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All you need to know - Cardiology part 3



This on-demand teaching session is delivered by Prin, a fourth-year medical student at GD PPA University in Romania. He dives deep into the topic of heart diseases and heart failure. The lecture covers congenital heart defects, including atrial septal defects, ventricular septal defects, tetralogy of Fallot, and coarctation of the aorta. It also touches upon valvular heart diseases and cardiomyopathies, leading to the end discussion of infective endocarditis and eventual heart failure. Precise examples of clinical cases are given throughout the session to test listeners' understanding. The session aims to enhance participants' knowledge about various heart disorders, their causes, symptoms, and treatments, making it highly beneficial for medical professionals or students specializing in cardiology or internal medicine.
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All you need to know for your preclinical cardiology exams!

Cardioresp Mechanisms - 10am

Cardiac Cycle and ECGs - 11am

Heart Disease and Heart Failure - 12pm

Pharmacology of Cardiology - 1pm

Learning objectives

1. Understand the different types of congenital heart defects, their manifestations, and potential surgical interventions. 2. Develop an understanding of how congenital heart defects can progress to heart failure if left untreated. 3. Gain insights into the separate valvular defects and learn to distinguish between stenosis and regurgitation. 4. Recognize symptoms of different heart defects, effectively read and interpret relevant tests such as transthoracic echocardiograms and angiographies. 5. Master an approach to managing heart disease and heart failure, including the understanding of preventative measures and surgical interventions when necessary.
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Computer generated transcript

The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hi, everyone. Thank you for bearing with us while we had a little bit of a technical problem, which is now sorted. Um So we're gonna start with our next lecture which is on heart disease and heart failure. So, over to you, print you. Thank you very much. Thank you very much Charlie and thank you to be a for this opportunity. Uh So today, um my name is Prin, let me introduce myself and I'm 1/4 year medical student at GD PPA University um from Romania. And we gonna uh I'm gonna present today heart disease and heart failure. Ok. So what are the topics that we're gonna cover? We're gonna cover the congenital heart defects uh um and valvular defects and the cardiomyopathies and infective endocarditis. And in the end how uh how all these um pathologies leads to heart failure? So, uh the congenital heart defect disease, as you know, it could be atrial septal defect, ventricular septal defect tetrology, phal and uh the coact so in the atrial septum effect, what is the problem? The there is uh there is a whole uh there is a passage between uh in the atrial se um uh in, in the a interatrial septum, sorry, in the a interatrial septum. So what happens, the blood will start passing from the left atrium of the left or the left side of the heart to the right side because and why uh there should be a question that why is the blood moving from left side to the right side but not from the right side to the left side? Right. So just because the pressure in the left side of the heart is higher than the right side of the heart, the blood is gonna move from the left ventricle to the right uh uh left atrium to the right atrium. Ok. So what, what's gonna happen is that there has to uh because of this transfusion of the blood, right. So the workload gonna increase for the heart as well as for the lungs because the oxygenated blood from the uh left side is mixing up with the deoxygenated blood on the right side. So, lung has to work hard to oxygenate the same amount of blood again and again. And the wo then the workload for the heart will also increase because it has to uh pump that amount of blood, right. So most of the time uh uh patient may be symptomatic, ok. Uh or or may present with reduced heart function. Uh Some um some presentation would be with the shortness of breath, murmurs, palpitation and edema. Ok? So, after childbirth, this atrial septal defect most of the times heals by itself. So we don't have to do any surgery or something. Ok. But if it's unresolved, then we have to operate the patient ventricle septal defect, it's the same mechanism. But this time the passage is, uh, in the, the hole is in the interventric septum. So, the blood from the left, uh, ventricle will, uh, move into the right ventricle and this diffusion of, uh, oxygenated blood into the uh deoxygenated blood. That's gonna happen. Uh It's same because um for um patient might not pre patient might be asymptomatic and may present with reduced heart function. Uh presentation is almost same murmurs, failure to thrive and some uh you know, uh uh fast breathing and shortness of breath. Uh uh uh this is again, same because it's gonna resolve by itself after childbirth. Ok. But if it's unresolved, we're gonna operate the patient again. Tetrology of palate. Tetrology of palate is something. It's, it's a syndrome and it is characterized by four defects. Ok. So what are those four defects? So, there is a ventricle septal defect that we just studied ventricle septal defect and then there is a pulmonary stenosis. So, pulmonary valve over here is a stenotic stenotic. What does a stenotic mean? A stenotic means that the valves are not opening properly? So the valves are not opening properly fully. Um Then there we have a overriding aorta. What does aorta means overriding aorta? Is that AORTA is displaced from a normal position to a position that it is placed just above the, above the interventricular septum. Ok. So just above the intraventricle septum, the aorta is placed. So what will happen is that most of the blood gonna enter into the aorta and the uh even from the even from the right side of the heart, the blood gonna enter into the aorta. Then the fourth defect is the ventricular hypertrophy. The right ventricle hypertrophy, you can see this uh look at the depth of the myocardium, it's hypertrophic, right? So how do the patient, uh the patient's gonna present uh to you, the patient might um uh deal with, you know, a S may have sinois, why Sinois again? Because sinois is gonna happen because what is happening here, you have to understand that in the other septal uh in the other defects, what we studied before the the oxygenated blood was diffusing with the deoxygenated blood, but it was going back to the lungs to get oxygenated, right? So there was no hypoxemia, there was no decrease in oxygen level in uh in, in your blood, right? Because eventually it was getting oxygenated. But what is happening here is that this mixed blood, that is the mixing of the blood is going into the systemic circulation, rather going into the uh pulmonary circulation. So, deoxygenated blood, some part of the deoxygenated blood is going into the systemic circulation. So eventually you'd know that there would be hypox, a little bit of hypoxemia, there would be little bit of uh decrease in oxygen saturation uh and partial pressure of oxygen in the blood. So that would lead to what sinois there that would lead to sinois and shortness of breath. OK. For this, we all um sorry again. Uh let's yeah, te fail to, to treat this patient. We al we always need to operate. OK. We have to do the surgery for this um coarctation of aorta. This is the fourth uh congenital defect, coarctation of aorta. What happens in coarctation of aorta is that there's a stricture kind of stricture. Um you can see over here. OK. So after the aortic arch, there's a stricture. So due to the stricture, what happens that there is stagnation of blood or high BP before proximal to the stricture or proximal to the coarctation. Ok. And um so this will lead to increased pressure in aorta in the, in the aorta and um the ascending aorta and also in the left ventricle. Ok. So this will lead to because there is increase in pressure in the aorta and the left ventricle, the left ventricle have to work harder. And when the left, then when anything has to work harder, we know that there is a proper uh I mean, if you guys were to study in morphopathology will study that the the skeletal muscle and the smooth muscles adapt to high work load by increasing uh you know, uh uh um becoming hypertrophic. OK. So the these muscles because they have to work harder. So, left ventricle uh uh smooth, uh the myocardial muscles will ha will get hypertrophic, right? Great. Uh uh It can also uh in sever cases of heart failure. Ok. Uh But, but what happens? So in this patient, we have to operate this patient. OK. So we have to do surgery. Uh these patient might present with difficulty in breathing, sweating and irritability and uh pale skin. So here's the question. And I wanna see a response from you guys. Uh I would wait for a minute to, for you guys to read the question and answer in the comments section. We've not had anything in the chart just yet. Oh, we just had d come up in the chart. OK. OK. OK. So I'm gonna read the question and we're gonna uh approach to that again. So a new a newborn baby is cyotic from birth. He, his cynos is worsen upon crying on examination, the chest is clear and systolic murmur can be heard and excerpt a summary from the transthoracic echocardiogram is below. So, atrial normal atria is of normal size, atrial septal is intact and then ventricle normal size, large ventricle septal defect. So first deformity, large ventricle septal defect noted with overriding aorta, overriding aorta and aortic arch is normal accompanying ecg normal and then a stenosis to right ventricle flow track above the pulmonary valve and the D arteriosis is patent. So we found all the, all the defects that could uh um highlight tetrology of fate and answer the option D is correct. Thank you very much. Moving on. Um Add to the second question, um I will hope for some more responses in the chat section. Thank you. Oh, sorry. All right. This was the answer slide out. This is the second question. I'm so sorry. Yup. One. Yes. This is the second question. Sorry. Yes, it, yes, exactly. So I'm gonna read the question again and we're gonna approach to the answer of a newborn infant is noted to have a Respi to distress too uh days after birth. Now, on examination, she is mottled and has a weak upper extremity pulses and palpable femoral pulse. Uh her arterial blood gas shows a profound metabolic acidosis. She has angiography done. So you have to just look at this picture and you will find there is a uh cot of AORTA. OK. This is a coarctation of aorta and this is uh um this is the stricture, you know, just after the aortic arch, this is the aortic arch and this is the stricture. Perfect. So what uh what you're gonna do? So you're gonna do surgery, as I said for uh tetrology of Fallot and for uh the coact of AORTA, you should just operate the patients surgery now to fix the issue. Perfect. Moving on, moving on to the valvular defects. So we're gonna study for valvular defects. OK. The first one is uh 1st 1st thing you have to understand what is stenosis and what is regurgitation, right? So, stenosis is when the the valves are not opening properly, right? So, valvular uh orifice has narrowed. Ok. Perfect. So what will happen whenever there is the valves are not opening properly? The blood through the valves would, wouldn't be able to um pass uh completely or properly in that. Uh if uh with that effective, OK. With that uh volume. Ok. Perfect. A regurgitation. What happens in regurgitation is that the valve opening is properly, but the closure is not proper. So the valves are not closing properly. So what will happen that the blood from the back will regurgitate into the proximal uh cavity? Ok. We'll, we will implicate this in the uh in the further topics and uh you guys can understand it properly. So normal heart sound, we all know that lub dub and L is the first heart sound. First, heart sound comes from the atrial ventricle closure. That is the mitral valve closure and the tricuspid valve closure lub sound. They make the dub sound is the second he he heart sound and they and uh it it is um uh done by the aortic and the pulmonary valve closure. Ok. Um Perfect. Uh perfect. Now, aortic stenosis, what about the aortic stenosis? That as I said, stenosis means the the opening is not proper. Ok. So when the aortic valve, so aortic stenosis means stenosis of the aortic valve. So, aortic valves are not opening properly. So what will happen that the blood from the left ventricle has to be sent in the aorta, right? The whole blood will not be able to pass through the uh this valve because the valve is not opening properly, it's not opening completely. So the blood will start the pressure in the left ventricle will start to accumulate progressively. And when the pressure will increase, I, as I said earlier, whenever the pressure increases in a cavity, there would be hypertrophy of those muscles. So there would be a hypertrophy of the left ventricle because the blood is not going there and it's come the pressure is building up in here, right? So that's uh gonna happen. Ok. So what is the cau cause for this? Why the valves become stenotic? That could be a question. Uh Perfect. So because of aging, because when we say aortic stenosis, there is this mostly present with aging. With aging, the valves become weak or they become calcified. So most of the times they become calcified uh with an age and they become stiff. That is the reason that they do not open properly. As you can see over here that these are some calcification on the normal tricuspid aortic valve, right. Another cause could be that a maybe the patient is born with a bicuspid valve. So you know that a normal aortic valve should have three cusps. Ok. But the maybe the patient was born with two cusp. Ok. So these kind of patient, like I have seen some patient who, who are with bicuspid aortic well, but they do not develop any symptoms till their like twenties and thirties. So after their third decade of life, they develop some symptoms. Um uh so this is one of the cause uh as well and then rare causes is rheumatic fever. So what are the symptoms? Symptoms? Is sri as for syncope, A for Angina, D for dyspnea? Perfect. So how are you gonna manage the patient? So well. So if patient is asymptomatic, you just keep the patient in under observation. So you do not do any intervention, you do not do anything, ok? For asymptomatic patient. But if the patient is asymptomatic and his left ventricle ejection fraction is below 50% we have to do a valve replacement, we have to replace the aortic valve. Ok. If a patient is symptomatic, then also we have to do the valve replacement. And if the patient is not fit for surgery, then we have another um another surgery which is called Ta Vi Tavi, uh stands for transcatheter aortic valve implantation device. Ok. So I'm gonna give you an overview about the valves here and the starting so that you do you will, you will have a better understanding of uh coming topics. So here we have the mechanical valve, this is a mechanical valve. So all the things which is uh you know, uh uh just based on mechanics basically. So because you, you can see these are the leaflets, there are two leaflets, they are right like this. But when the pressure builds up, it becomes like this and they close it. So they are doing like this moment, the prosthetic valves, prosthetic uh the bioprosthetic valves actually. So bioprosthetic valves are basically originated. Uh They are made from animals, OK. Then we have the sutureless, sutureless uh uh processes, but we don't have to really suture in because then you have to suture here, but you don't have to suture here. This transcatheter aortic valve is implantation device with this is quite good though because um you uh you just uh you, it's not, it's, it's like minimally invasive intervention because the, so basically you, you put uh you put a catheter, OK? And, and um you put the catheter inside the heart, uh the balloon catheter, OK. Balloon tip ca catheter. And then you put this valve on it and you just go to the aortic uh the valve area and you just inflate the inflate the balloon uh of the catheter there. When the balloon of the catheter inflate there, it is positioned there forever. Ok? Not forever. But yeah, until unless the patient is alive. Um aortic stenosis about aortic stenosis, you have to listen some murmurs. Um I don't know but because in clinical practice, I haven't seen really doctors listening to murmurs and then diagnosing. But it may narrow down some diagnosis for you that it's a systolic murmur or diastolic murmur. So it can narrow down, narrow down the options for you. But yeah, the the final diagnosis is basically made from uh uh the echocardiogram or EEC G and other things. Ok. But still we have to study the murmur so loudest over the aortic valve. So aortic murmur is always loudest at the aortic point. Where is the aortic point? Aortic point is over here, right? So on the right parasternal second, intercostal space, second, intercostal space on the right side, parasternal great and the sound, the murmur will radiate to the carotid arteries will radiate to the carotid arteries. Perfect. Now, I have added here, I wanted to add some add a video of the echo but I couldn't because it wouldn't play here. But then I took a screenshot of the video, then I added it here. Um Maybe it would be visible for you if you guys could see. And so the the valve. So the this is um uh parasternal long axis view of the heart. OK? And this is the mitral valve, OK? This is the aortic valve. This is the aorta and this is the left ventricle, this is the uh the left atrium great. So these are the mitral valves. So mitral valves are open and aortic valves are closed. So, could you guess what, uh what, what, which is, is the diastolic phase of the heart or is the systolic phase of the heart? So, it's uh, it's a filling. So it's a diastolic phase of the heart. Ok. Now, this is the aortic valve. This is a systolic phase, systolic phase that the left ventricle is contracting. Left ventricle has to pump the blood into the aorta over here. But could you see the aortic valves just this much open? They should open like completely but they are not opening completely. They're just this much open. So this is what is a stenosis, this is aortic stenosis. Ok. So echocardiogram really helps you to uh to the establish the positive diagnosis. This is a summary uh because of the shortage of time whatever I explained to you earlier. It's all in here. It's in summary, I'm not gonna I uh go through this over again. Ok, guys. Uh but let's see the aortic regurgitation. Ok. Aortic regurgitation. What is aortic regurgitation? The valves, the aortic valves this time are not closing properly. So the the blood from the aorta gonna reflux into the left ventricle. Perfect. So as you can see, this is a normal heart and these are the pressures as shown in the heart. We're not really, we don't really need to concentrate on that, but look at the aortic regurgitation figure. What what happens is that the blood should go from here to here but the blood is coming from aorta back into the left ventricle. That's abnormal, right? So that's the thing here that regurgitates the blood regurgitates from aorta back into the left ventricle, but not all of the blood, but few of the few part of the blood. Ok. So when this thing happens, so do you think cardiac output will be increased, the cardiac output will be decreased. Of course, it would be decreased. So less, less blood going into the system in circulation. That means cardiac output is decreased, ejection fraction is reduced and the blood is building up in here in the left ventricle, the pressure is building up again, left ventricle hypertrophy. That's what you would see. The causes. The causes are the uh the valve, the rheumatic heart disease, infective endocarditis and by asd aortic valve is again one of the causes for regurgitation. What are the sym symptoms? Symptoms would be palpitation, angina, uh syncope, autopia dyspnea and paroxysmal noc nocturnal uh dyspnea. Great. Now, how would you manage the patient? So, if there is any underlying infection such as endocarditis to first treat the endocarditis, right? If the patient is asymptomatic or have some mild uh symptoms, you keep the patient under observation. If the mild symptoms are present and the uh the if mild symptoms are present in the patient, you can uh give some drugs. So you can give some diuretics to decrease the afterload. You can give some vasodilators to decrease the afterload, um reduce systolic uh to reduce the systolic BP. We can give ace inhibitors such as um uh captopril. Ok? Ramipril. These are the ace inhibitors that you could give to reduce the systolic BP. I think my uh the second uh lecture gonna be about the drugs. So you might uh study them. Uh well, there um valve replacement and see where aortic regurgitation, we replace the valves. Ok? Um This is again, um So you have to understand that uh aortic regurgitation is a diastolic murmur. This is something you have to remember. Ok. So, systolic and diastolic. Ok. So, aortic stenosis was systolic murmur and aortic regurgitation is a diastolic murmur because this murmur is heard during the diastole of the heart. So you can see after the second heart sound, you can hear this murmur, ok? You're gonna hear this murmur more better when the patient is uh leaning forward. Perfect uh on the echocardiogram. Uh How would this appear? So, this is an image of a parasternal short axis uh view of the heart. Uh You can see this is the aortic valve. These are the three cusp of the aortic valve, but the aortic valve has some orifice, it's still open, it should be fully closed, right? But it's still open while they are still open because they are abnormal valves and the blood gonna regurgitate from aorta back into the left ventricle. You can see over here when we put on the uh color Doppler uh effect over here, we you can see that there is some flame sign uh which is visible. So this is aortic regurgitation. Uh This is again a short summary about that. And you could guys go over that because the presentation would be available to you after the lecture, mitral stenosis, mitral stenosis. So what is again, it's same, the the mitral valves are not opening properly. So, when the mitral valves are not open properly, the pressure will develop this time where the proximal chamber, that is the proximal chamber to proximal to what mitral valve, mitral valve. Uh then uh that is the uh the left aorta, right. So the pressure will develop into the left a uh um sorry what I'm saying? Left atrium, the pressure will develop into the left atrium. Ok. So this pressure due to the pressure developing in the left atrium, there would be a hypertrophy and enlargement of the left atrium that and when the pressure is increased in the left atrium, there would be a pressure increase in pulmonary veins and then into the pulmonary circulation as well. Ok. And then that that would lead to pulmonary hypertension. Basically, if you could just, you know, figure out like the whole me the whole uh pulmonary circulation, how it works. So, uh you, it would be easier for you to um imagine what's happening here. Uh So uh mitral stenosis is most of the times are always associated with rheumatic heart disease. Ok. Most common cause is rheumatic heart disease for mitral stenosis. So you can see that the mitral valve has narrowed here because of some vegetations of plagues, right of uh fibers, bacteria, uh fibrins and bacteria and platelets, uh mitral stenosis. The symptoms are quite same dyspnea, synopia, orthopnea. What uh what is the management? How would you manage this patient? So, if um if it's a mild mitral stenosis, we just observe the patient if it's severe asymptomatic. So we do balloon valvotomy. What is balloon valvotomy? This is balloon valvotomy. Ok. We, so we insert this balloon catheter from femoral vein into the, this is the inferior vena cava and from inferior vena cava, it comes to the right atrium and from right atrium, we make it across the interatrial septum into the uh mitral area, uh mitral valvular area. When the catheter reaches here, we inflate, we inflate the balloon so that the vegetation or any sort of calcification which are on the valves, they just breaks down and go away into the circulation and the valves are free to move again. Ok. So this is what we do balloon valvotomy. If the patient is very symptomatic, if it uh he presents with the severe symptom uh symptoms, we're gonna give beta blockers diuretics and we also gonna do this procedure to him and we gonna uh we may also do valve replacements. Ok. Um So mitral stenosis is a diastolic uh sorry middiastolic murmur. Ok, loudest over the apex in the left uh lateral obvius position on expiration. Perfect. Look at the echo echo over here, right. So this is a uh these are the four view of the heart. Ok. So first is the uh parasternal long axis of view of the heart. So this is the aorta, this is left atrium, left ventricle and right ventricle. So this is like a very good sign of mitral stenosis in echoes. This is called hockey stick sign because it looks like a hockey stick, you know, this kind of stuff. So it looks like a hawk sticks. So that's why it's called Hayti and it's very much seen uh in mitral stenosis. Ok. Sorry. Oh OK. And could you see left atrium is quite dilated here, right? It's quite dilated chamber is dilated. So it's because the pressure is building up here because the blood is not going able to go in the left ventricle and pressure is building up here. That's why they are dilated, right? This is the pa on the shot like says I get uh and you can see some ca uh some vegetation over here. C could you see these opacities over here? That's uh something um which uh and the mitral valve is not just not opening fully, it should open like till here, but it's opening just this much, right? Uh This is the apical uh apical view of the heart apical view. Uh This is the left atrium. Do you see how much it has dilated that it has almost like displaced the interatrial septum and you know, so the left, it, it's so much dilated when you put on the color uh Doppler here, you can see totally that um the how less blood is going into the left ventricle and most of the blood is just staying into the left atrium. Again, the summary mitral regurgitation about mitral regurgitation. Uh So again, the blood gonna go come back to the left atrium from the left ventricle. OK. So this reflects this is called mitral regurgitation increased in um Yes, yes, I can show you the summary if you have any questions. Let me know. Uh Do you want me to explain something? Yeah. OK. So I think I can move on. Ok. Um mitral regurgitation about the mitral regurgitation. Um So as I said, there would be a reflux of blood from left atrium, uh left ventricle to the left atrium during the systole. Great. So uh eventually the pressure is building up into the left atrium. It's same mechanism as what as it was in left uh the mitral stenosis. But uh uh when I in context of pressure development, so pressure is developing into the left uh atrium, increased palmary pressure, palmate pressure will increase and flu um fluid build up. OK. That would lead to congestive heart failure. OK. Um Prolapsing mitral valve is the most common c cause in developed world. There is quite a statistics about this that in developing world rheumatic disease is one of the cause for aortic regurgitation. But in developed world, there is prolapse of mitral valve prolapse because there is some uh uh uh uh how do you say connective tissue disorders? Again, mitral regurgitation symptoms are dyspnea, apnea, chest pain and fatigue. How you're gonna treat the patient? So that if it's um if the patient present with uh acute symptoms and acute onset, so you can give patient nitrates because he because he is having chest pain. So you have to give a vasodilator that is nitrate. So that nitrate because the, you know the coronary su uh the coronary supply of the uh of the heart is proper. So you have to give a vasodilator that is the nitrate. You have to give diuretics to decrease the afterload of the heart. You have to um give positive inotropic drugs. And this is a procedure procedure that we u that we do that. This is called intraaortic balloon counterpulsation. OK. And this is, this is done to increase cardiac output actually. Uh then we, we can also give uh uh if it's a case of heart failure, we have um many drugs we can give ace inhibitors, we can give uh beta blockers, we can give spironolactone which is a diuretic and uh you guys are gonna see it in the next uh lecture uh about the drugs and heart failure and all. So I haven't really get into depth about the drugs and all of them. Uh and see where regurgitation happens. Then you have to sur do surgery. Ok. So mitral regurgitation, you have to remember one thing. This is always, uh this always comes with a very important uh you know, highlight, uh it says pansystolic murmur, pansystolic murmur because you can s you can hear, listen, this murmur during the whole systole. OK. Uh So, uh during the whole systole, you can hear this murmur and it is loudest over the mitral area and uh it radiates to axilla. OK? When you look at the echo, this is um this is uh apical view of the heart. Uh You can see uh this flame sign. So flame sign, the flame sign is oh, sorry, flame sign is always as stated with um, regurgitation. So this is called flame sign. OK? It's look like a flame, a fire flame. Um So this is a high, OK. So the blood from the left ventricle, this is the left ventricle is coming back into the left atrium and this is uh the echo recorded as a flame kind of color. So that is flame sign. Um This is again the summary if you wanna have a look at it. Ok. Val uh valvular defect investigations. What are, what kind of investigation would you, uh would you like to do on a patient with va with val uh valvulopathy looks like, right. So you can do chest x rays, chest x-rays might just tell you about um you know, en enlargement of any compartment of the heart, such as left atrium, enlargement or left ventricle enlargement. But wouldn't be able to tell you more. It could be this enlargement if it's because of a stenosis, if it's because of um uh regurgitation. So for, to narrow that down, you always used echo echo is the best E CG might tell you about hypertrophy. Uh In E CG, you might uh uh you did the E CG part uh just the lecture before uh now. So earlier. So I think um in E CG, you might have learned about the hypertrophy of ventricles, uh left ventricle hypertrophy and how um uh bi fit B and um and uh the bifid P wave and uh you know, uh the aortic uh aortic hypertrophy. So this is, these are the all findings that you can find in E CG. Again, E CG doesn't uh precise the diagnosis. The precise diagnosis can only be made by echocardiography, which is the best. OK. Cardiac uh catheterization, angiography is also good, MRI and CT. Well, they're always good. OK. This is a question, I'm gonna wait and I would like to have as many as responses from you guys. Uh So have a minute. OK, I have got the first response. So I'm gonna get to the answer. OK. So what uh sorry. Um So this is the answer because the patient is symptomatic, right? The patient is symptomatic. So we have to do a valve uh um a valve replacement. Ok. So, because the pa uh as you said, uh the the patient, if the patient is symptomatic, you have to do the valve replacement. If patient is asymptomatic and the uh the ejection fraction is below 50% then we have to do valve replacement. So these are the two conditions for valve replacement uh uh indications. So we this was uh the question about um moving on to the next, this is the next question. A mitral regurgitation. Yes, because as I said, uh pansystolic murmur always comes with mitral regurgitation. So, pansystolic murmur, wherever you see pansystolic murmur, it's mitral regurgitation. Great. Thank you. Thank you very much, Aveed and Shreya uh for the response. Thank you, Miriam for the response earlier. Um Cardiomyopathies is the second topic that we're gonna cover. The cardiomyopathies. Could be of three types, dilated, hypertrophic and restrictive cardiomyopathies. The dilated cardiomyopathy, the ventricle stretch and thin ventricle enlargement. So, what happened is that dilated? You can just uh understand it from the term dilated that the vent the chambers are dilated. Ok. The they are dilated and the thickness of the myocardium is very thin, it's very thin. Ok. So when the thickness is very thin and the chambers are dilated, what's gonna happen? Do you think that the, the, you know they're gonna pump the blood very forcefully. No, they're not gonna pump very f forcefully. So there would be a decrease in um ejection fraction, there would be a decrease in cardiac output. And this is one of the uh one of the pathologies that could lead to heart failure. Ok. And it is mostly seen uh it just starts from left ventricle. So yeah, you know it's gonna severely affect the cardiac output. Uh OK. So what could be the cause? Could alcohol could be the cause? But most of the times you, you could, you would see that out of three patients. One patient, uh the cause is basically uh genetics. OK. So it's uh genetics and uh alcoholism, ingestion of some drugs, autoimmune disorders and thyroid hypertension and diabetes could be some of the other causes. Uh the present uh the uh the patient will present to you as a heart failure, pleural effusion, dyspnea, edema, chest pain, fatigue, and syncope. Uh how would you manage the patient? So, manage you have to restrict fluid and sodium intake because if you, if the patient is taking excessive fluid, if he's taking a lot of sodium. So you know, wherever the sodium goes, the water goes along. So sodium is, if the sodium increases in the system, the water will increase in the system, the the whole fluid level will increase in the system and already the heart wasn't working properly and you're basically increasing workload on the heart to increase more volume of blood. So that's something you don't wanna do, right? So you have to manage uh as a for the management, you have to first restrict the fluid intake and sodium uh uh intake. OK. Then you have to treat the underlying cau cause like as I mentioned, diabetes or uh HEPA thyroidism, alcohol intake and all these things, you have to treat all those underlying causes. If there's uh if there is presentation of heart failure, then you have to treat, manage the heart failure, then there are variety of drugs. The drugs uh will be mentioned in the next lecture, hypertrophic cardio uh cardiomyopathy. So, what do you mean by hypertrophic uh cardiomyopathy? That is the, the muscles uh the uh the myocardium would be hypertrophic. Ok. So, as you can see this is a normal heart and this uh this is a, a hypertrophic mus uh uh muscles of the um uh myocardium of the left ventricle. And could you see this um this mass? So this mass is basically obstructing the way of blood going into the aorta. So this is almost uh obstructing that um uh aortic valve. Ok. So the blood go not gonna go into the aorta. So there would be a dust uh uh and this is uh basically uh usually affect the left ventricle and you know, uh because there is obstruction, the this, this is gonna be a diastolic dysfunction. Again, this basically, this kind of uh hypertrophic cardiomyopathy leads to sudden card, uh, sudden uh death in young patients. It's one of the sudden cardiac death in young patient. Ok. It, it is most of the times a genetic cause, 50% familial inheritance and 50% is sporadic mutation. Ok. Um, the next is OK. The presentation, how would the uh patient present, patient will present with same kind of symptoms, some something similar such as it, uh, uh short uh shortness of breath, systolic, murmur, angina and sudden death. Uh Well, it's whenever you hear a young patients, sudden death and cardiac is the reason you should always think about hypertrophic cardiomyopathy. Ok. Management. How would you manage the patients? So you can give calcium channel blockers. Uh You can give um beta blockers which are basically the rate uh rate control drugs. Uh And um the then you have the um pacemaker which um for, you know, some sort of arrhythmias for that, you can indicate pacemakers, but something which is very important is we can do the surgery so we can resect this uh extra piece of mass. We can just resect it or we can do uh septal ablation. Ok. Uh So, resection is called septal myectomy because myocardium is being uh um uh cut off. So myectomy and then we have the septal ablations, ablation could be done by radiofrequency waves or it could be done by cryo uh cryos uh cryoablation. Uh Another one, another cardiomyopathy is restrictive. So, restrictive means something is restricting the myocardium to contract or stretch both. So most of the times the, the what will happen here is that the walls of the left ventricle will become stiff, become rigid. So there would not be any stretching. Ok. They will not stretch anymore. Are we running out of time? Ok. I'm going to be quick. Um, so they're not, they're not stretching very well. So during the diastole, when they have to fill with blood, so they would be able to stretch. So less filling. Ok. So less filling of the ventricles during, during diastole, this will lead to less cardiac output. Ok. And this is very much associated with uh some amyloidosis, sarcoidosis, a hemochromatosis kind of disorders. Um Again, um um the, the presentation is almost similar in all the cardiomyopathies, but the management is different. So if you treat, you have to treat underlying cause such as amyloidosis or sarcoidosis, you have to treat those, you have to give antiarrhythmic drug. If the patient will present with arrhythmia, most of the time they do present with arrhythmias. And uh you can do uh in severe cases, you have the only option you have is you have to do cardiac transplant. Ok. This is a question. Uh uh I don't have time. So I'm gonna read it and uh we're gonna uh discuss the answer. Ok. Great. So a 20 year old man uh present to the A&E uh depart uh emergency department following the fainting at home. He claims that he has lightheadedness of the from last three months. Ok. On taking a history, he said that the pa uh paternal uncle died of sudden card cardiac uh event aged 30 on E CG. They are narrow dragger like Q waves in, in fetal and later leaves as shown. So what do you think could be the reason? So these waves are basically showing um yes, sc yes. So it's hypertrophic cardiomyopathy because I in even because the, the drug like you is basically showing that there is a hypertrophy. And uh as I mentioned also that most of the times in at least stage patient died due to the hypertrophic cardiomyopathies. That's answer very good. Uh OK. Infective endocarditis, we have to jump into that quickly. Infective endocarditis is basically a multisystem disease because this bacteria which is in your system is damaging most of the organs. OK. So one of them is heart. OK. So heart valves and adjacent endocardium is damaged. So what happens that bacteria enters the bloodstream? OK. And they start forming vegetation on the valves. Do you see this valve? And they are forming vegetations, vegetations are made up of three components. They consist of bacteria, they consist of fibrins and platelets. Ok. So it's, it's not completely a clot, it's not a completely a bacterial culture. It's a mix of them. So they are, they form a vegetation on that and this becomes stiff and the valves are not working properly. This is the reason uh that lead to uh uh valvulopathy, right? The most common bacteria that is associated is streptococci. Ok. Uh M most of the time in clinical practice whenever you see um that a patient presented with a new murmur. Always remember, I'm emphasizing a new, new murmur with fever. It is more likely that the patient has infective endocarditis until unless it's proven otherwise. Ok. Uh infective endocarditis, we have Duke's criteria. We have Duke Duke's criteria to do the positive diagnosis. Great. So these are the major criteria such as blood culture. We did the blood culture and it came out to be positive. That would be one of the major criteria. Echo showing echo showing valvular vegetation, new valuable regurgitation murmur, new emphasize a new valuable regurgitation murmur. So these are the three m uh major criteria and the minor criterias are predisposing cardiac condition. IV, drug use IV, drug use such as any, you know, uh like cocaine or any kind of drugs. They, they used as an IV in uh in past recently, temperature more than 38 that is fever and then embolic phenomena um such as uh sprinter, hemorrhages and all and immunological phenomena such as glomer, nephropathies and rocks spots and pos and also positive blood culture, not meeting a specific criteria. So these are the minor criterias. Ok. So what how do we uh using this major and minor criteria, how we make the positive diagnosis for endocarditis. So we define um endocarditis, infective endocarditis as if the two major criteria are present. Then we say, ok, it's an infective endocarditis or we say if one major criteria and three of the minor criterias are present too. So it's a infective endocarditis or we say none of the major criteria. We don't care and all of the five minor criterias are present and we say it's a infective endocarditis. Ok. This is definitive diagnosis for endocarditis. But when we say, oh, maybe there is a possibility for infective endocarditis for that when it's only when one major and one minor criteria is present or three minor criteria is present. Ok, great. So here's a question. Uh I'm not go. Uh We don't have time actually. So we're running out of time. So I'm gonna just uh give you. So uh there, there is a 3031 year old patient present with one week of history of fever emphasize on fever, chills and fatigue. Ok. Now, here, past medical history includes me, includes mitral valve, prolapse, mitral valve, prora prolapse is basically telling you about what there is a predisposing cardiac condition. So one minor criteria check and hypothyroidism. She admits two infrequent intravenous heroin use IV, heroin IV drug use, 2nd, 2nd criteria check uh and 10 pack uh per year history of smoking. Now, uh physical examination reveals temperature of 39 that is fever fever that is third minor criteria, check her car. Uh her cardiovascular examination reveals a new emphasize on new pansystolic murmur, new murmur. That is one major criteria check. That is basically three plus 13 minus and one major. That is, we definitely know that it's a a def definite end infective endocarditis. Perfect uh investigation of heart failure. Uh So what is heart failure? Heart failure is basically a condition when the heart is not able to uh uh do its function uh effectively and appropriately. And uh with all uh you know, so basically heart fails to pump the blood. That's, that's how we can try to remember heart failure. There could be a lot of reason. It, there could be all, all the topics that we studied will lead to heart failure. Uh if not treated. Uh uh myocardial ischemia can also lead to heart failure and many other pathologies can lead to heart failure, heart failure. Ok. So chest X ray. Uh so how would you investigate uh heart failure? You can investigate it on chest X ray. You will see some cardiac enlargement, make sure pulmonary edema. It can be normal x-ray. Ok. Um It can be normal x-ray and still patient may have heart failure. So x-ray is not giving you all the briefs and details about the heart failure. So you, you don't really rely on that. But yeah, you can start with that E CG may show uh underlying causes uh arrhythmias and ischemia and left ventricle uh hypertrophy. That's all E CG could show as I discussed earlier as well. Uh Blood test, you can do blood test, you can do thyroid function test because when you have hyperthyroidism, there is a chance of heart failure when you have electrolytes, electrolytes such as hyperkalemia. When potassium s are increased in your blood, uh that will lead to atrial fibrillation and could lead to uh uh uh sorry ventricle fibrillation and could lead to a heart failure. Uh blood uh urea blood glucose test, uh liver biochemistry and look for anemia because anemia can also lead to heart failure. Actually, uh A NPA NP measurement serum A NP and BNP pro BNP. These are uh some of the which we, which you can distinguish heart failure from other causes of dyspnea, do dobutamine uh stress echo to uh identify those with hibernating uh myocardium uh uh myocardium disease. So, those people, uh those patient who in which uh myocardium uh disease is hibernating, that is no symptoms but still there. So you, you do the stress uh echocardiograph. So basically, you, you tell the patient to run a uh run on a standing bike uh uh to pedal that and then you check the echo and then you try to find out the, put on the positive diagnosis. What are the diagnosis? Uh What are the pharmacological treatment? These are all the pharmacological treatment II, wouldn't uh uh this wouldn't really help you to um if I take time to explain everything because you're going to learn all this in the next lecture in any ways, non pharmacological treatment, something I would like to explain to you. Uh um So you can do what, what you can do basically. So if it's, there is a myocardial uh infarction, if there is a uh my uh uh M I, so what are you gonna do in M I? So you revascularize the coronary artery, you rev you tried to revascularize the myocardium. How would you reco revascularize the myocardium? There is two possibilities. 1st, 1st, the one is uh coronary artery bypass graft. So basically, you take the internal mammary artery, which is not uh that useful artery, but you can take that internal mammary artery and then you l it it with in the coronary artery proximal to uh proximal to the obstruction and then uh to the tissue. So this is basically a bypass graft. OK. Uh Co bypass graft that you could do. You can do bi V pacing, which is always done in heart failure, heart failure is always uh do uh we do bi V pacing. Um And so the pacemaker is basically established is um again, uh and the pacemaker is basically sensing and uh in both chambers in the left and the right ventricles, that's why it's called biventricular pacing replacement of the disease valve. If there is any valvulopathy, you just uh do the valve replacement, uh surgery, cardiac transplantation. That's the end uh point. Um So this, this, this was it. Um Thank you very much uh for listening me so carefully and uh that's all. Thank you very much for this opportunity. Thanks. Thank you. Um We're gonna take a five minute break now. Um again, I put the feedback form into the chat for you. Uh So just please fill it in. Uh It only helps us. Um Yeah, so I'll take a five minute break. We'll set up for the next one and we'll start up again in about 1110, 17 past one, something like that. Um Please stick around. We've got one more lecture left and it'll be given by Rohan. So, yeah, see you in five minutes. See you. Bye bye.