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Yeah, bye. Right. Hi everyone. Can you hear me? Can people hear me? Just say? Yeah, there we go. All right, perfect. So, hi, my name is Doctor Beer and um I am a fy one currently um in the West Midlands and um I'm one of the final year, er, leads at mind the bleep er, and I'm presenting um just a quick session on acute coronary syndrome um with my colleague, Doctor El er Kami, who is uh one of the um medical leads at my I believe as well. Ok. So um we'll get started at around five past six. We'll just wait for a few more people to join and um we should be able to get started by the way uh on your screen. Is it just the slides that you can see at the moment? Can you see the red slides or is it just my face? I don't know which one we can see the slides on. Can. Perfect. So we can see the slides on camera. Alright, great. So yeah, we can make a start in about um five minutes all. Yeah, just um again, just to everyone who's just now joining, as I said to, um, everyone else, we'll just make a start in a couple of minutes. All right, we'll just wait for a few more people to join and, um, yeah, then we can go. Hi, everyone. So, as I promised, um, it's five past six. So let's make a start. I don't wanna delay you guys too much cos it's a Saturday night. So let me just put this on full screen. Hopefully, you guys can all see. Um, so as I said, um, we're gonna be talking about acute coronary syndrome today, which will, er, essentially, um it's synonymous with a heart attack, right? But we're gonna be talking about the three different forms uh from er, less severe to more severe, um, that can uh progress from unstable angina all the way to an ST elevation myocardial infarction. And um we'll explain further what these terms mean. So, thank you for joining us. So, what is um an A CS, what is an acute coronary syndrome? All right. So, um essentially, it's either a partial or a foot occlusion of a coronary artery. So we have these coronary arteries that supply the heart muscle, right? Um, with oxygen and essentially, when either any of these are blocked, um, essentially the muscle that is supplied and the area that it supplies of the heart can become necrosis or slash dead, right? Obviously, that occurs over time and during that time period is really the golden time for us to intervene and we'll talk about that later. And uh characteristically, this um occlusion is not relieved by vasodilation. So, in angina, usually what will happen is the coronary vessels vasodilate to compensate, right, for the obstruction, which is usually an atherosclerosis of kind. However, in this case, even though there's maximal vasodilation of the coronary artery to try and compensate, the occlusion is still there. The occlusion is getting bigger and bigger and bigger, right? And we'll talk about why that can be because of the causes and that is what is contributing to the pain. And the pain is just because of ischemia because there's less oxygen in going towards that heart muscle, right? And essentially that will cause pain in the heart muscle that will stimulate some of the pain fibers, right? Because of the lack of oxygen, right. And uh another characteristic feature is that the pain is not relieved by rest or GTN. Whereas Angina is relieved by rest or using GTN spray, which is a type of spray that is a vasodilator. Again, that's to increase the amount of oxygen supply to the heart. Ok. So hopefully, that makes sense. Now, again, how do we differentiate it from uh uh Angina? Usually, this is associated with hemodynamic instability, usually meaning a low blood, low BP or a high heart rate, right? Um And also associated with some nausea or vomiting, um which we will, we can um also control that we'll talk about later as well. Uh and also some cold and clamminess as well. Um As I've talked about angina a few times, usually, um Angina is what precedes this condition. Ok. So usually patients will have a history of angina history of intermittent chest pain before their acute coronary episode. All right. And, and without treatment, uh it, it will result in eventual death of the myocardial tissue. As I said, if we don't treat within that golden time period, then there'll be death of the tissue. Um And the most common cause is usually a rupture of an atherosclerotic plaque and atherosclerosis usually just builds up because of our diet because of smoking and other lifestyle factors and sometimes it can be genetic as well. Um And usually that when that builds up, eventually it can become weakened rupture and that rupture then causes an occlusion of the blood vessels. All right. Er And as I said, there's three categories um from less severe to more, more severe. Um And basically, their cattering is based on the amount of arterial occlusion. And also that therefore, um is synonymous with the cardiac markers that we'll talk about known as troponins. So you've got unstable angina and semi and then stemi, right? That's from least severe to most severe. Ok. And this image in the corner just basically shows that um what it kind of looks like the athero atherosclerotic plaque and then when it ruptures, um we have a complete blockade of that vessel in terms of the mapping um of the coronary arteries and exactly what areas we're looking at. The main things to really note here, right is that you have three types of arteries, you have the epicardial arteries and these are the main coronary arteries that we know of such as the right coronary, the left coronary, et cetera. Then you have the intramural arteries which are the arteries connecting the epicardial to the subendocardial, which is right on the anterior of the heart, right on the anterior of the cardiac muscle, right in the subendocardium, we call it right. And then you have the subendocardial arteries. All right. So what happens is usually during systole, when the heart is contracting these intramural arteries, they're pressed and therefore there's no blood flow going through them.