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Cardiac Surgery and Anatomy



In week four of the teaching program, we delve into cardiothoracic surgery, specifically focusing on cardiac surgery. We will be joined by medical student, James, who will provide a comprehensive presentation on coronary artery disease, its anatomy, and its clinical aspects. Multiple-choice questions will be administered throughout the session for active engagement with the topic. Attendees are also encouraged to ask questions during the talk, which will either be addressed immediately or at the end of the session. This interactive training will equip medical professionals with essential knowledge to better understand and deal with cardiothoracic related health challenges. As a bonus, attendees who fill out the feedback form at the end will gain access to the session's slides, recording, and discounts from our sponsors.
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Learning objectives

1. Understand the anatomy and clinical aspects of coronary artery disease and the coronary artery's system. 2. Recognize the sites of occlusion in various cardiovascular diseases. 3. Interpret ischemic changes seen on ECG leads in relation to the occlusion of a particular coronary artery. 4. Understand the correlation between the different coronary arteries and their corresponding venous systems. 5. Understand the procedure and purpose of coronary angiography in the diagnosis and management of coronary artery disease.
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The following transcript was generated automatically from the content and has not been checked or corrected manually.

It. Now, give me two seconds. I'm gonna read out my laptop to see if that's if that's working. No, it still says. Yeah. Yeah. Yeah. Is it working out? Yeah. Might be a like on my laptop, but Donovan's laptop works. So that's ok. Now, thank you so much. So, if people didn't hear me, I just said we'll be starting at um 635. Thank you so much for joining in the meantime, grab a drink, grab a, grab a snack and make yourselves comfy. Thank you so much for pointing that out, by the way, Abdu. So, hello everybody. Um Thank you so much for joining. Welcome to week four of Su's teaching program. This week, we are going to be focusing on cardiothoracic surgery and today we'll be joined by James who will be taking us through the cardiac side of things. Just before we begin, I would like to say a massive thank you to our partners. So the MDU teach me surgery, meddle pass the MRC S and more than skin deep. At the end of the talk, I will send a feedback form. If you fill in the feedback form, you will get access to these slides, the recording and also some discount codes for from some of our sponsors. Um throughout the talk, please pop questions in the chat. Um I will ask them at the end slash if I can answer them throughout, I will answer them throughout. But yes, I shall now hand over to James who is going to take us through the world of cardio cardiosurgery. There we go. Hi. Thank you, Florence. Uh Thank you for allowing me to present. Uh So I'm James, I'm a student at Queen's and today we'll kind of be going through cardiac surgery and anatomy and hopefully a brief but comprehensive presentation. Um So thanks to the partners. Um Here are the learning outcomes. So today we're going to be covering uh coronary artery coronary artery disease. So the anatomy of it and then uh kind of the clinical aspects. Um Next time we'll be looking at your disease again, first, focusing on the anatomy and then uh the clinical stuff and there will be M CQ throughout. So there'll be some polls coming up now and again. Uh So I'll just get started then. So first of all, having like a coronary artery disease, so gonna focus on the coronary arteries first. Uh If you can try and correlate with the t on the left or the diagram on the right. So we'll start off with the right coronary artery. What's a beat to the left of that diagram So you first off, you'll have your right coronary going on your sino atrial nodal branch. And that will supply the sinoatrial node in 60% of cases. And again, it's quite important because there's an instruction there. The sino arial node will go about the haywire and you don't want that. Uh then you have the right Conus, the right marginal. And then something to really consider is the posterior endoventricular artery. And in 85% of cases, uh this arises from the right coronary artery. So that would be right dominant. Uh next stem, we have the left coronary. So you have the left main stem uh then going into the left anterior descending. So this is one of the main arteries which is kind of located towards the right of that diagram there uh running down the front of the heart uh in the end interventricular septum, uh you then have the left Conus artery, left circumflex, which is kind of uh lipping around the left side of the heart and going around towards the back. And then you have your left marginal, which is a branch from the left circumflex. And then after that, in 40% of cases, you can have the sinoatrial nodal uh artery coming from the left. So this is just looking at the sites of occlusion then. So really just kind of focus on the first three. So for sites 1 to 3, uh they account for up to 85% of all occlusions. Um So this is an order of frequencies. The first one would be the proximal left anterior descending artery. Uh Second, that would be the proximal right coronary. And then the third one will be the proximal left circumflex branch. So these are kind of the main ones you'd be looking out for on ECG S. So again, then this is just kind of taking us through uh the ischemic uh changes that are seen on the E CG leads whenever there's an occlusion of coronary artery and the heart tissue isn't really getting the oxygen that it needs to perform properly. So you'll get these different ischemic changes. So on the left of that table, this is just telling you the area of the heart that is infarcted, the middle is the ECG lead. Uh You'll see the ischemic change in and then you have that corresponding coronary arty which supplies that territory. And if it's occluded, you will then get these ECG changes. So if it's anti receptal, it'll be leads to B1 to B four. And this is the left anterior descending. Uh if it's an inferior infected area leads 23 and aVF will have ischemic change. So this can be in the right coronary of the left, main stem anterolateral change, then can be from V four to V six or one or ABL. And that's the left anterior descending of the left circumflex anteriorly. Then uh you have B3 and B four. And that's the distal uh left anterior descending laterally. Then you have one A VL and B5 to be six, like normally just the left circumflex uh posteriorly. Then it's kind of a weird one. You need to look out for tall R waves and V one to V two. And this is usually the left circumflex that's affected lastly. Then you have the septal uh area of the heart which may be infarcted. And this is supplied by the proximal left anterior descending. And you'll see ischemic change such as ST elevation or ST depression in that case. And either B1 or B2. So this kind of ECG diagram is just taken from GP meds. It's just showing you the different leads on an ECG and it has a color coding labeled for you just to show you where uh different areas of ink will appear on an ECG. So you've got uh inferior, lateral, anterior and septal. So you can have a look at that in your own time. This diagram is quite nice because it shows you the different areas that each uh coronary arter supplies. Um So as you can see uh the left ventricle or a portion of the left ventricle along the anterior aspect of the heart is really supplied by the left anterior descending. And then as you can see in the diagram part of the right there, uh the right diagram, sorry, the posterior standing artery, which usually comes from the right, uh coronary will supply the posterior aspect of the left and right ventricle. So it's just again, another diagram to appreciate what areas are supplied. So we've done the arteries. Then next, we're going to move on to the veins. So four main tributaries are veins uh will run into the coronary sinus. And this is kind of located on the uh atrial posterior atrioventricular sulcus. And this is kind of more towards draining into the right atrium, but kind of coming from the great cardiac vein. So if you look at the diagram in the right here, the great cardiac vein really just follows the left anterior descending and we'll follow up the interventricular sulcus around to the posterior aspect of the heart forming the coronary sinus. Again, this is looking at an anterior aspect of the heart. So we're gonna look at the small cardiac vein mixed and the small cardiac vein really corresponds to the right marginal artery. Um so uh that will then go around to the coronary sinus. So just the next image then it's like in the posterior aspect of the heart. Uh In this case, we're looking at the middle cardiac vein and this will kind of correlate with the posterior descending artery. So it'll go from the posterior aspect of the heart and the endoventricular sulcus. And then you have your posterior cardiac vein, which would more be uh kind of coming from the uh the left uh marginal um and going up towards the uh left circumflex and then uh adjoining with a great cardiac vein to then go into this uh coronary sinus, which feeds all the venous blood of the coronary circulation back into the uh right atrium. So again, this is just three different diagrams. Uh The top left is kind of what we've seen before, but just with the arterial and vein supply overlapping, then we have uh two different diagrams. So the top one is the posterior aspect of the heart and the bottom one is the anterior, this just showing you it's a different color and uh different aspects color than really. So, uh I've come to our first question now. So a patient presents with symptoms of an acute coronary syndrome. Uh ST elevation is present in leads V one and V two, which coronary artery would then be occluded to produce the ischemic changes. So it would be a, the left circumflex branch B, the right coronary artery, C, the proximal left, anterior descending. D the left anterior as sounding or e the distal left, anterior descending. So looking for quite a specific answer in this one. So I'll give you a few seconds here and then I will start up the poll. OK. That's the pull up. So if you want the answer, give you another 30 seconds because there's 10 questions, there's plenty of opportunity, try and get a few more responses, just even try and see what you think. So it's good to give it a go bye. OK. So, and the interest of time I'll keep moving on here. So the answer for that then is C so it's the proximal left anterior descending artery. And if you remember back to the table, uh it was the first most commonly occluded site. So the proximal left anterior descending really supplies this septal area and you'll see the ischemic change occurring in V one and V two. So it's really quite a specific answer. So, uh like you are right to say left anterior descending, but it's really the proximal left anterior descending. So good crack out. So next, then we'll move on to coronary angiography. And this is really just one of the main uh modalities of looking at the coronary arteries and seeing if there's sites, sites of stenosis or uh uh occlusion. So, it's a, it's an invasive cardiac investigation um or it can be and this is whenever a radio die um will be kind of injected into the coronary Os, that's just the, the openings for the left and the right coronary arteries um at the aortic root. And this is to delineate the anatomy. So you can get access and it's normally through the radial uh if you can or if not the femoral. Um So you'll have this arterial sheath uh which is kind of insert into the femoral radial artery and this is used uh well done. So, through a modified cell downer technique. Um And it's done percutaneously. So you're using this guide wire to kind of feed up the catheters and uh have a look and inject things. So, with the coronary ostia, you're using a preformed catheters. So for example, you can have a Judkins. So you're gonna have, you're looking at the left coronary artery, you're gonna have a Judkins left, you're looking at the right coronary artery, you're gonna have a Judkins right. Um This might be slightly difficult this n next part, but we're gonna look at a few images in a second. So uh there are different views and the way it is described is stripped by the position of the X ray detector. So this will make a bit more sense in a second. So you can have kind of three main views. Um You have a right anterior bak and then a right anterior bleak image, the ribs will descend to the right hand side of the image. So that's going from the left to the right. And then the thoracic spine will be on the left hand side of the image in the left anterior like uh image, the ribs will descend to the left hand side of the image. And then the thoracic spine will be located on the right. You can now have an anteroposterior. So going from the front to the back and then cranial and caudal. So cranial towards the head, caudal, towards the feet, but these diagrams hopefully make a bit more sense. So uh if you look at the diagram on the left, you can see uh the detector um the table and then the X ray emet. So we're concerned with the detector when we're talking about the uh positions that these images are taken. If you look at the metal image there, uh this is really just showing you the cranial and caudal aspect. So cranial towards the head caudal towards the feet. And then when you look at the image on the right, you're looking for the left anterior blake. So that'll be to the left of the patient, the right anterior blake will be to the right of the patient, that's the for the detector. So the patient's feet will be coming towards us out of the screen. And again, this is just showing you the cranial and caudal aspect and then also the anterior, right and left anterior oblique. So there are three images here. Um This is looking at the right, anterior bla, anterior posterior um and anterior posterior cranial view of the left coronary system. Uh In each case, um it'll probably take you a while. It'll probably best to have a look at these and your own to really fully appreciate them. But the image on the left is a right anterior blink. Um You can see the left main coronary coming off kind of the top left aspect of that image. And really, if you look at the bottom, right part of that going towards the apex of the heart, you have the left anterior descending. Again, the metal image there where it's more of a caudal view. You're looking at the left main coronary and then looking at the left anterior standing, going towards the um apex and card and then again, like on the left main coronary and left anterior descending. So it's better to appreciate probably whenever you got a bit more time by yourselves. Next time, we've got both uh left anterior blake images. Um one cranial, one caudal and again, it's just looking at the left coronary system here. But again, it's better to appreciate. We've got a bit more time. Next time we're looking at the uh right coronary system cases. And it's really looking at the right coronary artery. Uh And both you can see they already going into the arial node. It's quite important and then you've got your posterior descending artery there. So this heart is right dominant that they're looking at. So next time we'll move on to the pericardium. And in that case, the pericardium, there's three layers um kind of from superficial the day, but really outer down there, you've got your fibrous, uh your parietal serous layer of pericardium and then your visceral serous layer, pericardium is also known as the epicardium. So if you kinda look at the diagram on the right there, you see the fibrous is uh the outermost parietal uh kind of intermediate, then you go to this pericardial space and this is between the parietal and the visceral layers. And this is where the serous fluid is found and it's produced by the epicardium. And this will prevent friction uh of the layers of the pericardium from rubbing together. Then um most importantly, then uh kind of an important clinical question. Pericardium is innervated by the phrenic nerve. So you have C three, C four and C five. And if there's problems with the heart, you can get referred pain. So it might not just be in your chest, sometimes it can be uh in your left arm. So if it affects the intercostal brachial nerve or if you get your left shoulder and neck, that's really kind of the superconductor nerve that's kind of uh passing on those pain signals. It's just kind of getting mixed up because the going on the same aspect of the spinal cord and kind of feeding back that oh there's pain here when really it's in the heart. Again, this is just the light you appreciate kind of the media style and that the heart is enclosed within the pericardium. These are just two more images um to have a look. Uh you can see the heart situated between the lungs and really the middle, middle mediastinum, see the great vessels coming out of it that aren't covered by the uh pericardium, but the heart is completely covered. If you look at the diagram on the right, then uh quite an important surgical uh sinus, it's a transverse pericardial sinus and this separates the venous and arterial outflow tracts uh and uh cardiac surgery. And most that'll be an important landmark for surgeons to kind of delineate what they're working with. Uh Then uh you can see on the right diagram, there's an a big pericardial sinus and this is just kind of towards the posterior aspect of the heart where the uh pulmonary veins are fitting into the left atrium. So we've kind of talked about the anatomy then uh for coronary artery disease. So now we're gonna talk about coronary, coronary artery disease itself. So really, it's this uh stenosis or occlusion of the coronary arteries. And you're gonna have this reduced blood flow to the myocardium. And this is kind of really termed ischemic heart disease. So, the heart really doesn't have the ability to uh get the coronary blood that it leads to the myocardium to match the metabolic demand from it, beating away. And the most common mechanism responsible for this is really atherosclerosis and this can present as angina pectoris and acute coronary symptoms syndromes, which we'll talk about later uh in a bit of detail. Uh It is the worldwide leading cause of death and really in high income countries, there's been a substantial increase in prevalence and this can be due to a sedentary lifestyle and really poor diets too. So we're gonna look at the pathophysiology then briefly. So there's a lovely image on the right. That's not how your coronary arteries should look. There should not be this sweet, small kind of lumen and then this massive collection of stuff at the bottom. So the stage of development is there's gonna be an endothelial cell dysfunction. So there's gonna be something that will disrupt the endothelium macrophages then and uh low density lipoproteins will then accumulate there some kind of fat stuff. These macrophages will eat this low density lipoprotein and then form these kind of foam cells will eat all of this fat and kind of get a lot bigger, you then get a linear fatty streak. So this kind of a line of fat that will form uh then on top of that, you're gonna get your smooth muscle muscle cell migration to that kind of site of injury. And that's gonna pro proliferate uh creating more cells and then extracellular matrix will be deposited around that area. Then because the smooth muscle and the extracellular matrix is kind of joined there, you have the fat and then the smooth muscle and the matrix come together from this fiber lipid plaque. And this is really a complex atheroma. And at that stage, you can get calcification of this a atheroma and this causes the vessel to become quite really stiff and stenotic in that area. And then once it kind of reaches a stage where it's too big and gets a bit unstable. It can then rupture uh then causing a thrombus. So you will have um the clot occurring there and this can cause ischemia distal to that point. This again, this is just a diagram kind of walking you through the different points. So you've got your normal, lovely wide lumen you have then endothelial dysfunction and you'll get your uh macrophages. Uh well, macrophages moving towards your monocytes, which are macrophages, eventually moving towards the damaged endothelium. Then you get your lipid laden macrophages, which are your foam cells and then your fatty streak and then you get your fibrous pack. So it kind of builds up over time. This is just another diagram that kind of appreciates how it can build up on starting from this initial lesion to this complicated one. So there's quite a few risk factors um to consider. So there's unmodifiable risk factors. So these are the ones that you can't really change. Um You have increasing age, male gender. Um if your family has a history of ischemic heart disease, modifiable ones there, the ones to really kind of be concerned with is smoking, diabe diabetes, mellitis, uh obesity, um alcohol consumption, low exercise and lifestyle. So again, talking about these high income Western countries that might be more disposed to that poor sleep and then a poor diet. So really there's kind of four main or well, three main things. So I can present as angina pectoris and acute coronary symptom. So you've got uh unstable angina, an Anstey or stabbing and heart failure. But I haven't really got into heart failure that much. Or else it would be a lot more to do or cover there enough as it is. So with angina pectoris, then uh this is really like a clinical presentation. So if someone appears in front of being a chronic, has these symptoms, you need to be able to recognize this is uh this diagnosis. So common thing between them, both of you have chest pain and angina pectoris then is gonna be central, heavy and gripping. It might radiate to the left side of the chest. Um and then to the left arm of the neck. Importantly, though angina pectoris, the chest pains really precipitated by an exertion and it will be relieved uh with rest or uh GTM and nitrates. Um It might not be present in the elderly or diabetics due to neuropathy where they might not be able to feel that pain. So you need to be quite conscious of that. Uh Again, you can have dizziness and breathlessness. Well, it might not really be that much nausea, lightheadedness and fatigue. Acute Corney syndrome is just a bit more extreme than. So you got your chest pain, but kind of importantly, differentiating this, it occurs at rest. So it doesn't, it doesn't precipitate by exertion, someone could be sitting doing nothing and then we will have this crushing pain might be breathless. Um, you're gonna have nausea and vomiting. You may be sweating, you may be experiencing palpitations and then there's a few atypical symptoms too. So this is looking at, uh, if you take a history or if you've seen the patient see they're experiencing, then you're gonna examine. So generally you're gonna have an anxious, restless patient who's gonna be sweating buckets in front of you. That's because their sympathetic nervous system has been activated. They might be quite cyanotic uh though this is in severe cases and that's because they're hypoxic, looking at the vital signs in uh with BP, someone might be hypertensive and this can be due to cardiogenic shock because that heart muscle is dying. Um You're not gonna have the same output really uh like as a result of that, then you can have a tachycardia and this can worsen the ischemia, respiratory rate. You're gonna expect someone to be quite tacky neck because if they are hypoxic, they're not getting enough oxygen in. So gonna be breathing more trying to get all that oxygen in and again with the pain. And because they're kind of quite unsolved, you're gonna be breathing a lot more anyway, uh hypoxia, then your oxygen shots, you're expecting to be a bit lower, but that's dependent upon the degree of cardiac dysfunction. So quite a good uh classification to use them as the Canadian Cardiovascular Society classification. And this is really functional relating to patients, symptoms of angina to their ability to perform activities. So there's four classifications and this would range from 1 to 4 with one being the least severe to four being the most. So one was really looking at there's really much limitations to the physical Act. Two, there's a slight limitation. Three, you're getting a bit more marked limitation and then four is an inability to perform your activities of daily level in your life. So this is looking at the investigations then that you might use. Um So with angiography, it really is the gold standard in cases of uh Angina pectoris where you're looking for suspected uh coronary artery disease, like we talked about earlier as an interventional and sometimes invasive procedure, you're gonna inject the contrast into the coronary arter. So you can kind of see the lumen and serial ct images can be taken in with a heartbeat. So you can have um one whereby uh you're looking for the sites of identification or you're looking what site is, knows and how stenos is it. So how much of uh as a atherosclerosis built up there to narrow that site and this will influence the management plan really. Uh So there's some quite good figures. Um If there's a 75% percent stenosis, you're going to have a 50% loss of arterial uh diameter. So in this case, you have your stable angina and this is angina with activity. If you have a 90% stenosis, you'll have a 75 to 80% loss of arterial diameter and this is really angina at rest. So, one of your acute coronary syndromes uh with echocardiography, then if you're gonna go for a coronary bypass graft, which we'll talk about later, um you will probably get an echo and this is to look at your left and check your ejection fraction and it's a strong pro prognostic factor. So this will end surgery. So it'll tell you how well you'll do afterwards. So for angina pectoris, then nice really recommends the following uh to kind of diagnose it. You're looking at first line ct coronary angiography, which is on the last slide. Second line is non invasive functional imaging. So this is looking for that reversible ischemia and third line, you're gonna have your invasive coronary angiography. So again, it's moving away from more invasive procedures. So if someone presents to you with chest pain, breathlessness, looking very sweaty and quite sick, uh you're gonna suspect an acute coronary syndrome and you're gonna do a few investigations. So you're gonna get troponins, uh troponin levels. Um It normally tells you within the first four hours what's happening and you're gonna have serial troponins. So you're gonna see the trend. Is it rising up or is it staying the same or is it decreasing? And it can be troponins can be quite elevated um for a few days afterwards as well. So an unstable angina, this is normal and a non ST elevation, elevation, myocardial infarction, it will be elevated and it will be even more elevated and an anesthetic. And then looking at these cardiac enzymes, your CK uh MB levels, it'll be normal on stable angina. It'll be less than two times the normal, but it'll still be elevated in a man's stomy, but it'll be more than two times normal. So it'll be very elevated in a sty. So with ecg changes, we know where the ischemic changes might show up whenever a certain coronary artery is occluded. So what is actually changing to tell you what area of the heart is being affected and what leads? So you're going to have an unstable angina transient ST depression or you're going to have at wave inversion or it could be normal. And this is the case in the unstable Angina and antemi, but in the case of an Anstey, um there is an infarct and this is subendocardial. So just below the inner layer of the heart, in the case of a stader that could be transmural and that's all through ST elevation or Q waves and transmural just means the full thickness of the heart wall. These two diagrams then are just to kind of appreciate uh the tripod levels on the left. So you can, as you can see, it rises very steeply in the case of an MRI and then it will kind of fall off, but it'll still be quite high for a few days afterwards. And then you can look at your MB, so your cardiac enzymes, they'll be raised but not as much as the components diagram on the right then is just another uh one to appreciate the different um lead changes or ischemic changes and then far locations. So another question, then um a patient presents with symptoms of angina. They find that they are limited in carrying out their activities of daily living as they become breathless and experience chest pain when doing so, they have never experienced chest pain at rest. So what Canadian cardiovascular system classification does this patient belong to? So A is one, B is two C, is 3d, is four uh through the pull up my and give us about a minute to 30 seconds. Just wait for a few more responses. Good, nearly 10 seconds. Again, this is just a good one to know. So you can kind of classify someone based on the history that they're giving you. So that's a decent amount. Um The answer is see. So uh you would give them a class three. So from that history, then again, sorry, I should mention throughout the questions whenever the answer comes up, if you look at the kind of the vignette or the stem of the text, it'll be highlighting the key word as to kind of what to look out for. So they're limited in their activities of daily living. But they have never experienced chest pain at rest. So this is three. So there's a marked limitation of physical activity, but this is precipitated by routine activity and not at rest. You're welcome. Done. So now that we've kind of had a look at it, we've classified it, we've diagnosed that we know the anatomy. How are you actually gonna manage these patients whenever they present to you? So, with coronary arteries, artery disease, uh really, I think this is for um kind of your uh angina, you're looking at uh for symptomatic relief, you're gonna have an antiplatelet agent. Next time you would consider a beta blocker. Uh We're a calcium tunnel blocker. Um But if one isn't working, then you may consider both, but you need to be careful with exactly what type of calcium channel blocker you're administering. So it's a monotherapy. You can do dilTIAZem or RMO. It's a combo, you need to do Nifedipine, uh short acting nitrates. So that is to try and uh dilate the coronary arteries. And this is quite an important thing whereby if someone does take the GTN and it relieves the pain, um that can be your stable angina. If it doesn't relieve the pain, you're starting to think about like coronary something. And then again, we have the modifiable risk factor management that is conservatives. This is lifestyle and trying to get people to exercise more, eat well, get good sleep. But really the definitive treatment and kind of what we're really interested in is this revascularization therapy. So, you have your percutaneous cornea intervention uh done by a cardiologist. And then you have a coronary artery bypass graft by your cardiac surgeons, psoriasis, maybe a bit of a bigger slide. But how do you manage an acute coronation? So there was a pneumatic going about. So your moac, so you've got your morphine. Uh but that is only in severe pain. Uh you can have oxygen, but this is if the saturations are less than 94% your nitrates, um that's sublingual or IV. And then you have your uh aspirin 300 mg and then you're gonna do your A CG to determine exactly what you're gonna do next. So in the case of a sta, then if we're thinking about PC, it can be offered if the presentation is within 12 hours of the symptom onset. So they need to get in quick. In this case, PCI can be given if it's delivered within two hours of time whenever thrombolysis could have been given. So this is, as you can see, this is very time dependent. However, though, if it's still present after 12 hours and there's ongoing evidence of ischemia, you can then consider PCI and quite important with PCI. You want to give this gel of the platelet therapy prior to doing it. So you can have your aspirin and your prazole or potentially clopidogrel. Yes, the pulmonary bleeding risk, then you're looking at thrombolysis, then if someone doesn't present in time and there isn't say a PC, uh lab nearby, then you're gonna be looking at thrombolysis. This can be offered within 12 hours of the symptom onset of, uh, if primary PCI can't be delivered within 100 and 20 minutes, or you're thinking of someone at a district general hospital who doesn't really, really have access to this or somebody who is quite out of the way. Um And this is delivered within 100 and 20 minutes when thrombolysis could have been given. So really, you need to be quite on top of your times here, next stem uh and stemi. So for those who aren't a high bleeding risk and don't need immediate angiography, you can give them from the paranox. Um However, if they need immediate angiography, you might be considering a fractionated heparin. If you are going to give them PCI or conservative treatment, you want to be really looking at the dual antiplatelet therapy. So your aspirin and then your um pra tag or quite importantly, then with an ending or unstable angina, you're thinking about this greatest score. So this is the global registry of acute Coronary events and this is really just a an assessment to to the stratified patients. This will allow you to make key decisions on whether what your management is gonna be. So it's gonna be coronary angiography with PCI potentially afterwards or is it gonna be conservative management with medication. So if we're looking at that, then if someone's is uh clinically unstable, so let's say they're hypertensive hypotensive, sorry, they're going into cardiogenic shock. You might need to immediately get them to PC, the CF lab to do PC. However, if it's within 22 hours and the greatest score is more than 3%. So this is this immediate high or highest risk group, you will then consider uh angiography with follow on PCI potentially. And then it's also considered if ischemia is uh experienced uh after admission. So with this greatest score, I'll kinda show you what it's talking about next. So the parameters of the grace score are age, heart rate, BP, uh C class renal function arrest on presentation, ecg endocrinal level. So you'll have all this data in front of you. You'll input it into this toe and it will tell you what the next step is. And as you can see on the table on the right, then you have your predicted s six month mortality and this will show you the different percentages of that predicted mortality. And these patients are then stratified through these groups uh for their risk of future adverse cardiovascular events. And if they're intermediate to highest risk, you'll be considering PC. So we've kind of mentioned these terms PCI and cabbage. Uh PC is really just coronary angiography, but you're doing procedures within that. So you have your femoral or perfectly radial access, uh you're using the Seldinger technique. So you're passing this guide wire up to the coronary artery. So this is under radiological guidance and you can do angioplasty. So this is using a balloon uh contained on the catheter. You'll wind up with the lesion to kinda get it in this kind of narrowing and you're gonna inflate the balloon to try and then restore the normal width and get that blood flow uh distally. Then again, you can add in potentially a stent and this will kind of be drug so it can stop uh thrombosis occurring. And this is like a wire mesh that will go in the stenotic area to try and stop it from happening. This will be permanently deployed across that lesion and this is to decrease the rate of post uh PC stenosis cabbage then is coronary artery bypass graft. And this is looking to circumvent the blood around the stenosis. So, if there's a blockage here, you wanna get the blood from here over to here. So you're gonna anastomose the graft of the coronary artery uh to a side distal to the lesion. So you're gonna go above the blockage to then below the blockage to get the blood past that. And it can be performed on or off pump. And it is preferred to PCI and the presence of complex coronary artery disease. But we will talk about that a bit more. So, these are the two main documents that you really want to be considering when you're looking at coronary artery disease management. So you've got your stable angina management and your acute coronary symptoms. So we'll kind of cover a bit of this next. So if we're looking at revascularisation, um and this is the case, looking at the stable Angina management guidelines, you can have uh revascularization coverage of PC for those with stable angina if their symptoms aren't really satisfactory, controlled with your medical treatment. Um So this is if the medications they're getting aren't working or relieving their symptoms or if the symptoms are really controlled and they're doing well on them. But you find out on angiography that their left main stem. So the kind of the beginning of their left coronary artery is affected or there's proximal. So that means closer to the coronary ostia, uh three vessel disease, then you'll be considering a cabbage and coronary angiography will really guide that treatment strategy in less complex cases. Then um really PCI is more cost effective and should really be done if both procedures are appropriate. However, there is a survival advantage of the surgery cabbage over PC for those with multiple vessel disease. So multiple coronary arteries are affected, affected, sorry, they'll be considering the surgery over PC and particularly in those patients who are diabetic if they're over 65. And if there's complex uh three vessel disease and this is with or without the left main stem and bone. So these are just a few trials, I'll quickly whizz through these. But this kind of gives you the rationale for PC or Cage. And this is really like on the European Society of Cardiology or the European uh cardio Surgery Society. So there's four trials really, you've got Noble. Um I'll just give you the main, main headlines. Statistically, uh the primary was a comp uh at five years of death and nonprocedural M I or repeat revascularization or stroke. There was a statistically significant difference between pizza and cabbage um in favor of uh cabbage with uh 90% of the primary outcome occurring there. But the other ones didn't really kind of follow this XL trial. Um It was looking up a five year composite of death stroke or myocardial infarction. There wasn't any difference between PC or cabbage. There was no statistically significant difference after five years. Then there's precombat. Um I was looking at uh PCR coverage for left main disease uh at 10 years. Then it was the primary outcome uh including death M I stroke ischemia or uh kind of revascularization procedures. And there wasn't any difference between PC and cabbage syntax. I remember briefly again, it had this 10 year uh kind of uh primary endpoint of all cause all cause mortality. There was no difference between PC and Cage. So then in 2022 this, I think they updated the guidelines from 2018 and 19. Uh They, there was this um meta analysis kind of carried out using these four different trials by 17 et al. And they were kind of looking at the drug elating stents versus this procedure on left main coronary disease. So they've got 4000, 394 patients. So that's quite good. And was looking at mortality uh over five years since the primary come. And for both of them, there was no statistically significant difference between Pisa and cabbage. But again, this is just kind of a general thing, there's different indications for them in specific scenarios. So as you can see, this is really just a uh kind of uh intimus curve. So you can see in the bottom. So the X axis, this is the number of years from 0 to 5 and then you have this a cumulative incidence on the Y axis going from 0 to 12 for PCI and cabbage there. PC is the blue line, cabbage is the red line. As you can see they kind of really tr each other with PC will be pulling ahead at last. But there's no statistically significant difference in that case. This then is kind of looking at the meta analysis, looking at more kind of in depth things. So looking at my infarction, there was differences here, but it's maybe best to show you the next diagram which will kind of explain this a bit better but more user friendly. So as you can see in this diagram then you have a whole bunch of variables down the left, you have PCI on the kind of left, left kind of chart uh and like blue and cabbage on the right and purple. And really this is just showing you the different um kind of uh the outcomes and the P analysis. So as you can see cabbage, um in this case, might have had more chance of graft occlusion, thrombosis. Whereas as you can see down towards the bottom really at death, uh any M I uh was kind of more um spontaneous M I was more towards PCI. So you can have a look through that and maybe or more time just this is to explain the rationale behind the guidelines. This is kind of a nice chart to maybe explain to patients. Um if you have 100 people who undergo this uh PC or cabbage at five years, out of those 100 people, how many people are gonna be affected by an event? So in PCI, you have 20% you will experience an event such as death stroke or M I. Um Whereas in cabbage, you're gonna have 16%. This is them just looking at the different kind of characteristics or aspects um that would favor PC or cage. It's not really worth going through all of this. You can have a look at it whenever you get the slides. So after all this trial data and all these experts come and gather them, what did they kind of, what did they really conclude about this? So um the guidelines in 2018, then it was looking at in stable patients with an indication for revascularization in left main disease. And this was looking at the coronary artery uh anatomy was suitable for both procedures and a low predicted surgical mortality. And really that concluded that both treatment options are clinically reasonable. Um that's suitable and this is based on uh the avail patient preference, the available expertise and kind of the operator volume. So this table there is looking at left main disease with a low or intermediate syntax score and for cabbage, then the level of evidence, well, the cost and level of evidence was one A. So that's greater and PC was two A but the level of evidence was there. So they can both be done but cabbage uh seems to have a bit of a higher level of evidence currently, but that can be subject to change down the line. So I mentioned syntax on the last one, we'll just briefly cover this. I'm gonna cover two scores. Um syntax then is they love to make up these lovely names uh for all these trials. So, synergy between percutaneous cornea interaction with taxus and cardiac surgery score, this is looking at quantifying uh anatomic complexity and then the severity and extent of multivessel disease. And really it's a surrogate of uh atherosclerotic burden. So it's a risk stratification tool and allows you to make decisions for the revascularization strategy. This is between PCI and cage and for multi multi vessel disease. And really, you're scoring it uh based on kind of angiography where you're gonna score uh lesions which are greater than 50% diameter and stenosis. And the only on those vessels though that are greater than 1.5 millimeters and dier. So you need to have a significant enough stenosis, but also the vessel needs to be big enough. And three risk groups were identified too, very low, intermediate and high. Next time is the Euro score. So this was done in 1999 and kind of revalidated in 2012 with the second version of the European system for cardiac operative risk evaluation. This is the production of early mortality in cardiac surgery. So really there's three groups of risk factors and they all have different ratings of 12 or three. This can be either patient related cardiac uh or operation related. And from that uh kind of different group of risk factors, then you get these three risk groups. So you got your low, your medium and your high and let's just let circles know kind of how patients prefer after the surgery when they not be suitable. So I've talked for enough. Uh third question now. So a patient presents ad with left sided chest pain that persists at rest, radiating to their left arm, they're breathless, sweating, profusely, feeling nauseous E CG is then performed and you get ST elevation and leads one B LV. Five to V. Six troponins are elevated at 0.92 Agras per milliliter diagnosed with an endemic. So which risk assessment score would you utilize to make the clinical decision uh on the patient's management as to whether it's gonna be conservative or you're gonna do corneal angiography, potential P CPC follow up. So A is your score, B is sometimes C is key risk 3d is the well score or E is grace. So about 30 seconds, 10 minutes. OK. Let's see what we've got here. Wait for a few more responses. So we're considering an ante, do we or do we not want to co geography follow on PC? Good, happy that. So the answer is OK. So we're gonna use the greatest score here to stratify this patient as to what the management would be so well done. Number one. So it's really a the risk assessment tool for an ending or unstable angina form decision. And uh it's looking at the uh predictive mortality of that patient if whether or not he did um PC. And again, it needs to be performed within 72 hours and the greatest score would need to be greater than three. That patient will be intermediate high or highest risk. It's well done. So now we've kind of moved on. We're gonna talk more about the surgical aspect of cabbage. So you can't really talk about cabbage without cardiopulmonary bypass. Uh in most places now, the caveat is nowadays, some people will not or some surgeons sorry will be up like cardio pulmonary bypass. But it's good to understand. So what does bypass do? It really just takes a bit of function of the heart and lungs. So you're providing that res support for the circulatory and respiratory system because whenever you're uh being operated on, you don't have any control. So it will deliver oxygen um to your end organs and this will allow surgery to occur. So it has several different functions. So it's gonna provide oxygen to the tissues, it'll ventilate the lungs. So getting the carbon dioxide out oxygen in, it'll facilitate the cir circulation on systemic uh systemic circulation around your blood vessels and it will control your temperature as well. Temperature is a very big thing. Cardiac surgery you need to be quite conscious of and then always looking at your electrolyte balance because you don't want your electrolytes going highwire. And again, this is really just to protect the heart and also kind of decompress it. So sorry, it's a lot of tax there. We want to make the image nice and big. So if we kind of consider it, so we're gonna hyper heparinize the patient because the tubing is all kind of quite thrombotic. And if you didn't have any um heparinization, you would get these clots forming and really the surgery would be pointless in the first place because you wouldn't have a live patient by the end. So we're looking at, if you look at the heart, then you can see that there's a blue line coming from it and a red line. So these are the bypass cannulas and these are inserted under the heart. So an aorto atrial one, so you're gonna insert one into the right atrium can be by cable. So both the inferior or inferior vena cava and then uh you're gonna have one into the ascending aorta. So you're gonna drain the blood from the right atrium and then the left ventricle uh into the reservoir. So the reservoir is kind of the center kind of bottom center of that image where you can see it's kind of uh called the venous reservoir. So it's kind of filled with a blue um blood and then you're going from the venous reservoir, it's gonna pass along the blue uh timing coming at the bottom of it. And that will go through uh the pump then to the heat and gas exchanger once it passes through the heat and gas exchange there. So we've gone along from the right bottom, right of the diagram to the middle, down to the bottom left, you're gonna get this arterial filter and the blood will then go back through the arterial line to the aorta uh through the aorta coming up to the aorta to the systemic circulation once that's established then you're gonna have your uh aortic cross clamp placed. So this will kind of separate the parts, you're gonna clamp off the uh kind of proximal and distal part of the ascending aorta. And this is to separate the coronary and the systemic circulations. Because importantly, in this part, you want to uh separate them because you're gonna be putting a potassium rich cardioplegia solution through the gas exchanger through the cardioplegia pump that will then pass into the aortic root to provide after grade. So after, to get, move forward, so this will be going uh the cardioplegia solution going into the coronary arteries directly. So whenever you look at cardiac surgery, you'll see them with these kind of um cannulas that they'll put into the coronary ostia that then feed the blood into the coronary arteries or it can be retrograde and this is through the coronary sinus and through the coronary sinus, it takes longer. It's not, not as great. So really, you won't be doing ade uh once you've done the operation, then um you stop the heart, you're then going to uh afterwards, once you're kind of finished, you're gonna administer protamine uh at the end. And this is to reverse the apps, this is to reduce the bleeding risk once everything's fine. So we've talked about bypass. You need them to consider, what are you actually gonna use to? What are you gonna use as conduits to ashes, to bypass the these occlusions So, very importantly, you're gonna hear of the internal mammary artery or it's also called the internal thoracic artery. It really is the first choice of conduct and it will arise from subclan come up here and it will then descend along the kind of power or power of be parallel and lateral to the sternum that's associated with an excellent long term patency as a late um or sorry, an early in late survival benefit um post cage and it's resistant to the development of atherosclerosis. We don't want that kind of closing over again. 10 year patency is uh 82 to 95%. So, as you can see, it's very good and really, you're gonna be using that mammary ra to then go into the left anterior deem long staph vein then is probably the most common conduit used. Um It runs from the anterior medial malleolus. So this is kind of the bump at the bottom of your ankle on the inside of your ankle and it'll go to the junction of the femoral vein and the groin. It's very easy to harvest. It's available. It's versatile, doesn't really spasm as much. However, because it's a venous conduit, there is increased graft failure. So it can kind of stenos and close over again. This can be due to intimal hyperplasia. 10 year patency as you can see is not as not as good but still reasonable. 61 to 71%. Now they're starting to use the radio a lot more. And this could be the secondary choice of con. And if you're gonna do uh use the radial artery, you really want to be performing the S test. And this is to assess the adequate the adequacy of the ulnar artery supply to the hand because you don't want to take someone's radial artery away if it's not sufficient to supply their hand. So you will be uh using an a hand, you'll clear the radial, you'll clear the ulnar. You'll then hopefully see the color go out of the hand, get them to squeeze their hand, then you'll take your fingers off of the ulnar. And hopefully, if the color flows back into the hand, you know, they can harvest the radial artery on that side. It is more likely to undergo a atherosclerotic change than tidal mammary. But as you can see, the PNC is a lot better than the softness. So it's 83 to 95%. So here's just a few images. Then uh the left one is what you'll see if you do a medium Steny and you open the chest, you're gonna see the uh internal mammary kind of para vertebra, uh sorry parasternally, and they'll be dissecting that out. So I can see in the meal diagram there, you can see a pedicled version, a pedicled version. So that means there's a bit of tissue surrounded and the bottom one then is a skeletonized version so that extra Soane fatty tissue will be kind of removed from it unless it's just the dog on the right. That's showing you how they dissect it from the chest wall, anterior chest wall next then is looking at the Smore. So in the bottom left there, it used to be done. Open my C it's not as bad, it's done endoscopically. So that's the top left image there. So they'll make small incisions in the leg and pass um a camera and a toe up to them and dissect that out. Then um you can see the radial uh kind of more of the diagrams on the right. And that's just how you access ra already on the bottom image is what you would see if you were doing that. But that's really an open procedure nowadays. Again, it would be endoscopic. So we've talked about everything kind of leading up to this stage. We've got our bypass, we've got our conduit, we've identified that. How do you actually do the procedure? So this is a very basic overview of it. So you can have minimally invasive ones, but we'll just consider that tried and tested the median sternotomy incision. So this is the big incision, find someone ster and then you're opening up the chest. So at this stage, really, you're going to be harvesting the internal mammary and this is prior to opening the pericardium and then you'll do your softness vein harvesting as well. So normally, when you're doing it, you'll have your mammary artery you're getting and then your, so this vein too, uh pericardial will be opened and then kind of held up with stay sutures for bypass, then you'll cannulate the heart, they'll initiate the bypass, you'll put on the cross clamp to separate the systemic with coronary circulation. And then they'll administer the cardioplegia and this is to arrest the heart and uh diastole, you'll then identify your coronary targets. And this will be done way beforehand with your angiography studies. And then you will do your bottom end anastomosis. And all that means is that you'll first be looking at, where am I going to put these conduits uh distal to the site of occlusion? So the bottom man anastos is taking the graft and putting it onto the actually the heart tissue. Um So you moving and the side. So you're gonna have your Bassa like that. So that's the side part of the heart. And then you're gonna have your uh condo coming down on the and this is using very small sutures using a parachuting technique. So you're gonna be putting your stitches in, you're gonna have your vessel like that. They'll be holding that for quite a while and then once they're happy with it, gonna parachute it down on to its target. Um Then you have your aortic cross C will be removed. If you're happy enough, the heart will be rewarmed, it'll be weaned from bypass. This is to allow them to see where is the bleeding is there? Um, conduit good. Is it being surgery on properly after that? Then you'll do your top end anastomosis. We've sutured on, uh, they call it onto the heart. Next, we need to then feed it up onto the aorta or in the case of the internal mammary, you don't need to, this is the bottom end anastomosis. So with aorta, then you're gonna have kind of a side clamp. So you're gonna take a heart like that there and then you're gonna have this lovely bit of aorta to then graft onto circular punches are taken and then you're really just adding on the top end. So you're gonna dr the grafts and the heart because if you have an air embolism that will cause a stroke. So you insert a cannula into the grafts and that's just to make sure all the air flows out afterwards, then you're gonna administer the po domain to reverse a decannulate heart. After cardiac surgery. Quite a lot of people run into problems with um the pacing of their uh heart. So go go in a bit of a funny rhythm, normal atrial fibrillation and these pacing wires will just kind of control the heartbeat afterwards to make sure it's able to recover properly. You put, put the drains in, so your mediastinal drains and normally they'll kind of be coming out just kind of just below where the sternum is, and then you close the the sternotomy wound with sternal wires, these big massive wires that will hold the sternum together. So the this is just the procedure really. So it's looking uh darker on the left to show you an actual heart that has been grafted. So you have your left internal mammary that'll normally go on to your left anterior descending and then uh kind of the left image. But the left aspect of that, you can see a so vein graft and it'll be going from the aorta to another vessel is the left anterior descending. The image in the right D is, is showing a, a diagram of that. So uh quick question, uh what is the main ion found in cardioplegia solution that induces arrest to allow cardiac surgery procedures to be performed? So, is it a magnesium B, potassium C iron D, calcium or E sodium? I'll give you another 20 seconds. This one should be OK. OK. And the un the time all par. So the answer is potassium. So a high dose, potassium chloride solution is prevalent cardioplegia. This will then induce arrest or mechanical. Uh so that'll cease the mechanical activity and result in diastolic arrest that allows you to work away. Next one, ma'am. Other quick question, which cabbage conduit is associated with the best long term patency. So a left internal mammary artery B, the radial C, the short softness D the lung softness or E the right gastro artery start to pull again. Ok. We got 20 seconds cause I realize it gone over quite a lot. I haven't even touched positive, but thanks for second on good. So everyone's getting that question quite well. So this is the best long term ency um As a result previously, it's the left internal mammary has the best patency. It's less resistant to atherosclerosis. And the 10 year patency is 82 to 95%. The other vessels do not reach up. That's why it's normally the most on to the left anterior. So come to the end of coronary artery disease. We have our co procedure. So here's a video, a good video. Here's a fantastic video. It takes you through absolutely everything. It's an hour. If you're interested. Um importantly, then you need to know I lead up to the operation, what the condition is. But you also really importantly need to know especially for patients, what are the complications. So if someone presents the clinic, you're gonna tell them this is the operation, but they're gonna wanna know what's gonna happen, what could go wrong. So you need to be quite cognizant of that. So, postsurgery, you're going to be in ICU and that's for monitoring, monitoring and supportive care. Overall mortality is quite low. So 1 to 3% and you can have a whole host of complications. So strokes quite a big 11 to 5%. POSTOP bleeding is a very big worry of surgeons and it can happen in certain cases. Um, sternal wound infection can happen. Uh not that common at 1 to 3% but something you'd be quite worried about and something that there's been quite a bit of research done on in the royal in Belfast here, there's been uh looking at renal failure. So we keep kidney injury and stuff. So, um if you're interested, look up those papers, um neurological complications you might be worried about, but kind of the main one atrial fibrillation, it's one of the most common complications that patients will kind of suffer from. So that's why they'll put the pacing wires in and then normally you might put them on a beta blocker as well um to stop it from arising. So normally if all things go well, you're discharged in about a week, you're gonna slowly recover from open heart very well, not open heart surgery, you're gonna slowly recover from a cage procedure. Hopefully in about three months after the operation, you can be back to your normal activities of daily life. So that's coronary artery, we'll try and whizz through valvular disease. Now, but again, another very interesting aspect of cardiac surgery. So this is looking at the functional parts of the heart, both internal or external. You've seen these diagrams before just slightly bigger. It's just swing in the right atrium, right ventricle, the associated uh arterial and venous vessels and then the great vessels above. And then the diagram on the right is the posterior aspect. So it's showing in the superior and inferior vena cava, you're looking at the pulmonary veins there in the left atrium and then you've got your coronary sinus swing in that uh ATRIO ventricular sulcus in the posterior aspect. So just briefly consider the heart chambers, there's 42 atria, two ventricles, you've got some on the left, some on the right, right atrium. Then you're gonna have this deoxygenated blood coming back to the heart from the S VC, the IVC and the coronary veins have this right ale oracle, sorry. And there's a smooth part of the right atrium. There's in this muscular ridge called the Crista terminalis. And then you have this pack in neck muscle. So it's kind of rougher area. And the coronary sinus importantly feeds back into the right atrium. While all this venous coronary blood is coming back then separating the right atrium and the left atrium, you're gonna have this interatrial septum. And importantly, here, there's a fossa ovalis, which is the remnant of the fore ovale, which would have been present until I blood to pass in the right atrium to the left atrium. Whenever um fetal circulation was present, he then you put the left atrium. So you have this oxygenated blood returning back from the four pulmonary veins. You have this left or so this left kind of points, your appendage. It's a very important thing in atrial fibrillation. So, heart's quivering uh in that aspect, up in the left atrial appendage there in the left or you can get the stasis of blood and that can then form a thrombus that will then turn into an embolism and that can cause a stroke. Next. Then you've got the smooth surface and then you've got your pack muscles, you're rough and your smooth. Next, we have the right ventricle. So this is the oxygenated blood coming from the right atrium down into it. You have this trabeculate carnea. So there's rough muscular ridges. Uh you have the supraventricular crest separating the that from the smooth corus walls. So that's kind of more of the outflow tract. It's gonna be nice and smooth and you have three pary muscles with the cord eye 10 to the eye. Next, then you have an interventricular septum separating your right and left septum or ventricular uh sorry, left and right ventricles. You have a superior membranous part, so slightly center and inferior muscular part and you have your left ventricle. So there is the oxidated blood coming from the left atrium down into the left ventricle again, like the right ventricle. You have this rough part, right, like car and then the smooth part on the outflow tract and you've got ta muscle. So this is just showing you kind of left floor of the blood, you're coming from the right atrium down into the right ventricle and then through the pulmonary outflow tract, then you have blood returning from the pulmonary veins into the left atrium, down into the left ventricle and then up out through the aorta. This is just showing you what I kind of talked about. So the diagram on the left is showing you the right atrium. Of note, there is the Crista terminalis and the fossa wallis on the right thumb, you see the right ventricle and this is just showing you the uh cordate tendineae with the valve and papillary muscles on your tuba cornea. Next time we're showing on the left diagram is in the left atrium. As you can see, it's quite smooth, you can see the other side of the fossa wall. And then the diagram on the right is showing you the left left tle again, you can see your um like car and your bowel muscles. So on the right then is a an image and this is just showing you the different tumors of the heart. And then on the right, you can see a chest X ray. So this is just kind of pointing at the different features of the heart that you might see. So in which chamber of the heart is the cresta located, is it the left atrium, left ventricle, right atrium, right ventricle, give it a go again and just time, give another 20 seconds. OK. So there's a previous slide, but you will get access to these slides. OK. So the answer to that question is the right atrium. So you have the crystal terminalis, which is this muscular ridge separating the anterior surface of the right atrium. So you have the smooth part sinus of an arm and you have your rough packing that muscle. And this sign of this crystal terminalis is the ridge that just separates them. So the valves um will quickly go through that the valves ensure you you need interactional flow. So the blood's not gonna go this way, it's gonna go that way and hopefully not come back away. So you have your itcher ventricular valve. So that's between the itch above and the ventricles below and they will close during cla when the ventricles contract, they will then close. So, uh the tricuspid, um it has three leaflets and it's kind of uh between the right and the right ventricle. Mitral has two leaflets and it is between the left edge and the left ventricle. Some of the inner valves, though they have three cusps and they close during diastole. So these are on the ventricular outflow tracts separating the pulmonary trunk from the right ventricle and they order from the left ventricle. So they're closed during dias. So whenever the ventricles stop contracting them, no more bloods being forced out through the outflow tracts. So you're gonna have this blood coming back down and these valves will then stop it from going back into the ventricles. So the top of these valves, uh cut of those valves, you're going to have your um so that should be the itch of ventricular valves have their propi muscles and Corini. But from the pulmonary valve, you've got your right ventricle to the pulmonary trunk, um the aorta, you're going to have the left ventricle to the ascending aorta. The diagram on the right, just kind of shows you the different positions of the heart. If you're legging from the top down, these are just more images to appreciate them. So the image on the left is showing you ventricular diastole. So you're going to have your seminar valves closed, but you get your ventricular valves open, ventricular cystic gland. So the ventricles are contracting, you're gonna have your atrioventricular valves closed, but then you're gonna have your semi linear valves open. And again, this is just showing you the uh pulmonary valve uh seminar valve. But if you can appreciate it on the right diagram, this is the aortic valve. Um you can see the left and right coronary osteo, that's where the blood goes to the coronary arteries. This is just looking at the kind of a sight on view of the heart valves. Um It's just showing you the cord tendon of the papillary muscles to too. So where are the valves of the heart? And if you look here, it's different from where you listen to them, but we'll explain that in a bit. So aortic is the left sternal border, third rib, pulmonary left sternal border, third costal cartilage, mitral valve is left fourth or fifth, intercostal cartilage, tricuspid down is the sternum level of the fifth costal cartilage. So why is it different where you auscultate? Exactly where the valve is? This is why? So the blood, well, the heart sign this snap close of the valve, the blood is being carried or flowing through the valve and that sound is then carried with the blood and the sound will therefore be our best downstream. So as the blood is drawing this way, say you hear the stop there, blood's going there if you're gonna hear the valve pass up. So this is why it's a different site from where the valve actually is to where you will listen. So you have your aortic, see all of these off by heart. So aortic is right second intercostal space kind of parasternally. The pulmonary is parasternally but the left second intercostal space, mitral is the left fifth under costal space might collect your line. So that's your apex and you've got your tricuspid left fifth under costal space really more external margin. So right beside the sternum and this is just diagram to appreciate where you would listen to the different bowels. So it should be like this aortic pulmonary tricuspid mitral. If you can't remember that, just remember eight point too many. This is just another diagram to show you what type of murmurs you might hear at those different points and it's quite a good one. So hopefully it'll be useful for your reason. So, so we've talked about the valve, we've talked about different parts of the heart. How does it all actually contract? What, what starts up? So this is the conduction system of the heart. So it'll initiate and coord coordinate contraction. So it'll flow through the heart. So if you look at the diagram on the right, it'll kind of start from the top left of it. So you'll be going through the sinoatrial node, the impulse will then pass through the atria. So you have backwards bubble going to the left atrium and then it'll pass down to uh the atrioventricular node. And this is kind of just the the bottom of the right atrium there. And at that point that will then pass on the atria through to the ventricle. So you go through this bundle of heme, you then have your right and left bundle branches on the left and right ventricles. They'll have these purkinje fibers which will kind of pierce into the subendocardial layer of the heart muscle. And then we'll get that contraction of the ventricles. These are just more diagrams to kind of appreciate where you're gonna find these different pathways of the conduction system of the heart. So we've talked about where stuff is where it arises. What does it actually mean? So if you're looking at an E CG, it will tell you exactly what is happening in the heart. So if it's atrial depolarization, you're gonna see that as ap wave ventricular depolarization, you're gonna see that as a QR S complex, a key wave them will be ventricular repolarization and the rest of the stuff it's interesting to consider, but these are just kind of the main points. So here's a quite a nice diagram that's color coded. So on the left, you're gonna see the different aspects of where this electrical signal is passing and rising from. And then if you look on the right, you will then see it corresponding to an ECG. So you've got ap wave for our atrial depolarization, you then have the kind of light green line and this is where it passes through the atrial and check renaud where there's about 100 and 20 millisecond delay. That's the light of the atria to empty their blood into the ventricles. You then have the red section and this is ventricular decoration is when the atria or sorry, the ventricles contract force blood out of the heart and then the yellow portion. Um it is then ventricular repolarization. So quick fire question, which structure of the hearts conduction pathway is responsible for the delaying the electrical active electrical actions canceled by approximately 100 and 20 milliseconds during the cardiac cycle. A bubble of his b sinoatrial node C Bachman's da ventricular node or E the pin G fibers like 20 seconds for this. Yeah. Mhm ok, nice 100% responses. And you realized it is the ATRIO ventricular node. So it's responsible for delaying these pulses going from the to the bubble of test and ventricles. And that is delay the A da to fill and do the content in before uh allowing ventricular cyle to occur to the next one. So we finish that on topical part. Now we're on to the clinical stuff that we're all interested in. So probably disease will selectively affect heart valves when a heart valve is affected by disease, nobody are gonna hear that sound. And that is termed a murmur and a murmur will arise whenever there is turbulent blood flow, just kind of a club. So you have these four main valvular disorders to denote what is actually happening and to denote where it's happening. So you have stenosis. So that's uh a valve that is kind of narrowed regurgitation is now the valve doesn't really function. So it doesn't ensure that you need directional flow of blood, your blood flowing back in and you have your uh aortic valve or your mitral valve. So, stenosis is narrowing, inability to fully open and regurgitation m incompetence or insufficiency, insufficiency, you'll hear it called, this results in a backflow of blood lesion. So there are an awful lot of causes of different valvular disease. So, aortic stenosis, three main ones are idiopathic age related calcification. So that's been getting older and calcium building up, congenital bicuspid valve that results in early stenosis and rheumatic heart disease. So, we're talking about developing companies in that case, aortic regurgitation or acute thing, acute presentation, but they're also chronic. So you game idiopathic age-related weakness, congenital bicuspid and uh connective tissue disorders. So, someone has ad or Marfan syndrome affecting the connective tissue that can result in regurgitation, vital stenosis, rheumatic heart disease, rheumatic heart disease, rheumatic heart disease, think of rheumatic heart disease Whenever you hear micro stenosis also as well, you can have a reactive endocarditis. Next step, mitral regurgitation. It's the idiopathic weakening of the valve. So, age-related, you have ischemic heart disease, calling it infective endocarditis, rheumatic heart disease or once again, either or more disconnective tissue disorder. So, if there's regurgitation, it's like is there a connective tissue disorder or you should know that by the history? So some nice images, hopefully the top left is a prosthetic aortic valve. Um endocarditis has occurred there. So as you see all of this stuff on, on the valve really shouldn't be there. Don't worry, Ashok, you'll get the slides, there's too many causes, it'll be fine. The bottom left one then is calcific degeneration of the aortic valve. And that is with people getting older. Usually, then you have a bicuspid aortic valve and this is what this is where the kind of infusion of these leaflets. And then the bottom one is your rheumatic uh aortic valve. Is it all affecting the aortic valve now we're looking up the mitral. So we have a rheumatic uh kind of valve and micro stenosis, one of the main causes. And then you have this papillary muscle rupture uh following an acute myocardial infarction. So, if someone acutely presents, having a heart attack, you listen to their chest and you hear what could be uh mitral regurgitation. That means that there could be a rupture of the pilary muscle following in infarction. So if someone presents with that stuff, what do you expect to find out from them? And what do you expect to see through stenosis? They can be asymptomatic for quite a long time. So it can be 10 to 20 years. You could have this exertional, breathless, chest pain, exertional syncope. So this fainting or it can be pre. So if someone does exert themselves, they can feel that I'm on the verge of passing out here. Again, you might have heart failure, but importantly, to hear the signs. So you're gonna have a loud mid to late peak ejection systolic murmur. Here's ejection, systolic like aortic stenosis. This is in the aortic area. It will radiate to the carotids and it will be sent you to see if you're setting forward an expiration. When ex sent you at that murmur. If you feel someone's pulse pulse, it's gonna be quite slow, rising and low volume. There's gonna be a narrow pulse pressure. So their systolic value, it's gonna be quite close to their diastolic value. It can be a softer, absent S two, you can have a heating apex beat. So if you put your hand on someone's chest and the heart beating out of their chest, it could be art stenosis, you might have heart failure signs. So this diagram really is just showing you, you can have an asymptomatic phase for like stenosis. And as soon as you have symptoms, if you do not have a uh an aortic valve, your survival is dire, it'll happen quite quickly. But with aortic valve replacement, you then have uh will be able to live hopefully a normal quality of life. Aortic reg regards them again. There's acute and chronic, you can have a sudden cardiovascular clots in the case of acute, um then looking at acute pulmonary edema. So uh that back through the blood, you're gonna get breathless, sweating, pallor quite vasoconstricted chronically, then it could be quite insidious. You got this uh exertional dyspnea or sonia, which is if you're lying down and experience breathlessness, pero turn dyspnea if you wake up in the middle of the night and are breathless, gasping for air can then get stable angina as well. So signs them, we really focused on the murmur here. It's an early diastolic murmur that could make sense you to lean forward, an expiration, you might have a soft s one, unlike the stenosis of the aortic valve, you're gonna have quite a wide pulse pressure. So the systolic body would be quite a while away from the diastolic one. And again, there's these names of different kind of signs. You've got the cranks, which is n bad pulsation. Water hammer is a coughing pulse whenever you have someone's arm up and you can feel it popping away and you've got head boing. So the music. So someone's sitting there in the heads going away like that could be our. Agree on my stenosis sounds symptoms. You get this gradual exertional breathlessness and reduced exercise tolerance. So if someone says, can't deal with the one dead, you might consider, could this be something oxen? So coughing up blood palpitations, you got this atrial fibrillation which can arise as a result of that chest pain, thrombo thromboembolism. So that's bringing it back to the left atrium or by you can get that stasis of blood in the left atrial appendage. And that can then form a thrombus which can then form an embolism which can pass up and cause a stroke, hoarseness, peripheral of signs them, it's a mid to late diastolic, low pitched rumbling murmur, her best in the uh apex era really accentuated, lying on the left and aspirations. We have a loud s one in this case, malar flush. It can just can occur someone quick red, you can have a low volume pulse, it can have an uh I regularly irregular pulse necessarily getting at that af occur. You have an elevated JB pace, leave the ve on your neck, look quite high and get up then checking your head and respiratory cramps, mitral regur them acute. You've got breathlessness, breathless on exertion, fatigue and weakness and it can be uh asymptomatic and chronic cases until it kind of reaches a significant degree. Looking down at the signs you got a blowing or a whistling. It's quite high pitched murmur, but it's p systolic. So it will go through out systole and it'll be lightest in the uh apex area. And unlike aortic stenosis, this one will radiate to the axilla, accentuated, light on your left side and aspiration and give us matter. You have decompensated heart failure, uh signs of bilateral lung lung cramps that raise J BP and peripheral or sacral edema. So this is just like up the murmurs which are quite important to know. So, stenosis you have this crescendo decrescendo. So you can see in the diag on the left gets light and then it gets quiet again. A murmur. It's at the aortic area and radiate to the carotids and they can put a weak uh delayed pulse with regurgitation. Then it early diastolic murmur, decrescendo. It gets quieter, starts on quite high pitched and blowing again. Aortic area is best to hear it with mitral stenosis. Then it could be following the opening stop and it's due uh with a delayed rumbling, mid uh diastolic murmur and this is uh next like a mitral regurge. It's P. So the same signs throughout um high pitched blowing murmur, heart pass the mitral area and radiate to the Ella. So another quick question 80 presents to your practice experiencing breathlessness, lightheadedness, chest pain on exertion. You have a slow rising pulse. Your BP is 132, should be 1 50/1, 32, sorry. And an ejection, systolic murmur may be auscultated in the aortic area. It does radiate to the carotid. So based on that history and that examination, so what's happening here? What is the disease? But what is the most common cause of this disease? So, is it a a bicuspid valve? B, an idiopathic age rated calcification, rheumatic heart disease, familial hypercholesterolemia or radiation therapy for 20 seconds. So, identify what is the disease and then what is the most common cause of that disease? The question is, well, the question is lettered with typical examples of what you would expect. Ok. Very good. So the answer is big. So it's idiopathic age related calcification. This is a typical presentation of aortic stenosis and that's most common in those over 65. Ok. Back to back questions here. So, on auscultation of the precordium. So, listening to the chest, you're a mid to late diastolic low pitched rumbling murmur which is loudest at the mitral, uh the cardiac apex of the mitral area. It is a accentuated when lying on the left side and expiration. The patient has an irregularly irregular pulse and a malar flush is present. What's the most common cause of this pathology? So, it's a age-related annular calcification, mucopolysaccharidosis, infective endocarditis, rheumatic heart disease, or carcinoid syndrome. So, again, what I'm asking here is what is the pathology and then what is the most common cause of that pathology? So again, by 20 seconds, only 10 seconds, just give it a go. Ok. Nice one. So whenever you hear that, you think rheumatic heart disease, which is the most common cause of v stenosis. And in this case, the body will produce antibodies will have an immune reaction targeting the streptococcal antigens that are found in rheumatic fever. And that will also kind of uh mimic um the tissue found on the valve, the mitral valve. So it's autoimmune molecular mimicry. So we've talked about kind of your signs and symptoms. Someone presents that. What are you gonna do next? How are you going to investigate their diagnosis? How are you gonna confirm it with aortic stenosis? Then you have this uh bedside, you're gonna do an E CG might get left ventricular hypertrophy with left axis, left axis deviation. You might do a chest X ray, see cardiomegaly, pulmonary edema, potentially. But echo is the definitive diagnostic mentality to uh look at this really. Then aortic regurge. If you look on the top, you wanna think about the bad side first, you're gonna look for a grip by strep a throat swab and then ECG you're looking for that L VHP my blood stem, you're looking at these infective causes. So you're looking for infective endocarditis. You're doing nephrology markers in culture rheumatology, you're doing an antibody screen and transthoracic echo is the definitive diagnosis or definite diagnostic modality. So whenever you think of these diseases, if you think of moval disease, what is diagnostic echo, vital stenosis, then again, we're looking an CG but this time because it's affecting um that side of the heart maybe have a bit of uh relax deviation. And then you're going to uh N A PDA. Actually, you're gonna have that pulmonary edema left atrial enlargement, which can cause that af occurring echo, definitive cardiac catheterization can lead look at pressures and cardiac MRI can really look if there's any uh vegetations. In the case of um in fact, carditis or rheumatic micro exam, you have an ECG, you potentially have your uh left axis deviation. Um left ventricular hypertrophy, you're gonna do blood exam, you're gonna do an anti pro B MP, which is like for signs of heart failure cause that will be produced in greater quantities. In particular stress, imaging them chest X ray, you're gonna have your pulmonary edema atrial enlargement. But once again, echo is the diagnostic mortality. We will give you a definitive diagnosis because it'll give you lots of different evaluation parameters. So, what does my say most importantly? So this is like kind of our investigation um uh guidelines. So we're not refer someone with echo with a murmur, no other signs based upon the nature of the murmur. So, what is the murmur? Do they have a family history? What is their age? What is their medical history? So, you really want that two week uh urgent referral for specialist assessment if it's a systolic murmur and they're experiencing exertional s syncope or there's a murmur and severe symptoms with chest pain or breathlessness. And you will refer to a specialist after the echo. If there's moderate or severe valve disease or you have a bicuspid aortic valve. So what is the indication for intervention? So, if it's symptomatic and severe disease intervene if it's asymptomatic and severe, but it does meet these criteria, which I'll talk about in a bit, then you would enter vein uh treatment. So you're looking at aortic stenosis, you probably don't need to know all of these values. It's just if you want them there. So, Vox is looking at the aortic jet losses, the blood being forced out. How quick is it going? So it's more than 5 m per second, you think about it. But really aortic valve area, aortic stenosis. If it's less than 0.6 centimeters squared, then a stenotic, if there's a left, left in e fraction or other signs of heart failure, then you'd be in aortic regurgitation, then again, if there's a reduced left ventricular ejection fraction or an increased end end systolic diameter. So the heart isn't pumping out as much blood and intervention. They like a mitral regards again, with less than 60% of left ventricular ejection fractions. So the left working as well, it will be potentially under medicine and then looking at the systemic pulmonary artery pressure, um if it increase on exercise test, but monitoring if you're asymptomatic with severe bowel disease, um you don't really need to do anything, you just monitor um but it's not currently needed. So if you are monitoring a patient that doesn't need endovenous, you want to review them every 6 to 12 months. And again, this is with echo. If you have mild aortic or mild stenosis, you wanna do echo every 3 to 5 years. So this is looking at the exam. So for aortic valve disease, surgery is a first line indication and severe aortic stenosis regards or mixed disease. This is in low to intermediate risk surgical patients. Tavi then is trans aortic valve implantation. There is a non bicuspid aortic uh stenosis and this is in patients with high risk. So we're gonna do Tavi patients who are high risk or low risk patients will go through the surgery, mitral stenosis. Then you could do transcatheter, Valvo valvotomy. Sorry. But there was a a severe mitral stenosis. Although um you will do a replacement um in cases of severe rheumatic rheumatic mitral stenosis. If the vulva isn't suitable. Primary mental regards, then you're looking at uh repair, surgical repair in case of severe primary mental regards, um that's suitable for repair. And then you look at a replacement. If the uh repair is not suitable, then you can do a trans catheter edge to edge if it's symptomatic and surgery isn't really considered suitable. And then secondary micro reg regards, um this is kind of looking at at repair, um and those who have cardiac surgery for another indication and then medical management in case of heart failure, surgery is unsuitable. So look quickly, look at the bottoms that you go conservative medical and surgical. So conservative watch and wait pretty much and you do it every so often. Uh six months for mild, severe um longer if it's less severe. So medical management for EEC stenosis, they're gonna the left particular failure management. Then you've got your isolated medical management and those who really aren't suitable for any intervention, surgical them for symptomatic and complex asymptomatic patients where you look at Tavi and those who are kind of more frail and less suitable for surgery who are higher risk than surgical replacement. For those who are a bit younger and lower risk regards them. You've got your conservative and a severity dependent for mild to moderate medical them, you're trying to slow the rate of aortic grade dilatation and this is in cases of connective tissue disorders that are quite high risk. You want to lower the systolic BP for those who are beta blockers or ace inhibitors. You then want to uh those who are severely uh severe a asymptomatic patients, you want to monitor them annually. So 3 to 6 month follow up surgical lamb, you're looking at cases of symptomatic or complex asymptomatic cases or in cases where infarction carditis is refractory. Then there if there's a significant enlargement of the ascending ada and then in emergency cases, if there's uh hematologic instability, vital stenosis, um conservative, you're looking asymptomatic and stable, might not require treatment. Um You can have a regular follow up with echo with mi stenosis. Then you're quite concerned about uh atrial fibrillation. So you want to re control out patient and anticoagulate them. Diuretics um are for symptomatic relief of kind of heart failure, symptoms with pulmonary congestion and peripheral edema. Long acting nitrate will help with breathlessness and uh better someone's exercise tolerance to give them beta blockers, symptomatic cases. Then you can do uh percutaneous foul plasty. You can do a percutaneous mitral valve valvotomy or if it's severe disease that isn't too high risk. You're gonna do an open valve replacement and valves likely gonna be metallic regards management. Then conservative again, common, the asymptomatic and stable with regular uh echo followup medical. Then atrial fibrillation with weight and anticoagulation, weight control of anticoagulation, heart failure. You gonna give the medications for symptomatic relief and then acute pulmonary edema guidelines. You're gonna follow that in acute cases. Surgical is really definitive in symptomatic cases and you can either do a repair which is really preferable, preserving components. Whereas uh the replacement, you're gonna have the patient on lifelong anticoagulation. Um, and that'll be lifelong. Um But if you did a bioprosthetic one, though, you might have a lesser ability, but the requirement for anticoagulation would not be there. TBI them. This is for those patients who are high risk and quite old, minimally invasive procedure is not open heart surgery for those who have the severe disease that can be done under local or general anesthesia. So it's kind of like um the angiography we talked about earlier, but you're having your femoral access guide wires inserted up, got it be passed under X right? Guidance to the aortic valve area sheaths with the heart valve will kind of be positioned over where the guide wire is and then you'll do your valvuloplasty and it can deploy the valve, then echo will be used afterwards. It's very important to check that the function of the valve is actually working and there's not much leak. So these are just ti mean just to kinda show you what's happening on the top way, you're gonna pass the wire up, position the valve, deploy it. Hopefully it'll work to quickly go through open heart surgery. It's really location dependent. What valve are you approaching and that will depend on what you'll go through. It's not a median stheno will be used, but there are less invasive procedures. They'll place them on cardiopulmonary bypass and then the valve uh will you will incise the heart to access the different valves. So the ascending aorta will be used for the aortic valve. The left atrium could be incised for the mitral valve. So you're gonna dissect the stenotic valve from its annulus and then suture the valve, the knee valve onto the annulus and mitral ARDS. And we mentioned before, valve repair is really favored over replacement. And you normally put in a ring to reduce the size of the ul and that you can also repair the cord eye tendineae, we then close the cardiac incision and they'll perform a echo and that's leg of the valve function and the valve leg because you need to make sure it works before you finish the operation. Because if it doesn't work properly, you need to go back and fix things like caram you want to look at doing pacing wires and then mediastinal drains and then you will then close the door. So the choice of valves, we've talked about it before. You can have either have your bowel prosthetic, which has lesser dil lesser durability in another effective ORAC area. Or you can do mechanical valves which will be longer lasting, but you will have to permanently anticoagulate these patients due to the higher thromboembolic risk. So this is just a quite a nice diagram or sorry, not a diagram, a table of aortic valve disease. Let's just take you to see the different advantages and different advantages, disadvantages and the lifespan of these different bowels. So this is looking at the kind of the approaches of the aortic valve disease. So in this case, it's really looking at a calcified aortic valve. So you're kind of dissected by all that calcified area to make sure there's no uh risk of some then dissected the valve. The metal dia diagram is showing you them sizing the valve. And then on the right, you can see this kind of para technique where you kinda you are sit around the uh annulus area and then you are parachuting the valve down to where you've excised. The previous one. This is just color diagram. So you um went into the commissars, um you then excise the valve, you then size it and you then parachute the new valve into its uh position. So what's the it comes from that them again, complications are quite important and this is what patients want to know if you're going to operate on them. So, POSTOP mortality is about 2 to 5% survival. Post five years is like 80 to 90% 10 years, 68 to 89. And then um we want to look at the risk factors for surgery. Now, if you're above in age, you have a lower Jackson fraction, you heart failure with coronary artery disease or renal failure, you've got a greater risk of maybe getting an adverse outcome. So the early complications to really keep an eye on a hemorrhage. Bleeding is always a big consideration. Infection, arrhythmias and potentially stroke leg complications. You can hear your thromboembolic events, para valve in your leak, which is where the valve doesn't release, set properly. And you get this blood going pass the through the valve and then you get hemolysis in the case of a mechanical valve. So, mitral surgery, as you said, repairs for a replacement and repair does have an improved survival. So, uh in our case of repair, 10 year survival is 68% whereas a replacement um is 52%. So try and do repair if you can uh most common approach to the left uh atriotomy, although you can have a se transseptal approach, that's through the right atrium and then through the atrial septum, this can be done on a operation complications. Then you wanna be conscious of the circumflex artery, coronary sinus and the atrial grove, mitral stenosis, percutaneous mi mitral blade valvotomy or the open surgery. This is just like a mitral stenosis surgery. So the diagram on the left is just like an accessing the mitral valve. And then on the right, you can see a repair as that's in uh inserting an the strength to try and decrease there. And then this one is showing me a transeptal approach um to the radium and then to the and to yourself. So you have to know this is kind of the last bit we've talked about how to get those valves, diagnose treatment, all of that stuff. What type of valve do you want to put into the past history of your bioprosthetic valve? Limited lifespan, but it doesn't require anticoagulation or you have these mechanical valves, they have a really good lifespan, but they will require lifelong anticoagulation. And that's just the inr target there. And really, nowadays, the valve types that are used would really be the s dudes with the bi leaflets with two leaflets, two tilting metal discs and that the least uh strongest risk. So if you hear a metallic click, whenever you're listening to someone's chest, it's a metallic mitral valve. If you hear uh s two click, it's really gonna be me metallic aortic and any complications that might arise on thrombus formation, infective carditis or hemolysis. These are just different valves. So on the top left, you can see uh this g so the Bileaflet valve and then you can see the bioprosthetic valves are uh on the middle, on the right and then that one's just the bottom, show you the different types, the star which isn't really used anymore. So again, this is just showing you mechanical or bioprosthetic mechanical used in younger patients. Bioprosthetic, older mechanical will last longer with bioprosthetic may have a shorter lifespan and you will require anticoagulation of a mechanical valve but not with bioprosthetic. So, last question for those who are left. So a patient with a past medical history of downs, presents to your practice, complaining of breathlessness, fatigue and weakness on examination. A high pitched pan systolic murmur is heard loudest at the left fifth intercostal space, midclavicular line and this will radiate to the axilla. S one is quiet. You hear bilateral lung cramps. Um They're prove and uh sorry, they're empty. Pro B NPS come back elevated. Given the history and the examination, what valvular pathology is present here. So, given the history and the examination, what do you think's happened? Give it molly 10 seconds. OK. So the answer is the mitral reg regards. This is really a classic question. So we're gonna connect the tissue disorder disorder. You're immediately regurgitation. So it's pan systolic high pitched, blowing her best of mitral area radiating to the axilla, heart failure, present lung CRPS raised anti p signs of heart failure. You're thinking mitral well done. This is just uh already valve replacement, um mitral valve replacement videos if you're interested, this is the relevant nice guidance that I've taken from or stuff that you might wanna look up. These are the references that were kind of used to put together. So quite a wide variety of things to read up on uh that was put into this. Um Thank you for starting in. Um I appreciate you hanging in that long. Thank you. So, if there's any questions and thank you to uh Abdu uh Ran and Mr Peter man who is our surgical supervisor. A massive thank you to James as well for doing that talk. So much stuff in there was incredibly useful and also the NC QS, which are very, very good, especially after pass me was down over the weekend. Um I would also like to say a matter thank you to Abdu who coordinated this week and organized our speakers. Um I've been answering questions on the chat throughout. We go. Well, I don't know whether you saw but we had a question about Wean syndrome and also about the difference between class one and class T um class two and three on the Canada um cardiac score, but I answered those ones. Um I will send the feedback form once more in the chat. Please send it, fill it in and you will get um links to the recording and the slides as well as the certificate. Um They just take a while to process. So if you don't get them straight away, that will be why. Um Also a massive thank you to our sponsors yet again and please follow us on Medal and on Instagram just to keep in touch with our talks and our next talk is going to be on Wednesday and that's on the thoracic side of things. So, thank you so much, James yet again and have a nice evening. It's no problem. Thank you very much, looking forward. Thank you so much. Bye.