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Or will it start now? Yeah, I think it's started now. So what I'll do is I'll just restart. Everyone should be able to hear now. Yeah, there we go. Ok, so I'll just repeat kind of the first day I was talking about um this, yeah, I'll wait for you guys to refresh the page. Ok, cool. So hello. Really? Uh my name is I'm one of the foundation year two doctors at U HB uh currently working in, at Hartman's Hospital in cardiology. And today I'm going to be giving a talk on cardiac emergencies. So that kind of follows on from respiratory emergencies, which was one of the talks. Um I gave a couple of weeks ago and in the feedback, there were a couple of people who asked for a cardiology based session in a similar way. So that's what we're doing today. So similar to the first session, we'll kind of talk through it in a scenario based approach, looking at common acute things that you'll see from a cardiology standpoint. Um So we won't be covering kind of the long term management of chronic conditions and some of the more new cardiology stuff which can be covered in a different talk if you guys would be interested. Um And with that, I think we'll get started. So we'll cover some aspects of the UK MLA curriculum. Um And the actual four things that I was sent through from the curriculum were um covering acute coronary syndromes. So including mis um cardiac failure and arrhythmias and then cardiac arrest as well. Now, cardiac arrest goes more into that a s algorithm side of things. So we'll briefly touch upon that, but that is kind of a session within itself. So that can be covered in more detail. Um at a different time, there's other cardiac emergencies in terms of stuff you'll see on the front door such as hypertensive emergencies and what to look out for and then stuff like tamponade as well, which is a bit rarer, but it has kind of a very much exam based um exam focused bunch of findings that you should be aware of. So with that, I think we're ready to get started with the first scenario. So let's go. Um The first one is a 76 year old male who's presenting with chest pain on a background of a previous dey, I'll um give you guys about 30 seconds or so to read through the history and the A two E assessment. And then if you could just pop in the chat, um what you guys think would be relevant, further investigations. These, these sessions are meant to be kind of as interactive as possible. So do feel free to pop any questions at any time in the chat, um, as well as answers and each one's based on kind of a, a two E approach as well because that's a kind of a prerequisite regardless of whether it's a cardiac emergency or a respiratory emergency or whatever. So, with that brief, we've got usually has transient chest pain on exertion. Now, he's having severe chest pain at rest as well and, uh, GTN improved it. What would be some kind of further investigations that are crucial to do in this scenario, just popping in the chart. Yep, we would do an E CG. Definitely often that's just kind of a part of C regardless. But yes, an E CG. Anything else? Yep, we would do a chest X ray and the scenario as well. What else would help us kind of differentiate between the potential diagnoses at this stage? Ok. Yeah, you've done kind of a physical examination, um, as part of E as well as, um, in terms of the circulation as well and it's just a gentleman who's a bit sweaty but, um, otherwise there's not anything too over on physical examination. Yeah, exactly. So chest pain bloods as well. So, uh, troponins as well as uh, one that you've not mentioned they d dimer are important in this scenario as well because it can be, um, you know, secondary to something like AP, that'd give you chest pain, although, albeit not usually relieved by GTN, but something you've got to rule out. So, yeah, that's all right. I've, um, of course there's more investigations that you do, but the two that I've kind of highlighted are on the next screen here. So you do an E CG and I've just shown you kind of the, um, lateral leads on this one and then also you've got the blood test results. So now trying to piece it all together, we've got, can anyone tell me what this E CG is showing? And we can kind of infer that the other leads were normal in this scenario. Any abnormal kind of just going through the ECG? Is there anything abnormal about? Yeah, exactly. So we've got some T we versions in V five and V six and ABL as well actually. And also, I don't think we've got any ST depression in this scenario. Um Not that I can see, but yeah, we've got two, we versions which are kind of a nonspecific change but can indicate ischemia. Um And then the troponins are negative. It could also be a sign of previous ischemia. Exactly. Yeah. Um alongside Q waves and things like that now, so we've got that right. We've not got any kind of ST elevation or anything like that, but we've also got the bloods with the troponins being negative. So, going back to the history now, you've got proponents negative and you've got severe ch central chest pain, which has been present at rest and improving on GTN. What would that indicate to yourselves in terms of what the diagnosis could be in this scenario? Yeah. So unstable Angina. So in terms of a CSS, um unstable Angina is an A CS. Um and the reason why it occurs is because of critical vessel stenosis, but the kind of differentiating factor from the others is the fact that it's not causing an infarction. Um I probably should have asked this question before switching to the slide. But the main difference between stable Angina and unstable Angina and why unstable Angina is um you know, an acute coronary syndrome and therefore, a cardiac emergency is because it's occurring at rest. Um and therefore, it's treated similarly to an NSTEMI. So we've kind of gone through by looking through the history, the key differences between Temi and unstable Angina, but I've made a table as well, which I think outlines it well. So starting off with the mechanism of what actually is going on. Unstable Angina is that it's called vessel stenosis, which is causing transient ischemia to the endocardium, but it's not going through the cardiac layers and it's not actually infarcted tissue there. Either en es come almost like a step above where you've got that um stenosis and you might have partial plaque rupture. However, it's not extending throughout the layers of that cardiac muscle. So it's still endocardial um but it's infarcted, the tissue there and then Temi is transmural. So it's going not only in the endocardium but also in the myocardium and epicardium. Um And therefore, that's why you get ST elevation uh on the ECG EC GS can be normal in Anstey and in unstable Angina. But you may also see t wave inversion, which is what we were seeing um in the E CG earlier, you may also see ST depression. Um the way to differentiate then between an NSTEMI and unstable Angina is as we did earlier by looking at the cardiac markers such as proponents. So you'd expect raised dynamic troponins in antemi um dynamic, meaning increasing by over 20%. Um And when you do serial troponin measurements in a stemi, you don't need a race drop for the diagnosis, you would expect a race troponin. However, if you see that ST elevation with the um history matching that presentation as well, then you treat it. You're not gonna wait for a troponin to see whether it is a stem or not. Um So, in terms of management of a CS moving to that.