alec Chrystal is obviously uh exogenous book for giving it as a form of medication. But endogenous prostaglandins will maintain the patency of the doctors arteriosus. Now, if we go back to embryology, the doctor's arteriospasm allows us to bypass the lungs and essentially oxygenate the blood through the placenta. Now, what happens is when we get rid of the placenta and the stage three of labor, what happens is the placental Rwandans will gradually reduce and then over 2 to 3 days, the doctors should close spontaneously by itself. Um continuing on. We want to limit oxygen therapy because that can again promote the closure of the ducks and we want to correct acidemia and then investing in investigative underlying disease. So generally, in terms of exam point of view, if you see central cyanosis, the first line management, apart from A D C would be across the London's. And uh other things you want to do is you wanna correct acidemia and investigate underlying disease the next flight. So this little bit of a case I brought up, I thought it'd be good to look at it from this point of view. So this is a two week old baby was okay at birth. However, struggling to feed on, feeding and crying, she turns blue. I've given the chest X ray there, you know a couple of headings as well. So I'll give you like five seconds. I mean, if you want to think about what it is before I move on. So couple of things I've highlighted here was okay at birth. Now, this is another rule about cyanotic heart conditions. If you see a patient that is cyanotic at birth, it's most likely gonna be from exam point of view, it's most likely gonna be transposition of great vessels. As I said, that's the most common, one of the more common diseases to bring it exams. But if the baby was okay at birth and then 2 to 3 weeks later is when the problem is occurring, that's when we're gonna start thinking about tetralogy. Of fallot. So this is one of our high yield sort of cyanotic heart conditions that we want to be looking at. So the Trelegy of fallot has four sort of uh four sort of uh anatomical changes that we have to be aware of. So we have an enlarged right ventricle, we have a ventricular septal defect. We have an overriding aorta and also a pulmonary valve stenosis. So they're just four things you have to learn. But what you can kind of uh attribute the one thing you have to understand about the presenting symptoms is that the symptoms or the severity of the symptoms is directly in proportion to the this the notice of the pulmonary valve. So if you ever get a question exam saying this patient, this baby's got tetralogy of fallot. Why is this patient experiencing all these symptoms? What is the real cause of the symptoms, the cause of the symptoms of the pommery valve stenosis, which is dependent on the overriding the of the aorta. So the level of overriding aorta resulting in a probably valve stenosis is what's going to cause your symptoms. Now, if we look back at what the case, it was maybe it was fine at birth, but the problem happened on feeding and crying and then she's turning blue. So that's something that we want to consider. So I've written above is hyper cyanotic spells which are tech spells. We refer to them as tet spells. What happens is we were having an increased oxygen demand which the heart cannot cope. So, increased auction demand, crying, feeding and exercise, that's when you have that cyanosis, increased respiratory rate, increased heart rate. So a common question that they can maybe asking preclinical Zoran post clinicals as well is something about why the baby squat. So if they ever, if you ever see, they sometimes say that when these patient's are having these hyper cyanotic or tet spells, the child will squat and this is do kinking the femoral artery. So I've said before, the anatomical problem in technology is a ventricular septal defect. So to visualize that you have to think that the pressure in the left ventricle is going to be higher than the right ventricle. So that's what we think. However, in this situation, because of the enlarged right ventricle, there is a right to left shunt. So normally in normal human beings, the pressure is higher in the left and the right ventricle. And that's basic physiology, basic cardio physiology. But here then the right ventricle enlargement and the pommery valve stenosis means the pressure is larger in the right and compares into the left. So you can have a high to low shunting, which is from right ventricle to left ventricle. Now, back to what I was talking about the squatting. So the squatting will increase the systemic vascular resistance. So if you get a kink in the in the femoral artery, you're gonna have an increase of increase of afterload. Now, I'm throwing up like around a lot of cardiac physiology terms here. So after load is essentially the force the heart has to overcome, to maintain its stroke falling. So after load, after load is really determined by two things, the systemic vascular resistance, which is the sort of the the blood vessels, the peripheral arterial blood vessels, which is what's gonna increase your books for kinking it. So, by kinking it, you're gonna increase the pressure there and uh your afterwards going to increase or by the aortic valve. So that's why it's diseases like the aortic stenosis, etcetera, there's an increase afterward, but that's not relevant here. So an increasing of the afterward, what that's gonna do is that's actually gonna cause a reversal of the shunt. So the pressure will then actually rise in the left side of the heart because the left side now is having to work harder. So the left side is still even in tetralogy, fact, the left side is still the one pumping to the rest of the circulation. So when the pressure on the rest of the circulation is increasing, the left side, left ventricle, in particular has to has to increase it increase its own pressure. So as left ventricular pressure rises to match the increase in afterload, that's when there's a reversal, the shunting. And that's why that's the baby sort of physiological attempt to maintain their oxygen sort of their their, their stroke volume and keep up with the increased oxygen demand. I hope that makes sense. If it doesn't, I can't see any questions, but if that didn't make sense, you just write it and I'll try to explain the best I can. Um, going to some more clinical sort of exam things. The murmur is an injection systolic murmur. Uh One would have thought okay. The patient's got a whole system, the patient's got a ventricular septal defect. VSD S are classically presenting with holosystolic members, commonly known as pansystolic members. So I've written, why not a whole systolic murmur, essentially ventricular septal defect is so large and tetralogy of fallot that it's uh that there's no holosystolic. So another thing that will come to later on is that the, the, the larger the, the whole or the larger the defect, the softer the murmur and then child you file the murmur, the defect of the ventricular septal defect is so large. There's no hole systolic murmur, looking at this chest x rays. This before this is our pathognomonic with tetralogy of fallot. It's got that sort of boot shape to it. And that's, you know, that's just something that you should learn. And then, yeah, this the baby since have surgical correction. So, um again, quick summary of that is that maybe presents fine at birth 2 to 3 weeks later when they're eating when they're crying, when they're, when they're walking around, they get cyanotic central cyanosis and they maybe can start thinking or squatting, that's gonna be to charge your fault. You know, the four, the four anatomical changes, surgical correction. And uh that's really everything into Trelegy folate. One thing maybe you should note is that associations tetralogy of fallot is tend to be associated with, it can be associated with the George syndrome. Um And then again, we'll come to that later on transposition of the great vessels. This is the second most common that comes up in exams in terms of cyanotic disease. Um It's very, very simple. Essentially, the aorta is coming off the right ventricle and the pulmonary arteries coming off the left ventricle. Very, very simple. Of course, that's the wrong way round and this is a failure. It is a cocoa no trunkel abnormality, which is again seen the George syndrome and there's a rotational failure that's occurred in this situation. Um These patient's are cyanotic at birth. So just remember in comparison to tetralogy of fallot, whether get cyanotic a couple weeks later, this is cyanotic at birth as soon as the duck closes. And when I'm in, when I say doctor, I mean, the doctors arteriosus and uh the, the, the only sort of good quote unquote, good thing about this disease is there's normally a concurrent ASD or A VSD promoting mixing of blood because it like, for example, if you close off the VSD, the ASD and the doctors arteriosus what you're having here is, then you're having just uh deoxygenated blood in the right ventricle going to the systemic circulation. And obviously, that's gonna cause cyanosis hypoxia and ultimately death. So the advantage of the, of the ASD S and the VSD is promoting the mixing of oxygenated and deoxygenated blood. So there is still some oxygenation getting to the peripheral tissues. And that's why we, again, in the situation, we have to, we have to get prostate gland and to maintain that mixing. And the management here is the arterial switch procedure. Um Looking at the chest chest X ray is a little bit different. It's called an egg on a string. I mean, yeah, that's just the definition of it. That's uh that's sort of pathognomonic with that. Um Yeah, so I'm not gonna focus on too much on the other cyanotic heart disease is because obviously, I don't want us to take too much time, but we'll go into ventricular septal defect now. So this is the most common sort of um congenital cardiac defect that you'll see in babies. Um It's associated with fetal alcohol syndrome and Down syndrome, Trisomy 21. And it's a right to left shunt, meaning that the blood, the, the oxygenated blood is going to the left hand side. Uh Sorry, it's a, it's a left to right shunt. I don't know, I've missed uh that wrong. So, but it's an acyanotic shunt. So we're going left to right, high pressure, too low pressure and yeah, high pressure, too low pressure left to right. It's a acyanotic condition. These patient's will not present cyanosis at least in childhood. So, in terms of exams, you want to know about a whole systolic murmur. And I've written there, the noise paradox, the largest the defect, the quieter the murmur. And that's because I've mentioned that already, there's a failure to thrive and they can eventually develop features of heart failure. Complications include right ventricular hypertrophy. It makes sense because the blood is going from the left ventricle to the right ventricle, from an area of high pressure to an area of low pressure, you're obviously gonna increase the increase the wall tension in the right ventricle, which I don't know if you guys remember the places law that's gonna promote a right ventricular hypertrophy. But don't worry about uh um event. Again, heart failure mentioned an infective endocarditis, non laminar flow, which means um the ventricular septal defect. So you have a ventricular septal defect. And when the blood goes from that area of high pressure through an area to an area of low pressure through the whole, it's like it's something called venturi force is what happens is they're going from an area of high pressure to an area of low pressure. It's gonna speed up through the whole. So it's gonna, it's gonna go from the left and go to the right range, but it's so fast to the whole the defect and that's called non laminar flow. A non laminar flow flow uh predisposes to uh to nonbacterial thrombotic uh thrombosis. So that's when infective endocarditis can happen. And that's because there is a pro thrombotic state in that situation. And you should Meyer syndrome. Again, this is something quite important that you should be aware of is that this general presents maybe 30 to 50 year olds, longstanding, left to right shunting. What happens is there's a vascular remodeling within the lungs. So there's a pulmonary vascular remodeling because the pulmonary pulmonary vasculature is going to have such a increased volume of blood that it's getting exposed to. So from the left to the right, so it goes from the left ventricle to the right ventricle to the pulmonary artery to the pulmonary vasculature. Because of that shunting, there's a recirculation of blood and the pulmonary vasculature is getting exposed to more blood than it would normally do. And because it's getting exposed to more blood, it's gonna incur vast the remodeling and it's gonna this vascular remodeling predisposes to right ventricular hypertrophy. And then what happens over time is the right sided pressure is over greater than the left side of pressure. And when that happens is the reversal of chanting because again, we're always going high, too low. So when the right side of pressure increases, it's going to go to the left, it's gonna go from right to left. And that makes sense that's gonna cause cyanosis because in the right ventricle were predominantly, we have, we only have the oxygenated blood. So, from the right ventricle to the left ventricle, back to the aorta. And that's when we're gonna get the presentation of cyanosis and the only man and the and the other things you get in this patient's maybe finger clubbing as well. And the only management for Asian Mark syndrome is a heart lung transplant and these patient's turned have a poor prognosis and this general presents around 30 to 50 years of age, anywhere in that sort of middle aged period, atrial septal defects. Um These are again very, very common. The most common type of atrial septal defects is osteo condom, which is more common than the other one which is osteo premium. So 70% of atrial septal defect. So, due to an ostium secundum defect, again, that's just sort of a definition. Um You guys should be aware of clinically. This patient have a failure to thrive and there's a key sign, you may have an injection systolic murmur, but the key exam finding that you'll see on your M C Q S is a fixed splitting of S too. Now, what this means is if you look at the diagram of the photo that I've inserted above the thing that you normally have is you'll have the, it, the aortic valve. Well, so back to basics. What is S two S two is the closure of the aortic and pulmonic valve because at the end of systole. So what happens is in physics and physiology, normal physiology, the aortic valve will tend to close before the pulmonic valve. And that's just normal physiology. So you can have a physiological splitting. And that's because what happens is when you're, and that's on inspiration. So when you breathe in, what's gonna happen is the intrathoracic volumes are going to increase. And that's because and then more blood will be in the right uh in the right ventricle. So it's gonna take a bit longer to close, you know, that, that gets a bit too complicated. But if you just from the basic standpoint, you're gonna get a fixed splitting of s too. So you can see it is that the A two, the aortic valve will close before the pulmonic valve. And this is because due to increased right ventricular pressure because there's more blood in the right ventricle because of the V S because of the, because of the ASD again, asd left atrial pressure will be greater than right atrial pressure will go left to right, right left atrium too, right atrium into the right ventricle. And that's again, a recirculation of blood. So the right ventricular pressure will increase there by the pulmonic bowel will take longer to close. And that's why we get a fixed splitting of s too. Again, the treatment is depending on the size of the defect. It's a small defect, we can leave it alone if the larger defect will go for a surgical fixation, I brought, I'm trying to bring your attention to something called a paradoxical embolism here. And this is something that can come up in exams quite commonly. And actually actually saw a patient, I was placed in a stroke ward a couple months ago and I saw a patient 21 year old male with a severe total anterior circulation stroke. It was the emcee AMC A stroke and an A C A stroke. And the reason for this was the patient without my mountaineering, he complained them some swollen calf, something like that. And what happened was what happened was the stroke, the clot from the, from the deep vein, uh the deep veins of the leg went from the veins to the archery. So if you think about it, the veins and arteries shouldn't be mixing. So if you have a DVT, it shouldn't go to the arterial side. But the only way for that to happen is for there to be a hole in the heart. Okay. So as mentioned, there it goes venous occlusion too, arterial occlusion through a temporary reversal of the shunt. So there's three ways it can go through an atrial septal defect, which we're talking about. Now, it can go through a ventricular septal defect, which is a bit rarer and finally, a patent Foramen Valley. So there's three ways there are three shunting that can happen here and it can go through there. But I've already told you that generally these shunts are going from a higher pressure to a lower pressure. So how will it go from the right to the left? If normally it's always going from the left to the right, when I say left, right, I mean, left side of the heart, which is higher pressure on the right side of the heart. So it's normally gonna go left side of the heart to the right side of the heart. But in these situations, the venous circulation will obviously enter into the, into the right atrium. So how does it go from the right atrium to the left atrium of the left ventricle? And that's because of the temporary reversal of the shunting. So, in periods of increased intrathoracic pressure such as coughing or straining, there can be a temporary reversal of the shunt. And that's when Venus inclusion has gone up to the right atrium and gone into the right ventricle. And it's not going away to the pulmonary artery causing a pulmonary embolism, which is the normal path of physiology or pes. It stayed in the right atrium or the right ventricle. More commonly the right atrium, the patient will be called for strained or going to the bathroom. And what's happened is is a temporary reversal that shunt and it's gone from the right atrium to the left to the left atrium or right ventricle to the left ventricle and then from the left and then from the left ventricle is gone to the rest of the body and the arterial circulation. And that's why the patient had a stroke. And that's something to be aware of because that can come up in exams. In clinical practice, you might be on the stroke or did you see your, how is this 21 year old had a stroke? And most commonly, it's because of this complementary diagnosis of these intraseptal defects or ventricle. Several defects can be done by echocardiogram, paid Informant Valley because it can sometimes disappear. You can sort of expose it on a sea lion bubble test again, something you should be aware of moving forward to the persistent doctors, arteriosclerosis. Again, another high yield acyanotic condition causes include congenital rubella syndrome, presenting with sensorineural deafness and cataracts and prematurity being born premature or high altitude births, which you know, I mean, it's not something to be aware of, maybe just be aware of that. So generally, what happens is how does the doctors are serious uh function. So I mentioned to you, the doctors are serious um is a right to left shunt that's being used over to sort of skip the lungs because all we know that in, in, in fetuses, the lungs are not really developed okay. So to skip the lungs and the oxygenation occurs via the umbilical vasculature, want to skip the lungs. So we go right to left and that's what the doctor materials is However, when the babies take their first inspire a tree breath, this is the vast, the pommery vascular resistance will grad will dramatically fall and this will cause a reversal, the shunt. So I know it gets a bit complicated, but right to left is so we can bypass the lungs. You can just think right ventricle, well, normally go to the lungs and then back to the left atrium, but we're bypassing the lungs were going right to left. However, when we take our first breath, the basket resistance and the lungs will drop. And that's the reversal of the shunt because it goes from an area of high pressure, too, lower pressure. So we'll go left to right and left. The right is the common denominator that we're seeing in these acyanotic conditions, which is A P D E A A S D and A B C D F VSD. We're going from higher pressure to lower pressure. So, from the left to right, and that's causing a recirculation of blood, which is again the same thing that's happened in A S D and A VSD. So uh that's, that's something to be aware of and classically in exams, these patient's present with the failure to thrive difficulty and feeding per a weight gain. Clinical examination findings are continuous machinery like murmur along with a subclavian thrill and a wide pulse pressure and the management of these patient's is endo thumb is in or Ibuprofen, um especially if it's, if it's early on, later on, if it's been there for a very long, long time, and the patient will be seen that a surgical fixation, but early on in life, you can do a bit NDTA missing or Ibuprofen. And the reason we are suggesting these are because these are prostaglandin antagonists. And as we said before, prostate landing is what maintains the patency of the PD A. So if we can remove the prostate gland and that's we can promote the closure. Infectious disease is something that comes up quite commonly. There's two types really that I'm gonna talk about. It is rheumatoid, rheumatic heart disease and Kawasaki's disease. Sorry, rheum, rheumatic heart disease, very, very common in the sort of Asian population or in the developing world. It's a group of streptococcal infection. A primary group of streptococcal infection and the streptococcus pyogenes or a throat infection. Then a couple of weeks later, the patient's represent cardiac symptoms are not sure why. This is because of something called rheumatic heart disease. And how does it work patho physiologically is a type two hypersensitivity reaction between molecular mimicry. So what happens is um there's antigen deposition on the heart valves. And what happens is we have self, the antibodies are created and the antibodies to the group of streptococcal will attack the heart valves causing the problems here. And then the UK the diagnosis made through the Jones criteria, which is utilizing a major and minor criteria you need a couple of major and a couple of minor or just two major. I don't know the exact breakdown. You should maybe look it up but it's not that important. Undergraduate level four things is erythema Marguerite. Um, Margon. It, um, is a, it's a sort of rash that you can see. I think it's best to put a photo over here but you look it up. It's very, very simple. It's just a sort of spreading rash. Cinnamon's corach cinemascore, a sort of involuntary corretora movements. Something that you may be seeing Huntington's disease. It's a sort of a similar presentation in here. Pancarditis is any sort of cardiac abnormality that can present on 80 kg, maybe valvular disease, endocarditis, anything that presents in relation to rheumatic heart disease and almost pancarditis. And then some Catania's nodules. We also want to have an A S O titer, positive titer S O is basically indicating the previous group. A strep tickle confection, um, in the acute phase will treat this with non steroidals. And we can also consider long term Benzel penicillin, prophylaxis to avoid um, rheumatic heart disease. And that's so the the rheumatic fever will be treated with the NSAID and to avoid the rheumatic heart disease progression. We'll use benzoyl penicillin, rheumatic heart disease. Classical presents can lead to long term micro stenosis. It can also result in aortic stenosis more commonly mitral stenosis. But just for knowledge sake, if you ever see an exam question and the patient's called aortic stenosis at a younger age. Um Obviously, one of the options from your cardiology learning will be a bicuspid aortic valve. But if they mentioned to you that there's been few JRL of the commissaries of the aortic valve. So fusion of the commissaries, that means that it's dramatic heart disease. So if you have an aortic stenosis due to calcifications or bicuspid valve, they'll mention about, they'll mention uh mention this calcium deposits. But if it's due to rheumatic heart disease, they'll mention a few Jher of the aortic commissaries. But again, mitral stenosis is much, much more common than the aortic stenosis and you can get dramatic heart disease. Cava sake's disease. It's a sort of a, it's a sort of syndrome which is a resistant pyrexia over five days. No improvement with antipyretics symptomatically. These patient's present with strawberry like tongue conjunct, uh conjunctival injection, cervical lymphadenopathy and cracked lips and these patients can get very, very unwell. You treat them with high dose aspirin and I V I G. Um could not hear that this is the only indication for aspirin and Children because it can cause rice syndrome. It's something you guys should look up. But I think it's got hepatic involvement. So this is the only indication. Another high yield factor know about Kawasaki's disease is that you should be screening for coronary artery aneurysms with echocardiograms because that's a complication of Kawasaki's disease. Um Coronary artery aneurysms do to Kawasaki disease can actually predispose these patient's to my cardio infarction. Even if they don't develop a coronary artery aneurysm. Kawasaki disease can cause a sort of vasculitis of the corner of the coronaries resulting in end of the dysfunction. And that's you can cause another M I there. So Kawasaki disease can actually result in M I is later on in life as well. But yeah, they're the high you'll facts. But the the the infectious diseases, coronary artery aneurysm echoes needed high dose aspirin. The only indication for aspirin and children's and Kawasaki's disease. If you got a patient who's having a fever, that's just not going. Think about Kawasaki's Medicare diseases. Think about mitral stenosis later on in life. Think about the Jones criteria type two hypersensitivity. But yeah, that's it. And then going on to exam associations. These are just sort of basically random facts of pediatric cardiology I put in because they didn't fit into the cyanotic diseases, but they can come up in exams, innocent murmur. So if you get a patient in an exam or in real life, young patient, completely healthy asymptomatic, the murmurs, you kind of hear it but then it goes away and it comes back and there's no symptoms. Think innocent murmurs, two in particular is a stills murmur is that the left sternal edge and venus hum czar infraclavicular early. It's just turbulent flow through the great things. And again, the stills murmur, it generally comes and goes depending on the positioning as asymptomatic cardiac tumors that we should be aware of. The most common cardiac tumor is met in all populations. So, if a patient has a cardiac um are the most common causes met. But in Children, the most common cause of tremor in cardiac in cardiac tumor is rhabdomyosarcoma and this has got an association with tuberous sclerosis. Uh discourses is another condition you guys should be aware of because it's got quite a high, quite, quite like severe clinical presentation in Children um with rushes and sort of e G abnormalities as well. Atrial myxoma. It's uh it's a bit, it's very uncommon, it can really present it later on in life, but also in teenagers, something to be aware of it presents with a position dependent syncope. It's occurring in the atrial is and uh histologically represented the mucopolysaccharide stroma cardiomyopathy in Children. Generally, you can have restrictive cardiomyopathy and that's due to end of cardio fibroelastosis. So, endocardial fibroelastosis is the most common cause of restrictive cardiomyopathy. In Children. You can have a hypertrophic obstructive cardiomyopathy, which is an autosomal dominant inherited condition. And classically, these Children will present with a diastolic dysfunction. So they'll be having an S four exertional syncope, a sudden cardiac death and there's a left ventricular outflow tract obstruction, sometimes some high level questions. They can ask you what, why is the left ventricular outflow tract obstruction occurring. There's two reasons. So, one of the reasons. Obviously the, the hypertrophy of the, of the, of the most commonly of the interventricular septum. But another thing is there's also a systolic anterior motion of the mitral valve and that I I didn't think you people would need to know that, but that's actually come up in an exam, I've done past medical school. So something, something to be aware of genetics and the exam associations. Again, cooptation of the order, which we haven't really mentioned. But some key examination or some buzzwords to be aware of is unequal pulse is between the upper and lower extremities. There might be a delayed femoral pulse and you want to do a pre doctor versus a post doctor, oxygen saturation. So you can do oxygen saturations of the maybe the right hand of the left foot and you want to see what's happening here and they'll generally maybe hire to normal on the right hand, but very, very low in the left foot. And that could be due to a cortisone of the order. It's gonna association with Turner Syndrome. Turner syndrome is 45 X O, you know, short stature, web neck, endocrinologically disrupted. And the card actually cardiac manifestations, cooperation of the order. You can, you can also get a bicuspid aortic valve entire syndrome as well. So there are two things you want to be aware of VSD S I mentioned, associate with Down Syndrome and fetal alcohol syndrome, gonna Trunkal abnormalities such as um such as the uh forgotten, but I mentioned it before but the our arteries coming off the wrong parts. That's the door syndrome. Uh Epson's anomaly, it's uh if the mother has bipolar disorder or she's taking lithium for some reason, other than bipolar disorder, it can result in absence, anomaly absence. Anomaly is a condition with this atrial ization of the right ventricle. There's a very, very low insertion of the tricuspid valve. So there's a very, very large right ventricle. This patient centered right ventricle, I perch free right bundle branch blocks and tricuspid regurgitation as well. How come I've mentioned already? But the genetic association is a bit of mice and heavy chain and protein C mutations and then dilated cardiomyopathy um is a bit different. It can cause TTN all those almost, it comes from TTN autism a dominant. So I'll just send one second on this as well. So how come is due to be itemized and heavy chain and protein C mutations but results in uh diastolic dysfunction of the heart. Whereas dilated cardiomyopathy is a systolic dysfunction of the heart. So, in how come you'll get an S four? Whereas in dilated cardiomyopathy, you will not get an S four. And one thing to be aware of is that if in an exam situation, they mentioned a 19 year old with an F three under the age of 30 years of age, an S three heart sound can be physiological. So don't always be concerned. But however, if they mentioned the presence of an S four heart sound, that can indicate that it's a uh got a hypertrophic obstructive cardiomyopathy. Um But yeah, that's, that's everything I had to say about all the different cyanotic acyanotic, some other infectious diseases and other things as well. Um If you guys have any questions, sure you can ask away. I think one question um in the chat function saying, can you please explain why babies can be re squat for T U F? Yeah. So squatting is as follows. So when you have T U F, the hyper cyanotic or tet spells that you're experiencing is because of an increased auction demand. So let's say babies crying, he was exercising or feeding that you know, that's going to require an increase of blood flow to particular organs or increased auction demand. So they're working harder. But because of the cardiac uh anatomical disruptions due to tetralogy of fallot, they can't keep up with that oxygen demand. So that's when they go blue. Now, what babies do is they'll squat, okay. So they'll squat and they'll sort of kink their legs. What happens is if you think about it, when you're squatting, you're gonna cause a kink in the femoral artery, the femoral arteries are very, very important artery, very large artery of the body. If you guys are aware, what happens is when you kink an archery, you're increasing the systemic vascular resistance. So essentially systemic vascular resistance is very simple. It's just sort of pressure in the, in the arteries of the periphery. But when you're kinking it, you're gonna increase the pressure that it has to overcome. So, an increase in the systemic basket resistance will cause direct implications because an increase in the systemic basket resistance is an increase in the afterload. These two are interchangeable, as I said to you, after load of the heart is the force the left ventricle has to overcome to, to pump blood or maintaining stroke volume. So, afterload most commonly is uh illustrated through systemic basket resistance and also the patency of the aortic valve. So remove the thought about the aortic valve for now. So afterload in this situation is equivalent to systemic vascular resistance. We had just increased the systemic vascular resistance by kinking the femoral artery. That's what what babies have done by squatting. So the afterload, the systemic basket resistance increased. Therefore, the afterward has increased. Therefore, the left ventricle is to pump more to overcome that afterload. Now, to pump more left ventricle acid, thereby increase the pressure within itself as well. So at the pressure in the left ventricle will increase the the shunt will reverse. Because remember in tetralogy of fallot, it's a right to left, it's a cyanotic condition. So it's going from the shunting is going from an area of high pressure in the right ventricle to an area of lower, comparatively lower pressure on the left ventricle, but to compensate for the increase afterload, the left ventricle increase its pressure and the increasing pressure in the left ventricle will then override the pressure in the right ventricle. And there's a reversal of the shunt, thereby decreasing the cyanosis it's occurring. Yeah, that sounds okay. Um, I think that was fabulous. Thank you so much. Tell her, I think that's the end of the talk for today. I've just posted the link for the certificates down in the chat box. If you can fill it up, you can get a certificate automatically onto your metal account. And if you do have any questions in the meantime, posted onto the chat function right here and we do aimed to run these sessions over the next few weeks every Monday around this time. So just stay tuned in, keep a look out on our social pages. So we'll be posting mainly over there. So, thank you.