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Yeah. Um Hi everyone. Sorry about the latest start. Um Hope you're having a good evening. Uh I'm gonna be uh presenting uh syncope and chest pain. Sorry. Um We've only got 40 minutes, unfortunately. Uh So it's gonna be have to going to have to be rather quick. Um But hopefully I'll get through it all. OK. So just um in terms of how I structure my lectures, I usually go definition background diagnosis and management and I think that's the best way to learn, in my opinion. Um Through understanding, I think memory will help but understanding we'll get you those last few marks to get awards like distinctions and distinction stars. Um So let's get right into it. So we're gonna be focusing on a lot. We're gonna be going through ischemic heart disease, cardiac arrest, tiny bit syncope and all the arrhythmias um in terms of the presentations that are covered um cardio respiratory arrest, chest pain, palpitations, blackouts and fades and decreased slash loss of consciousness. Um So I think I'm gonna have to be going through it all quite quickly and if there's anything you want more teaching on all my notes, for example, do email me, I've got it at the beginning and at the end, um just conceptually the heart has two main functions. It acts as a pump and it acts as a battery pump relates to its circulation and functional roles and battery to its conduction and electrophysiological roles and stuff can go wrong with either one of these and this covers most conditions. So for example, pump failure is often heart failure and a number of the stuff will be talking about today and battery often leads to arrhythmias. So let's talk about pump. So let's start with ischemic heart disease. Uh definition of of ischemic is pretty self explanatory, just ina inadequate blood supply to a local area due to a blockage of the blood vessel supply in the area. Apply this to ischemic heart disease. It is the term that's given to heart problems caused by narrow heart uh arteries, coronary arteries that supply blood to the heart muscle of the myocardium. And we can basically categorize these into two at first, stable angina and acute Coronary syndrome. And acute coronary syndrome is further er further classified into unstable angina and stemi and stemi. So let's have a look at the bit of the background of coronary artery disease. Um basically uh ischemic heart disease or coronary artery disease describes the gradual build up of fla fatty plaques within the walls of the coronary arteries. Now, two main problems occurs with this, there's a gradual narrowing which means less blood, less oxygen. The tissue demand is not met. There's bad myocardial damage which leads to symptoms of angina and further down the line. Uh heart failure. The second problem is a gradual build up of the plaque. Plaque instability increases, which I'll go over very, very briefly in the next slide uh causing sudden plaque rupture. Um And this can cause a sudden occlusion of the arteries uh through a thrombocyst or an emboli embolism. Um And on the left, you can just see a diagram, a very simple diagram of an artery slowly uh becoming more narrow as the plaque builds. So why does this happen? Uh atherosclerosis. This is by far the most common way to develop ischemic heart disease. There are other types of er of ways of developing ischemic heart disease um that this is uh outside of the scope of this lecture. Um Hopefully, there's another lecture talking about atherosclerosis in a bit more depth. Um but just very quickly the digger on the bottom left and below the dotted line. Uh is just a quick summary. So there's endothelial dysfunction. This can happen for a number of reasons like smoking, hypertension or um turbulent blood flow. This induces a proinflammatory state in the vascular endothelium. We then get uh um endothelial um endothelial cells, er overexpressing VCA M one which causes monocytes to adhere to the vascular endothelial wall and migrate through the wall. These often er bring in LDL particles as well. These monocytes turn into macrophages and because of the fatty infiltrates turn into foam cells and this builds and builds up to form that lipid core. And at the very center of the lipid core because there's less blood flow, you get a bit of necrosis. And on top, there's smooth mus muscle pro proliferation to try and like handle this big lipid core. This eventually turns fibrotic um and it gets very, very unstable because of the necrotic core, which is uh obviously not very structurally sound and a fib uh fibrous capsule. So what happens here is uh over time, this gets bigger and bigger and it can either narrow the arteries or break off and cause an embolus in a slightly smaller artery in terms of risk factors. This is really important for just cardiovascular disease in general, but specifically ischemic heart disease. So you've got unmodifiable risk factors such as family history, age and being male. You've also got some modifiable risk factors and these are really uh big things to focus on. These always come up and uh they're very pertinent. So, smoking diabetes, mellitus, hypertension dyslipidemia and obesity. And remember those five cardiovascular risk factors, they do come up a lot. So as I said, a couple slides, a few slides ago, we can categorize ischemic heart disease and stable angina and acute coronary syndrome first. So let's talk about stable angina. This is an interesting condition because to be honest, it's not really a condition, it's more of a symptom, um, but uh, often gets defined as a condition. Um, so it's characterized by chest discomfort that is provoked with exertion and relieved at rest. Um, just in terms of ischemic heart disease, in general, coronary disease is the leading cause of morbidity and mortality worldwide. So, it's, um, you're gonna see it a lot in, in practice and in your exams, uh, what's common is common and that is actually true. Uh Faculty says that all the time um and uh they're not trying to trick you. Uh these may be more simple conditions but conditions that come up a lot um do come up a lot. So, uh in terms of the etiology, stable angina, ischemic heart disease, um a supply demand mismatch as we get ischemia and atherosclerosis. Um So I've just got in the top right there, the Socrates, which I put on the next slide as well. But in terms of the approach, uh what you do is look at the symptoms and the risk factors and you determine if they're stable or not. So how do we determine the symptoms? Angina? That's pretty obvious. And we'll use Socrates er in the OSC but also in the exam will help. And what exactly is Angina? If you look towards the right of the screen, it's often a triad of substernal chest discomfort. So right beneath your sternum. So, which should provoke by exercise and relieve with the rest and that's what we call stable angina physical exam. Um, you could see maybe signs of heart failure if you've got angina, maybe HCM if you've got chest pain or other risk factors, uh, like a previous surgery, for example, um, like signs of a previous surgery, in terms of investigations, I like to group them into bedside bloods and imaging. So in terms of the bedside, we have an E CG, you might see a pathological Q wave, which I'll talk about a bit more, but it basically means a prior infarct and that you would get that in stable angina, sometimes bloods, um just a normal set of bloods, most importantly, troponins at the end. Um because that rules in or out uh in semi as well. Um anemia versus unstable angina. So important to include an imaging echo, chest, X ray, and coronary angiograph echo. We could see structurally how the heart is doing chest X rays often rule out other causes of chest pain. And I'll talk about this again later. But it comes up a lot that the first thing you want to do with anyone that comes in with chest pain other than E CG and history and exam uh is chest X ray and the coronary and may be um considered if uh this patient becomes unstable. So going through the Socrates, substernal chest is the sight onset is sudden, but may have had it before or it comes on with exercise characters, heaviness, tightness. You often see this over just classical pain radiates to the neck jaw, the left arm, sometimes even the right arm associated symptoms, you get dyspnea, which is shortness of breath, fatigue, nausea, timing. There's not really a lot to say there. Um, exacerbating or leaving factors. So it's provoked with exercise, lie by rest as characterized by stable angina and severity is often quite high like above five. Um, in terms of that Q wave, it's basically, so AQ wave is obviously normal, it's part of the QR S. Um but it can be pathological or signs that patho pathology exist if it's 40 milliseconds wide, two millimeters deep or more than 25% of the depth of the QR S complex. And it's seen in leads V one to V three and it's a sign of previous ischemia. The management er, is often just improving quality of life and improving outcomes. And that's two really important things, especially in the cardiovascular world, which is um that uh there will be drugs for quality improvement, quality of life improvement and there'll be drugs to improve outcomes, um which is er, stuff like a further my myocardial infarction or death. Um send you on to the treatment algorithm. I