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Ok. Um Sure, I'll make a wee start then. Um, so my name is Courtney. Um I am a final year medical student. Um just uh finished, we've literally just finished our exams and we're doing our assistanceship at the minute. Um You might see us about whatever hospitals you are in. Um Right now I am in Antrim Hospital doing my assistantship, my F zero. If you're in Antrim, you see me about say hello? Um I am actually um one of the final years in charge of the peer share kind of scheme in um in Antrim. So if you want to stop me, ask me about anything brilliant. Um If you see me and you're like, oh, there's Courtney. Um, you know what? I haven't done a blood this year and I really want somebody to come and watch me do a blood or to show me how to do a blood, like just grab me and I'll be, I mean, I'll, I'll be more than happy to come with you. I can't promise that I'll hit the blood, but I'll, I'll definitely, um, I'll definitely be willing to give it a go. Um, so yeah, Um I'm going to be doing the peer lecture on cardiology. Um I think this is the 1st 3rd year topic that you're getting um a peer share lecture on. So you're very, very welcome. Um These are, well, for me, anyway, when I was revising some of the peer share lectures were the most useful um things that I had like right up until my finals there, some of the lectures was literally the only material that I learned for that topic. Um So for example, our gynecology peer lecturer in fourth year, I literally flicked through the Gynecology powerpoint and I never looked at anything else for gynecology. So, um they are really, really helpful. Um Sometimes I think it's better being taught by someone who's just learned this material. Um as opposed to someone who's an expert in it because the people who are experts in the topic maybe aren't always teaching at the level of which you need to know. Um Otherwise somebody who's just learned, it can say, oh, I would learn this and, you know, I would probably wouldn't learn that. Um So yeah, normally what we find peer share is that like at the start, the numbers are quite low. Um And by the end of the series of lectures, everybody's went into placement and told their friends. Um, oh, that lecture is actually quite useful and by the end of them then, um there's a much bigger turnout. Um I hope this is useful. Um, sometimes you don't vibe with the slides or you're just not really, um, listening or whatever and, and the pear lectures aren't, aren't that useful to you? But I hope this is useful and please feel free to stick any, um, questions into the chat box and I will try my best to answer them again. I can't make any promises that I'll be able to, but I'll definitely give it a go. Um, so cardiology then one of the biggies in terms of medic medical specialties, um One of the ones that people fear, I think, um I don't mind it equally. I'm probably not going to be a cardiologist in the future, but I don't mind it as a topic. Um It always kind of made a wee bit of sense to me. I had a couple of really nice doctors who took the time to explain a lot of cardiology stuff to me as I was going through. Um, which, you know, yourselves makes a massive difference in terms of whether you like a topic or not. Um So cardiology then and so some topics. So you've got your stable angina, um your acute Coronary syndromes, heart failure, valve disease, hypertension, um arrhythmias. Um So your tachy, your braies and that includes atrial fibrillation, infective endocarditis, um and pericarditis and I'm going to go over some osk stuff as, as well at the end. Um I understand there's gonna be some fourth year students here who um have already done cardiology and just need to blitz through maybe some third years here who haven't actually looked at cardiology much yet at all. Um So I'm going to try and pitch this at a level somewhere in between um and try to hopefully get you to understand as much of it as possible. Um OK, so Angina then. Um ok, so you know what Angina is that there are pee and discomfort to the chest, it's brought on by exertion. Um, but the important thing about stable Angina is that it is alleviated by rest. Um, um, and that is rest like under five minutes. Um Usually by the time they're sitting down for a couple of minutes, peeing will be gone, um, it'll be alleviated by that or they have their wee GTN spray and it'll be alleviated by that. Um There's at their grading class system there for their, um, Angina, um, on how much it limits their regular activities. Um, you know, yourselves about risk factors. These can be most mo both modifiable and nonmodifiable. Um, so some of the, um, modifiable risk factors would be um, your smoking, your lifestyle, whether you're obese or not managing your hypertension, managing your diabetes. Um, non uh, nonmodifiable end is going to be getting older. Um, males are unfortunately, um, predisposed to it more and then your family history as well. You can't really do anything about that. Um, but it is a risk factor, um, investigations then, um, ECG you might see some ischemic changes on an ECG do your bloods, um, anemia and th and hypothyroidism can make any sort of stable angina symptoms way worse. Um, so it's worth doing those and, um, a CT pulmonary angiogram. So let's see what the vessels are actually like, how, um, occluded the vessels are in the heart using that CT pulmonary angiogram. Then, um, in terms of management for stable angina so conservative, um stop them from smoking, probably the most important thing that you can do. And to be honest with you, that kind of goes for anything um heart or lung really related, um stop them from smoking. Um Glycemic control if they've got diabetes, manage their BP, manage their cholesterol um and encourage them to lose weight, some medical management. So GTN spray, nitrate dilates the vessels of the heart. So um helps perfusion of the heart tissue. So prevents um those um angina peeing symptoms um by dilating the vessels. Um and it's quite effective. Um If you give a couple of sprays of it, it, it works um for more long term relief, then in terms of medical management, they can take a beta blocker or a rate limiting calcium channel blocker um or a more long acting nitrate that's not the GTN. So something like isosorbide mononitrate there. Um And what we really don't want is for these people to go on and to have a heart attack or a stroke. Um, so let's give them some aspirin, let's give them a statin, let's make sure their BP is under control and that'll prevent that hopefully from happening to them in the future. Ok. So, surgery then if it's none of that stuff's helping, you're really, really worried about this person and you think that they could easily, um, progress and, um, and have a heart attack in the future. Um You're gonna do a PC Coronary angioplasty and stenting or a CAV, so coronary artery bypass graft there. Um Yeah, that's, I think that's what I have to say. Ok, so your acute coronary syndromes, then what we would class as mis or heart attacks. Um So I want you just to think about three things. Um when you think about an acute coronary syndrome, um think about the pain, um the troponins and whether or not they've got ST elevation and that'll tell you which of the acute coronary syndromes they have. So, um acute Coronary syndrome can be an unstable angina. So one step up from what we've just talked about uh a non ST elevation, myocardial infarction or an ST elevation myocardial infarction. And we call those NSTEMI or sties. Um So, pain which does not get alleviated by rest, but there's no troponin rise or ECG changes, but it's not being alleviated by rest. So it can't be stable angina that's unstable angina. It hasn't progressed enough yet for there to be um serious uh cardiac death. So there's no troponin rise. Um and there's no CD changes yet, but it is still an acute Coronary syndrome and it probably will or it definitely could progress to an end demy or a stemmy if it's not dealt with um appropriately. Um So that is unstable angina, especially if like symptoms are lasting over like 15 minutes. I don't write that on the slide but over 15 minutes. And you're thinking, ok, um this is an unstable angina, an all ST elevation myocardial cardial infarction. Then they also have the chest pain, but they also have the second um thing that I want you to think about, they also have a trope rice. Um So we know that troponin um is was released by the cardiac tissue as it's dying. Um So it's a sign of dead tissue, um cardiac tissue. So, um that is chest pain and an elevated trope is um but there's no ST elevation on the ECG. Um Now, there might be other changes on the ECG and I've written them on there. So they're ST segment depression or at wave inversion or just no ischemic changes, you might just see an ECG and it'd be totally fine. Um But the important thing is there's no ST elevation sty, it's the biggie, it's all free. Ok. So it's yes, chest pain, really severe chest pain. You know, the pain is gonna be sitting on the chest and they also can, uh, there a troops will also be, um, enlarged and, um, they will have ast elevation and that'll be quite marked on the ECG and, you know, they're the ECGS that you'll know and you'll see and you'll know what they are right away. Um, so symptoms then, um, we know that constricting central chest pain, we know it can radiate to your arm, your jaw, nausea, vomiting, sweatiness and clamminess. Um, as I indicated that your patients are actually quite unwell if they're sitting sweating and clammy, um, the patient themselves feeling um, impending doom, they ask, are you, am I going to die? Doctor? Um, shortness of breath palpitations. Um, and I, oh, I did write on 15 minutes. It's there 15 minutes. Um So yeah, I think when you're thinking about acute coronary syndrome, you're going pain troponin ST elevation. And I'm going to send you these slides, these slides will go out to you. I promise. Ok, this is something which I hated. And when I was learning that I just couldn't really get my head around it. But, um, this is which artery then and the heart attack or the M is in. Um, so this is something which I think you need to just don't, don't wrote, learn this. You'll hate yourself if you wrote, learn this. I tried to learn this and it didn't work. You have to understand this. So I'm going to try and chat it through here. Um and, and go away and like look at it yourself as well. Um So your right coronary artery. Um You can see it in that wee picture at the top. Hold on. Can you see my mouse? Can you see my mouse? Yeah, we can see it. Oh, thanks. Um Yeah, so your right coronary artery um kind of looks round, where'd it go? Oh, yeah, it looks around the heart and goes down and feeds the inferior part of the heart. So, as you see, there it goes down to the bottom of the heart. Um So it, the important part is that it looks around the right ventricle and inferior aspect of the left ventricle. Ok. Your left coronary artery, then it splits. Um So it's either the left common, um which is here or it goes into your left anterior descending or your circumflex artery. Um So your left anterior descending is um feeding the left atrium. Uh sorry, the left ventricle, I'm just ignore me, I'm talking rubbish, but um the left ventricle um and it's going to be on the anterior aspect of the heart. Um oh, and then the left circumflex, it's looping around the side and it's going to feed the lateral aspect of the heart. Um the left atrium and like kind of the posterior aspect of the left ventricle. Um So what does that mean? Then? Think about an ECG um you are, you have your um chest leads an ECG leads 1 to 6, um, especially 1 to 4 and they're sitting, um, right over the heart. Um And we know the heart doesn't sit kind of straight in the chest. The left ventricle is sitting out of the heart. Um And so those four leads 1 to 4 V, 1 to 4. Your four chest leads are going to be sitting on the anterior aspect of the heart and that's your left ventricle and that's gonna be your left anterior descending artery. Um If you go on around the side, then um hold on. So you go on around, on around the side and you put your leads, um V five and V six. and they are going to be looking at the lateral side of the heart. So we're looking at the heart from this side and we know that that's um supplied by the circumflex artery. Um And then if we're looking up at the heart, we know that there's leads that go in the feet. Um We're looking up at the heart. Um So that there's your lead two, your three and your VF and that's going to be looking at the inferior part of the heart, which we know is um supplied by the right coronary artery. To be honest with you, this has been explained to me many, many times and I didn't get it. Um You nearly need to sit down with a pen and a bit of paper and draw out a heart for yourself and go. OK. Where, where are these leads looking at of the heart? Um and I would really recommend that you do this because to rope, learn this, it's just no crack. Um And you'll understand it a whole lot better if you just sit and learn it. Um OK. So mm oh Why is this not moving? Oh, there we go. OK. So let's talk about an our ECG placement. A wee bit better. So, um it's called a 12 lead ECG, but you only put 10 leads on a patient's body. So why, why is that? Um So you're putting six leads on the patient's chest and you have four limb leads. Ok. To confuse things even more. The lead that you put on to the right foot is a neutral lead. It's only purpose is to complete the electrical circuit. It doesn't do anything. It doesn't actually read when you see an ECG and I'm going to show you ECG S in a wee minute. There's no like left foot lead reading on it. It doesn't do anything. It's a neutral lead. So now we're technically down to nine leads and it's a 12 lead ECG. So how does that work? So leads, one leads, two and leads and lead three are leads which actually exist by comparing the electrical um like circuit of two different leads. Um And two different limb leads at that. So if you look at this here, image here. Um Lead one doesn't actually exist as an actual lead that you will see. Um But it um it compares VL, so your left arm lead to your AVR your right arm lead, it compares the um electrical activity in those two leads and that's what comes up when you're reading. Uh One lead two compares the left foot with the right and lead three compares the left foot with the left arm. So what does that mean? Then your heart is up here. So leads two leads three and F are gonna be looking up at the heart. If you picture your patient lying flat, they are looking up at the heart. So they're going to be looking at the inferior aspect of the heart. They're going to be looking at what the right coronary artery. So if we go back to here, the right coronary artery looks up and round and um supplies the inferior part of the heart. So leads two leads three and aVF are going to look at that. Um then the lateral part of the heart. So if we go over here over here is the lateral side. So, oh, this is lead five, lead six and also, then VL and one as well, we'll all be looking at the lateral side of the heart as if it's looking that way at the heart. Um So that's where you'll see if there's like a lateral or a left circumflex artery blockage or a lateral stemi. Um That's where you're gonna see the changes. Ok. Um And then an anterior part. So we know that, that there is the left, anterior descending artery. So left anterior descending artery um is the, is the anterior part and you're gonna see the changes in V one, V two, V three and V four right at the anterior part of the chest. I hope that makes a wee bit more sense. Um But as I say, I want you to like if I were you and what I had to do for my finals was to actually learn it and to work out why everything read the way it read if you know what I mean. Um So if I go on then, OK, so this is a stemi, how do I know it's a sty and that's your massive big ST elevation on these leads here. And so instead of this returning down to the baseline, it stays elevated. So it's ST elevation. Um and well, where is it in the heart? Well, here it is in lead one, it's in lead two. Definitely, it's in lead three and it's in um V four, chest lead V four as well. So V one, V two, V three and V four and a little bit in V five as well are all big ST elevation. Um And we've just talked about how that means that then that is a anterior stemi. Um So if you look across your other leads. There's not really anything that remarkable, a wee bit of something but nothing really that impressive but V one, V two, V three and V four, the anterior part of the heart, the left anterior descending artery. Ok. And so some more then this is ast elevation here in V two, V three, V four, V five, V six and in VL as well. Um So when we say it goes into V five and V six, they're looking at the lateral part of the heart. Um And so is VL as well. So that's your left arm. So coming lateral um into the heart. Um so that there is gonna be a lateral stemmy um or, and that there is gonna be in the left circumflex artery. OK. Um And here's another ECG then uh ST elevation big time um in need two and in lead three here and in aVF. Um and remember that foot lead and then lead two and lead three are looking up at the heart comparing the um foot leads with the two arm leads to lead two and three. And aVF are looking up at the heart to the inferior part of the heart. So the right um coronary artery there, um I hope I haven't just said a lot of words that actually confuse you. Um Oh, somebody asked a question. Is there ST depression in lead three? I wonder which ECG that was about? Let's go back. Oh, this one? Yeah, there is, um, big time and you'll see that a lot with ecgs. So, um, quite often the changes that you'll see. Um, so if you see a massive ST elevation in V two, V three, V four, V five, V six, you'll see like a reciprocal change in your other leads where they'll actually be depression in the other leads. Um, that doesn't mean it's not a semi. You still take it as a semi because V two V three V four, V five V six all um still have the elevation, but it's actually just a reciprocal change. It's just another sign of ischemia. It just hasn't um properly came out yet. Um ok. Nope. Ok. So, um a 68 year old female has presented to the emergency department complaining of a sudden onset crushing chest pain, ecg shows sinus tachycardia. Nothing else to proin level returns as four at one hour and five at five hours. They're not impressive. They're not really um notable results there at all. Um So, um what is the most likely diagnosis in this patient? Then you can pretty sure you can send me a message privately or you can just send it into the chat if you want, I'll be fit to see what you said if you have an answer. Yeah. Yep. So getting a couple of answers there, um And the answer is b it's unstable Angina. So if you think about your three things, you have the chest pain. Um It's not relieving with rest. Um but there's no ecg changes, there's no trope rise. Um It can't be any sort of m I it's unstable angina. So management then. Um so we think about mona, so morphine uh you titrate morphine to effectiveness. Um You don't want it to be toxic for the patient or overdose the patient either. And obviously everybody's um kind of opioid um toxicity like threshold will be different. So give them wee 2 mg initially and then you just kind of titrate that to effectiveness. Um oxygen if required, don't put oxygen on someone if they've got um normal oxygen saturations, um it only increases free radicals and damage. There's no point in doing it. Um nitrates then. So give them their two puffs of their GTN if they haven't had it already, um it'll help their peeing. Um And it also, as I say, dilates the vessels in the heart. Um So it actually does like improve um myocardial perfusion. So give it um and then aspirin. Um So mona ends on aspirin, but you also have to think it can't just be aspirin, it has to be a two like dual antiplatelet therapy. So um Aspirin 300 mega loading dose plus either agre or clopidogrel. Now, that's just trust that's just based on trust. Um I know northern trust at the minute are um on the tag 180 mg. Um I'm not sure other trusts are on clopidogrel, you just follow trust guidance for that. So, um if you were in an exam situation, um both of those are right. Um Either of those are right and they're not going to give you that in an M CQ, you know, and go, which one do you want? Tag or clopidogrel? They're both fine. Um It's just a second antiplatelet. Um So mona that's initial management for all of your acute Coronary syndromes. And then you can kind of think about semi. Um so, er definitive management for a semi is a PC angiography. Um and this um needs to be delivered to the patient within two hours of them presenting. Um So this isn't within two hours of their symptoms, like the onset of their symptoms. So, if, if um you're learning a wee bit about strokes, um you know, stroke license calls and stuff have to be done within like 4.5 hours to six hours of um their initial symptom. That's not the case for a semi or an acute Coronary syndrome. It's from when they arrive in hospital, you have two hours to get them PC. Um So, and you know what northern Ireland is a small country that's actually not that hard to do. They come into Causeway Hospital and you send blue light them in an ambulance to Atla Van. Um they come into Antrim Hospital and you blue light them in an ambulance to the royal. Um, and I, yeah, they're the only two places with, um, PCI in the country, I believe. Um, but you can get anywhere in northern Ireland in two hours. Um, so the, it's more just you don't want to delay in diagnosing them, um, because you need to get them PC within two hours. Um, if thrombolysis or if PCI wouldn't be available in two hours or that's not gonna be an option for you. Um You consider you can consider thrombolysis. Um um and that comes in the form of alteplase. Um but that's gonna be with a cardiology input um to help you kind of make that decision. Um an NSTEMI then um they are not rushed right for PC. Um but a lot of them actually will get um A PC. So you calculate their grace score, their grace score is going to um tell you their risk of mortality um in the next year is it, I'm not actually 100% sure. Um But depending on the score, they can then go for non urgent PCI in a couple of days, 48 hours. Um, whatever, you know, just whenever I suppose they can get them slotted in, I think it's ideally supposed to be within 48 hours, but I've seen patients sitting on the wards awaiting PC for um a week after an end dey. Um and then you can cabbage them as well. Um Coronary artery bypass graft there if their arteries are just um totally occluded. So, ongoing management um echo. Um So you don't know what damage um the event the M has had on the heart. So you want to kind of review um ventricular function, you want to review um the like valve function, et cetera in the heart. So get them an echo, um cardiac rehabilitation. Um and there's a team for that and then secondary prevention I learned this is six days, you can see what you think of this. Um So you have to give them aspirin and other antiplatelet. So, um again, that's clopidogrel tag. Um Then atorvastatin an ace inhibitor atenolol, but it's actually not Atenolol. Atenolol is just to remind you, it's, it's to fit in with the six A just to remind you that they need a beta blocker and the actual beta blocker they need is bisoprolol normally. Um And then uh aldosterone antagonists as well. So that's something like Aleen um or spironolactone. Um So there is your six A if you hate that and because some of them don't actually fit into an A um that's fine, you don't have to use it. Um It was just something that kinda help me post M I complications then. So um A and it's like the most rudimentary description of a myocardial infarction that you can come out up with is the heart is not getting enough blood. So what can happen if the heart does not get enough blood for a while. So, obviously, death, that's one of the biggest ones. Um but also you can just damage that cardiac tissue. So, um, arrhythmia if you're damaging cardiac tissue, which has um the electrical pathway of the heart in it. So, for example, if part of the area which is not getting well perfused during the M I is like your SA node or your A V node or other like the bundle of HS or, and the other parts of that electrical pathway of the heart arrhythmia um can appear and you'll see that. Um oh, they had um uh mi a week ago and now they're here with f um so rupture um so they can get like a big wall rupture. Um a tamponade then. So um that there's like a cardiac tamponade, an emergency um uh blood fluid around the heart preventing it from pumping. Um One of the reversible causes of um cardiac arrest, um heart failure. So the heart's just not working as well as it was because it's been um killed off. Um Valve disease can damage the valves of the heart because they're not being well perfused aneurysm Dressler syndrome. And for some reason, they just love um examining Dressler syndrome. So, um Dressler syndrome is a post M I um like inflammation of the cardiac tissue which presents as pericarditis. Um So in uh M CQ, it's gonna um give you all of the symptoms of pericarditis, which we'll cover in a wee bit. Um, it's gonna say, um, they've got, um, chest pain, it's sharp. Um, the patient has, they're sitting there leaning forward because it's worse when they lie back. Um, uh, they have an ECG and, oh, look, there's ST elevation all throughout the ECG. Well, then, um, you're thinking, ok, this person has a pericarditis and it'll also say, um, but two weeks ago they had, uh um an M I. Um so and then you're like, ok, so it's a Dressler syndrome. So it's effectively all like the pericarditis after an M I is Dressler syndrome. And they do just simply love examining on it. I think they just find it cool. Um But it is just inflammation at the end of the day um of cardiac tissue. So just anti-inflammatories, nsaids, steroids. Um And if it's really bad and there's fluid around the heart, you can do a pericardiocentesis. Um Yeah, I hope this is making sense. So, oh, is there any questions? Hold on on me? It says if they are already on. Um I'm actually not 100% sure. So this person has asked, uh on past me, it says if they're already on an anticoagulant, you give um clopidogrel. Is this right? I don't know. I don't think so. Um In northern Ireland. No, I think you, you treat as um per trust guidelines. You give aspirin and clopidogrel or tag, I think. But honestly, um maybe you would check that yourself as not something I learned from my exams. Um Great. So was there another question there? Hold on. Yeah. So, um how long they're kept on the dual antiplatelet therapy? Um So again, consultant dependent, normally about two weeks and then they come off. Um but a very consultant dependent. Um So normally aspirin doesn't go on long term. Um And is only so yes. So they're putting an aspirin at the start and the tagal, the tagal will be kept for a year, 12 months. The aspirin will be stopped in a matter of 2 to 4 weeks. But again, um depending on the consultant, um heart failure, then let's move on. Oh, ok. So heart failure, the inability of the heart to pump or to supply blood around the body. So, um why might it not be fit to pump? Well, um it just, it, it, the, the muscles aren't working? Ok. Um The muscles aren't working. They are not producing enough blood when they pump and they squeeze enough blood doesn't come up. They have no good, no sufficient ejection fraction. So this is what we call half ref or heart failure with reduced ejection fraction. It's a systolic problem, squeeze but not enough blood comes out. Um Another reason for heart failure then is um a more diastolic issue. The heart's not filling properly for whatever reason it can't relax. So it's only relaxing a little bit. So it can't fill. So then when it squeezes, it's not pumping enough blood. It's not actually an issue with the muscles. The muscles are fine. Um, it's more the, yeah, the heart can't fill properly. It's being restricted by something. Um, it's a diastolic issue. The heart's relaxed but it can't fill. Um, and this is heart failure with preserved ejection fraction still has a good ejection fraction, but it's just not filling properly. Um So, um this is like ischemic heart disease. So, uh um systolic um heart failure then um reduced ejection fraction. Ischemia affects the muscles, um dilated cardiomyopathy. The heart's got big and so the muscles are all stretched and can't really pump the same. Myocarditis is an inflammation of the muscles of the heart. The heart's muscles aren't pumping the same um arrhythmias as well. The heart's going just maybe too fast to pump properly, um or aortic valve disease um that they're preserved ejection fraction or the diastolic issues where it can't pump or supply the blood. Um because it's not filling. And so that there is more like a restrictive cardio um myopathy, it's obstructed in some way. Maybe there is a big tamponade there and the heart just has nowhere to go. It's surrounded by fluid. It can't fill. Um again, if it's got a pericarditis and it, it's a constrictive type of pericarditis, it's got nowhere to go. It can't fill. So therefore, it can't pump um or a mitral valve disease for that one as well. So presentation. So this is based on what side um of the heart um is affected. This takes me ages to get my head around every time I was making this slide tonight and this took me ages to get my head round. So blood backs up into the opposite supply. I don't know if that makes any sense but rightsided heart failure, blood is coming from the legs into the right side of the heart to go to the lungs, um to get oxygenated to come back to the heart. So it is coming up and into the heart. Um But if the heart's not working, then it's all being backed up. It's been backed up and backed up and backed up. And so the symptoms are gonna be peripheral edema, sacral edema, um, ankle edema A JVP, um Hepatomegaly ascites, um anything kind of edema around peripheral like leftsided. Then, um the heart, the blood is coming into the left side of the heart from the lungs to then go around the rest of the body, but the heart's not working. So it gets backed up because it's coming from the lungs. It gets backed up into the lungs and they, they're, that's the type of heart failure where your patients are going to be breathless, um Breathless on exertion, waking up breathless in the middle of the night. If you listen to the back of their lungs, you're gonna hear those bibasal fine crackles in the base of their chest. Um And that's gonna be the ones who show up with the type one respiratory failures as well. Um Doctor I can't breathe. Um And yeah. Um so some causes hypertension, um causes heart failure. Um, ischemic heart disease, obviously death of muscle causes heart failure, um valvular heart disease, cardiomyopathy. Um And here's another wee handy classification um of how it um affects your like function. Um So one physical activity is effectively unlimited. Um two mild symptoms with ordinary activity, three symptomatic and walking a really short distance and four symptoms are present at rest. Their life has really been around with their heart failure. Oh, see, sometimes these sides move and sometimes they don't. Yeah. Ok, here we go. Um So um investigations then um just do your standard bloods. Um but especially ABM P. So B na peptide um is released in response to myocardial stretch. Um So it's quite sensitive for heart failure. Um So do ABM P. Um Now is B MP diagnostic. No, but it is going to help you kind of see how your treatments are working. Um It's, it's a quite a good marker. Um If the BMP is getting a lot worse that they're getting a lot worse or if the BMP is getting better. Oh, actually, my treatment might be working. Um, chest X ray quite important, especially um if you're like suspecting some sort of pulmonary edema. Um an echo you want to see how the heart's working and that's how you see a heart, the heart's working. So that's probably going to be a transthoracic echo, um ventricular function, valvular function or structural abnormalities. Um And you can obtain an ECG, maybe you'll discover the cause of the heart failure in the first place. Maybe they have had um, uh nstemi and um, their heart has gone off because of that and that's causing the heart failure symptoms, but they actually haven't had much chest pain or something. So you're, you can do an ECG as well. Pretty much anything. Heart, you're like a tip for Aussies, you're in a station, they're like, oh, what investigations do you want to do? And you know, it's a cardiac station, echo ecg pretty much, um, obviously bloods and et cetera, but like echo and ECG are too good, like you're going to do those with pretty much everything. Um, ok, so, um, if your B MP levels are over 100 arrange a specialist referral referral um for the heart failure within six weeks. If BBM P levels are over 400 arrange a specialist referral within two weeks. It's quite bad at that point. Ok. Um, some um, chest X ray findings then um, of heart failure, the curly bee lines, um, a big heart, um, increased cardiothoracic ratio. So they have a big, um dilated and engorged heart and their muscles have all become very um hypertrophied because it's the heart's been working harder. Um This person here is clearly some, some sort of surgery because the wires in their chest. Um So that's another like important thing to note. Um And just in general, there, vessels around here are just very um you can see them, they're opaque. Um Here's a big pearl or here's just a little pleural effusion. Um and quite often, um people with heart failure will have bilateral um pleural effusions actually. Um So there might be one to miss your other side as well. Um uh Yeah, so management of a chronic heart failure, um lifestyle modifications, stop smoking, um fluid restriction. Um You'll see patients on fluid restriction, although the evidence I believe for fluid restriction is actually quite low. Um it actually doesn't really help them that much. Um But doctors do recommend it. Um It's just becoming less and less common for them to be recommending it. But yeah, still fluid restriction diuretics. Um So a big loop diuretic, for example, um is going to provide them with symptomatic relief. So they appear in A&E um uh doctor, my legs have just been getting more and more and more and more swollen over the past um week. Um I think it's this heart failure again because quite a lot of them have had this before. Um Do you think, can you just admit me and give me that same medication that you gave me the last time? Yes, that's no bother. And cardiology wards are full of people like this. Um heart failure patients, they're literally just there to get their IV um Furosemide, get them all dried off and send them home again. Um So yeah, diuretics will give them symptomatic relief. However, diuretics will do absolutely nothing for the actual outcome of that patient's story. Um They're not going to improve mortality, they're not going to improve the long term condition. What will um ace inhibitors? Um beta blockers, um mineralocorticoid receptor antagonists. So, spironolactone. So um like a di that's a type of diuretic, I hate spironolactone cause honestly, you could put it in three different drug classes but um like a potassium sparing kind of diuretic um or a mineralocorticoid um receptor antagonist is going to help keep them dry. Um And also increasingly an SGL two inhibitor, which obviously an SGL two LT two inhibitor. Um getting lost. What I'm saying that SGL T two inhibitor. Um so obviously these were originally diabetes medications. Um but they've been found to be extremely effective um in the outcome of left heart failure. Um And so you'll see um those four medications prescribed pretty much universally. Um definitely an ace inhibitor and a beta blocker. And then after that, um they might add all those extra ones, you know, OK, what about um um you hear doctors talking about flash pulmonary edema, that patient had flash pulmonary edema. Um So this can be a wee bit of a story of a patient comes into A&E, ok, you're having a stemmy. We need to get you sent to Alevin for um, your PC. Um, ok, we're awaiting the ambulance to come and blue light you to Alevin. Um, and then within next half hour, they acutely become really unwell and um extremely short of breath. And you're like, I wonder what was actually happening with this patient? And you do a chest X ray and they have just pulmonary edema everywhere. Um If you had done the same chest x- half an hour earlier, they wouldn't have had any pulmonary edema. Um And I actually learned this today, not for my finals today about this wee um pneumonic for the acute management of heart failure. If it's like a real cute case um for flash pulmonary edema. Um L MN O PLM nop um loop diuretic. So a furosemide 80 morphine, these patients quite often will be in pain, but it's not even pain that you're given the morphine for morphine reduces the preload of the heart as well. Um If you remember that from your physiology lectures, um morphine reduces the preload on the heart. Um So it will actually massively improve the symptoms of flash pulmonary edema, um nitrates again, um oxygen and then posture set them up. But that's just common sense. If a patient is sitting there breathing away, you're not gonna have them lying down, they're probably gonna be sitting forward themselves anyway. Um, yeah, valvular heart disease then. Ok. Again, this is something which I just don't, just don't advise rote learning. Um, again I tried it and it was not good crack. It's just not good fun. Um, so think it through, work it out for yourself. Um, so think pretty much exclusively about the left side of the heart. Um, the right side of the heart do have murmurs but we rarely examined on them. They're a lot quieter than the left hand side of the heart. Um And yeah, I probably just wouldn't. The ones you need to worry about are the aortic stenosis, aortic regurgitation, mitral stenosis and mitral regurgitation. So again, think this through. So in systole in the contraction of the heart, um blood has been flowing in um oh, I'll use my pointer. It, it is flowing in. It's sitting here in the left ventricle in cysto, the left ventricle contracts and pushes it out through the aortic valve to the rest of the body. Um When it's going through the aortic valve, if the aortic valve is calcified or stenosed, um it's gonna cause a murmur. Um it's going to be a ejection, systolic murmur. So as the heart contracts, it's going through, it can't get through it's turbulent blood flow, it causes a murmur here. Um If when this, if the mitral valve is leaky. So um if the opens narrowed, it's stenosis. If there's black backflow of blood when shut it's regurgitation. So, if the mitral valve is leaky, if there's backflow of blood on um systole, on contraction of the heart, um the blood goes back into the left atrium and this is called mitral regurgitation because it's clearly regurgitating right back through the mitral valve. So, if you sit and think that through um on um systole on contraction of the heart, um it has to be aortic stenosis because that's when the blood's going through the aortic valve. And it has to be mitral regurge because that's when the um that is when the um blood is going back up through the mitral valve. Um on diastolic murmurs then are gonna be the opposite. So it's gonna be your mitral stenosis. Um when the blood is coming through that um to fill the left atrium and aortic regurgitation. Um So it's just the opposite. But again, sit with a bit of paper and work it out. Um It's really, really helpful to do they're just your area um areas I always use the pneumonic annual parent teacher meeting, annual parent teacher meeting, um aortic um pulmonary tricuspid and mitral. Um So here's your little, little bit. Um When I was thinking through what I would actually learn about these murmurs, this is it um aortic regurgitation. Um It's an ear, early diastolic murmur, wide pulse pressure, collapsing pulse. And it's normally in effective in um endocarditis or rheumatic fever, but normally infective, endocarditis, aortic stenosis is the biggie ejection, systolic murmur, um caused by the calcification of the valve. Or if a patient is one of those people with a bicuspid valve rather than a tricuspid valve, they have a narrow pulse pressure and this is the one that radia radiates up into the carotids. If you listen to their college, you'll hear it. Um, mitral regurgitation is a pan systolic murmur. Um again, systolic because it's going back up through. Um, and this one's caused by um infective endocarditis. Um, ischemic heart disease, af cardiomyopathy or a mitral stenosis is a middiastolic murmur, um, caused by rheumatic heart disease. Um, pretty much always caused by rheumatic heart disease, but it's quite rare now because we don't really have much of um, rheumatic heart disease in this country. So, murmurs, um, investigate them. Um, transthoracic um echocardiogram, um cardiac catheterization stress test in them, especially in aortic stenosis. Um management treat the symptoms so they might very well might have heart failure symptoms to treat them. Um, re reduce their systolic hypertension, um, medically manage them with ace inhibitors, et cetera. Um surveillance. So, some of these patients are fine. Like you just listen to their heart. Oh, they've got a wee bit of a murmur. Oh, it's not that like it's not causing them any um, serious issues. Um, let's just kind of keep an eye on them. Let's just do some surveillance dental hygiene. Um, an important one because they're, if they've got a dodgy valve in any way, they're already predisposed to get an infective endocarditis. Um having bad dental hygiene is also one of the things that make you predisposed to getting um infective endocarditis. So, um yeah, uh just if you keep that, then it'll reduce your risk. So good dental hygiene. Um and then you can do surgery and if you go over so surgery, valve replacement, you can do that in any valve. Um So you can do uh uh surgical aortic valve replacement for aortic stenosis or at. So this is a, you know, um less invasive way of doing it if the patients maybe not that well and won't tolerate a surgical aortic valve replacement. Um Blue angioplasty. Yeah, they can dilate the valves and mechanical valves are typically used in younger patients simply because they're going to last longer. Um However, when you're on a mechanical valve, you need anticoagulation. Um So there's risks and benefits to both um bioprosthetic valves um or tissue valves. Um These are normally in a wee bit older patients. Um maybe patients over the age of 60 or whatever and they don't last as long. However, um but they don't require any um anticoagulation or anything. Um because they're not going to uh clot more um like a mechanical valve would. Ok. Any questions? Let me see. Yeah. So somebody there just mentioned if the heart can't fill, how is the ejection fraction still preserved? So, yeah, I mean, it's more like in theory, the ejection fraction is still fit to like it's still, if the thing was removed, that was stopping the heart failing, the ejection fraction would be preserved. Ok. Um Now, will it be? No, they've still got symptomatic heart failure. So therefore, their ejection fraction isn't being preserved. We know that um they've got symptomatic heart failure, their body is not pumping enough blood. Um However, removing the um issue and their ejection fraction would be preserved. Hope that makes sense. Send me another wee message if you need. Um So hypertension, then this will probably be um covered in like a GP. And here's your a lecture. But maybe the third years don't get actually access to the GP ones. I'm not actually sure who gets access to what? Um But let's cover it here anyway. So, um hypertension really anything over um systolic 100 and 40 or diastolic 90 complications. So, we know um high BP has many complications in terms of um predisposing you to an acute Coronary syndrome, a stroke, chronic kidney disease, um hypertensive retinopathy, so, damage to the back of the eye um and aortic dissection or aneurysm. Um These patients are quite often totally asymptomatic and they don't understand why you want them to get their BP under control. Um But due to all these complications, it's actually quite important. So, um investigations then, so the BP at the clinic and we can do ambulatory BP monitoring, um, as well. You know, we don't want to diagnose somebody with hypertension in the actual fact, they're just actually scared of the doctor and they've got white coat hypertension. So send them home with a wee monitor. Sure. Um, and it'll take their BP many times throughout a 24 hour period and take an average of that and work out if you have to treat it. Um, additional investigations, then, um, you want to see, I suppose what the high BP has already affected. So, um, have a wee look, see, um, the, the creatinine, the E fr for their kidney function. Um, have a look, do they have any diabetes or fasting blood glucose? Um, and an echo and an ECG because it's always the correct answer um in a cardiac kind of station management then. So management for 1st, 1st line for um, hypertension is an ace inhibitor or a calcium channel blocker. How do you decide? Well, there's a flow chart in the next slide. If an ace inhibitor or a calcium channel blocker aren't working, let's add them together. Maybe they'll both work in combination if that's still not working. Add in a thiazide diuretic. If that's still not working at that point, you're gonna need to go to spironolactone and alpha or a beta blocker. But that's gonna be AAA very much a uh consultant, um, kind of call. So, yeah, if somebody has type two diabetes they get an ace inhibitor, doesn't matter what else about them. They get an ace inhibitor type two diabetes. They will get an ace inhibitor and it kind of trumps all if they are under the age of 55. So they have no diabetes but they're under the age of 55 and they're white, they get N ace inhibitor if you're over the age of 55 or you're 45 but you're black and you're black African or African Caribbean family origin. Um You get a calcium channel blocker. Why? Um because they just are more effective and the pathways and we know that the es pathway in older people doesn't really work as well. Um And the c the calcium channel blockers are just proven in clinical trials to be more effective um for people of um Black African or African Caribbean family origins. So uh 65 year old per a 65 year old person with diabetes still gets an ace inhibitor. Uh 5065 year old person with a 65 year old person without diabetes gets a calcium channel blocker. A 45 year old person who is black gets a calcium channel blocker. Um but if you are 45 and you're white, um and you then you get an ace inhibitor, you know, um just take a wee while digest that um flow chart and kind of make it make sense to yourself arrhythmias then. So you'll be tachycardic, you can be bradycardic. Um And if you're tachycardic, it can be narrow complex or broad complex. Um So what I mean by that? So let's talk about atrial fibrillation. First of all, it's the one we all no one loves. So, um they can be totally asymptomatic. They can have palpitations, they can have chest pain, shortness of breath. Um They can be lightheaded or um have syncope. Um they can have irregular, irregularly irregular pulse um with uh kind of, I suppose, variable volume. That is me at an hour. It shouldn't be that much longer. Um But if you do have to shoot on like obviously, no worries, go on ahead. Um So irregularly irregular pulse um with a variable volume. Um So they have no P waves on their ecg um their pulse is normally going fast and they, it's totally irregular. Um But if you look at their QR S complexes, they're nice to be narrow. They're how they should look. They're just nice to be narrow. Um QR S complexes, this is a type of narrow complex tachycardia, atrial fibrillation, risk factors, there's loads of them there, sepsis, hypertension, um thyroid issues, um mitral valve disease, ca caffeine alcohol. Um You'll get a 35 year old man who comes in after a binge drink of alcohol. Oh, I complain to my heart racing. Um ok. Just you don't just maybe don't drink the binge binge, drink of alcohol again. Um It's it's, alcohol is something which, um, some people just have to totally abstain from because it will, um, send them into af, every single time. So FF management, yeah, I have to think about three things when you think about the management of AF, rate control, rhythm, control and anticoagulation. So, rate control. Normally, first line, um, you can use a beta blocker that's normally the first line. Um, these are, are however, um, totally contraindicated in asthmatic patients and hypertension. And that's one that if I'm skim reading a wee M CQ, it'll say in the middle, oh a 25 or yeah, a 25 year old asthmatic and I've just totally missed it. You can't give them a beta blocker and it can exacerbate their asthma. So um first line is a beta blocker, but if you can't, then you do a rate limiting calcium channel blocker. Um So something like dilTIAZem or verapamil, those are the rate limiting ones. Um Digoxin, it can be used in combination with either of the above. It's not really started as first line as a monotherapy anymore, but if you're at full dose of beta blocker, um and it's still not slow enough, you can add in digoxin, you cannot give, you cannot give a beta blocker and a rate limiting calcium channel blocker together. Um You will slow them too much and they'll become bradycardic um or they will die. Um So yeah, just don't give, just don't give beta blocker weight, limited calcium channel blocker together, you can rhythm, control them only. However, if the onset is within 48 hours or if they have been anticoagulated for at least three weeks, this is due to the risk of stroke. So, um in practice, you select patients based on um how likely you think it is that you will get them back into rhythm. So, for example, my granny has af she has permanent af, she has af, for forever. Um, she, um, doesn't even know she has it, she has no symptoms of it. She doesn't know when she first got it. There's no point in ever trying to shock that woman back into rhythm. Um, you're not going to get her probably back into rhythm. It's just unnecessary. She has permanent af, it's not worth your time. Um, but, uh, at the same time, if a younger gentleman comes in, he's like I, um, took cocaine and within 10 minutes I could feel my heart racing. Um, I felt, feel really, really unwell and this all happened an hour ago. They know exactly when their af started, they have an exact, um, on time. Um, something knocked them into af, so it's quite possible that you'll be fit to knock them back out of it and you can consider cardioverting them. But only if the onset is within 48 hours because the, um, the clot, um, that can develop in the, er, atrium of the heart. Um, if you shock them, I say that 48 hours, the likelihood of there being a clot, there is a clot, there is actually quite high and it can shoot up into the brain and they can have a stroke. Um, so we don't want that. Um, if you think that, oh, I would actually quite like to shock this person but they're not already anticoagulated and they've had symptoms now for 72 hours, you can put them on an anticoagulant and bring them back in three weeks. Um and then shock them and that might work. Um You can also use amiodarone or flecainide um for your rhythm control, amiodarone using like structural heart disease for maybe patients, older patients who won't tolerate the um paddles fide is that one that you can take as a pill in pocket? Um So we have your wee uh the patient knows they go into af every so often. Oh, I take that wee medication. It's just a wee single dose medication. Um And it knocks me back into rhythm. Um Brilliant, great. They can have that. They don't ever have to come to the hospital then anticoagulation, stroke prevention. So calculated chads vas score for everyone who has af everyone. Um And if they have a chads vac a chads vas score greater than three or, and it's indicated um you use a Doac first line um um to anticoagulate them and a warfarin, then if it's valvular af um there's other things that you can't use wax in. So if they've got really bad renal function or if they are an obese patient um or something like that, you're going to need to use Warfarin. Um But mostly it's do that are now first line. Um so to calculate your child's vas and for every single af patient, not all of them are going to need um anticoagulation, but some of them will and a lot of them will. So tachycardia is then um we're ready kind of on this. Um So, um you can look at this here algorithm. It's on the resuscitation um council um narrow complex. So we've already talked about af and um flutter, just sinus tachy and sinus tachy is quite often just physiological. I've just ran um for a bus and my heart's going in 90. Um I'm in sinus tachy. Um Just that's just physiological um SVT um supraventricular tachycardia. That is um again, that can um is a narrow complex one or uh Wolf Parkinson White syndrome as well. Um Which I'll show you in a second here. OK, narrow complex tachycardia. Then um as I say, sinus tachycardia can be either physiological or pathological. So, physiological secondary to me running um pathological, secondary to sepsis or to pee and, or to illness. Um So, yeah, either um we've already covered atrial fibrillation or flutter. So, flutters just the fluttering baseline, but still irregular rhythm. Atrial fibrillation is the is the absolutely no P waves and totally irregular rhythm. A super ventricular tachycardia. And if you just want to go down to the bottom, this is your ECG here, this is a super ventricular tachycardia. They are, their heart is going fast, but look, they've got nice narrow, regular um QR S complexes. Um They don't have um a total absence of any P waves. Um It's a regular heart rate, it's just supraventricular tachycardia, they're just going fast. Um sinus tachy big P waves still present, but they are fast, big P waves still present. S VT, you can't really see your P waves. So basically, you see a narrow complex tachycardia, um narrow complex, obviously being normal. Um narrow QR Xs complex tachycardia. If it's a regular rhythm, it's af pretty much universally, it's af um if it is a regular rhythm, um it's probably ASV T um or something else like that. So first line is vagal maneuvers. So you can do carotid sinus massage. You can do a modified valsalva maneuver where they blow into the syringe um or any other vagal maneuver that you may choose. Um Second line is IV adenosine. Um And you can, so you go 6 mg first that doesn't work. You do 12 mg that doesn't work. You do 18. Um Third line, you can do a verapamil or a beta blocker. And then fourth line is a synchronized DC cardioversion. Where am I getting this information? Just this algorithm. Um So, yeah, Wolf Parkinson White then um again, I just love examining Wolff Parkinson White just because it's different and you can't see it all the time. So, what is the ECG changes? Well, um this up sloping of the QR S complex um is called a delta wave. It's slurred upstroke. Um It doesn't just come along, come along, come along point, it comes along and kind of loops up into it. So that's a delta wave and that's probably the, the, that's the Wolf Parkinson white E CG change that everybody remembers. They also will have a shortened pr interval. Not that this one, not that this ECG really does like three small squares is kind of pretty average, but sometimes they will um and a tachycardia as well, they'll be going fast. Sometimes they don't really have any um symptoms, sometimes they will have like a syncope or dizziness or palpitations. Um And they'll arrive in A&E and that's what you'll find. Some because some don't have symptoms, some don't need managed. Um But you can give them antiarrhythmics um or they've, they've just got a part of the electrical circuit of their heart going wrong. So if you just radiofrequency ablate them, um that's def definitive management and to tell you the truth, um interventional radiologists doing radio frequency ablation is going to become more and more common in the cardiology field. So I've been told reliably by a couple of cardiologists so broad complex tachycardia is then OK. So look at this ecg here, big broad, no points anymore. Big broad um ac a big broad QR S complexes. Um ventricular, oh where did that go? Ventricular tachycardia? Um check for a pulse. It very this can be an arrest rhythm. Um So if you are walking past the patient, they're lying, sleeping or what you think is sleeping and on their um monitor on the wall, you see a ventricular tachycardia go to that patient and check for a pulse. They might not have one, they might be in a rest. Um However, they might and they might be sitting talking to you while they have the VT. Um So if pulseless follow the A LS algorithm, your um advanced life support, I know in third year you haven't done that. That doesn't matter if you haven't done it, you'll not be assessed on it. But um ventricular tachycardia is a shockable rhythm. You can shock them. Um and you can give IV adrenaline and amiodarone and that will get them sorted. If they do have a pulse, they might be sitting talking to you with a VT. Um You can shock them three times and you can give them amio. If you've got adverse features, you can give them amiodarone over 10 to 20 minutes if they're stable, give the amiodarone 300 over an hour. Um Ventricular fibrillation, ventricular fibrillation is always pulseless and they always don't have a pulse um you never see this ECG and them be sitting and talking to you, it's always pulseless. So just follow a LS toads the points then um it is uh a specific form of polymorphic VT um that occurs kind of because the QT interval is prolonged. Um It's management is a little bit different. If they're unstable, you cardiovert them as normal, but if stable, you can give them magnesium sulfate. Um And I suppose they often say toads is um the notable ECG findings is it looks like it is twisting around um the baseline, the isoelectric line. So, yeah. Um and you can kinda see that on this ECG down here bradycardias. Ok. Bradycardias usually don't get as much talked about because they're not as exciting. They might be physiological. Somebody might be really, really fit and sit with a heart rate of 49 all the time. Um Athletes for example, and they might be pathological. Um Have we given them anything, any drugs, any beta blockers um to slow their heart? Do they have a heart block? Do they have um an acute M I do they have raised intracranial pressure. There's a million reasons why somebody might be going slow, hypothermia, hypothyroidism, heart block. Um I understand this is a gross slide. I wouldn't want to look at this either. But um yeah, so first degree heart block is just a prolonged pr interval. Um It's pretty much always asymptomatic and rarely need to treat it. Um second degree win back the pr interval progressively lengthens before a QR S is dropped. So we short P ra little bit longer, a little bit longer again. Oh And now we've dropped total QR S complex. Um mos two then or second degree two is pathological. Um They have dropped QR S complexes normally at a certain ratio. So you might see a 3 to 1. So um or a 2 to 1 block. So that is where they have two P waves to every one QR S that is actually fired. Um So again, if you see here, 12 QR S 12 QR s third degree PS have absolutely no association with the QR S complexes. PS are firing. QR S complexes are firing, but they're not firing together. It's pathological and they're, they need a pacemaker. Um If not life threatening, just observe them for bradycardia. Um if they do have some signs of life threatening symptoms, um you can give them ap pain and you can repeat this dose six times until a total of 3 mg. Um You can give them other things as well. Ultimately, they're gonna need paste, they're gonna need something telling their heart to fire because their heart's not firing as it should, the electric electricity is not firing as it should. So um transcutaneous pacing there or a permanent pacemaker, ultimately, probably a permanent pacemaker. You can do transcutaneous pace pacing until they get to that point. Ok. Last couple of slides, then you'll be so glad to know. Um In fact of endocarditis. Um So this is an infection um within the heart, usually an a valve of the heart. Um So this is normally caused by staph aureus, pretty bog standard infection, but in the heart can be catastrophic. Um And strep um viridians, these patients can be so sick and they'll come in with a really rip roaring sepsis. Um And it's actually quite hard to diagnose as well and they'll be, it'll be like mm sepsis of unknown origin. Like we really don't know what's happening with this patient. Um And eventually they'll get an echo. Oh, look there it is. Um they have an infected endocarditis. So risk factors, prosthetic heart valves, anything that a wee bug can latch onto, they will um or structural heart defects. So, if somebody does have a bicuspid valve, for example, they're more likely to get an infective endocarditis dental procedures. Just a, it's a, it's a favorite question on a ward round of a consultant. Um Some risk factors for infected endocarditis. Yeah, like I in dental um procedures. So something to do with the blood supply if the teeth on the heart and everything, if you rip teeth out, um an infection gets in, it will go to the heart valve. It's uh yeah. Um I also don't know, maybe ask a dentist but dental procedures is one. uh IV drug use is a massive one. So a again and introduce an infection straight into the veins that's gonna go straight to the heart. Um and it's set in there. Um and immunodeficiency um clinical f uh features then, so they're just unwell, they're septic of the murmur and that might be a total new murmur. So, if there's no murmur documented and you hear one, that is maybe something that's something to think about um embolic phenomena. So they can actually throw off clots to other parts of the body. So maybe they've got a PE um or a DVT even a stroke um and secondary to their infective endocarditis. And then you've got the textbook stigmata um as in, they've got the splinter hemorrhages, they've got the osler nodes, they've got the JM Y lesions. They've got funny things. They actually are very rare and you rarely actually see them in practice. I've seen um what was it I seen was it JM Y lesions? I think it was GM Y lesions. I seen when I was on my elective there over the summer, but uh they're not by any means um common. And then the Juke criteria is the gold standard then for diagnosing um infective endocarditis and this is them. So you have major criteria and minor criteria. Um So major criteria is blood culture. So you need to take blood cultures twice out of two different sites in 12 hours, 12 hours apart. That is, um, now, does that always happen exactly as it should? No. What if somebody has really rubbish access and you can't get into them twice, um, in two different places. Um, sometimes they are just both ticked separately but it's best practice is to take, um, them at two different times. Um, if you can and from two different sites of the body, so both arms or whatever and, and, uh, echo. So again, that's another major criteria. If you see it there, it's there. And so quite often these patients get a transthoracic echo and then they end up actually getting a transesophageal um to confirm um temperature, the the phenomena, the ulcers, nodes and rough spots and uh gi lesions and stuff and the then the microbiological evidence and the positive blood cultures, um embolic phenomena and the risk factors as well. Um And so if you kind of have a combination, so it's two minor or two major, one major and three minor or all five minor criteria. And that gives you a diagnosis of a diagnosis of an infective endocarditis ready to treat them. Um Investigations take your blood cultures, take, this says three sets, taking at least three hours apart. Normally two is fine. II actually think that might be a typo on my part there. Um Two sets, two different sites um arrange an echo. Normally they do as I say a transthoracic and then it actually quite often has to be, uh to a transesophageal. And so that obviously involves like sedation. Um, and the echo probe going down into the esophagus to get a good look right at the top of the heart. Um, they can basically set the probe on top of the heart when they go down that way, dental evaluation as well. Call your friendly hospital dentist. Um, to have a wee look at the teeth management is really, really hard. Um, they're on IV antibiotics. They're in the hospital for weeks and weeks and weeks and normally six weeks. Um, they've, so you start treatment right away. Um, broad spectrum antibiotics and then when sensitivities come back, um and cultures and sensitivities come back, you kinda work out exactly what antibiotic they should be on. Um Normally they're on Van Gent Rifampicin. Um Really if, if the uh prosthetic valve, they're definitely on rifampicin. Um Normally it's, and gent, apart from that, they might just be sitting on tws until they come, until you come back with some sort of sensitivities, sepsis, six and surgical management. Um Sometimes the valves is not seeable and they need a valve replacement. Um But normally you look quite like the infection to be cleared up before you can go ahead and do that pericarditis. Then I told you I was gonna talk about it and I am, I think this is the only slide. Yeah, this is the only slide in pericarditis though. So, clinical features, the virally before sharp pain. So it's not that dull, heavy pain that II uh M I is, um, the pain is quite often worse when they lean back. This is different from a pe, the pe pains are worse when you lean forward. Um, but this, this pain pericarditis, pain is actually better when you're sitting forward. Um, they might have a new pericardial effusion, um, fluid around the heart ecg changes. So I didn't mention this when I was talking about ST elevation earlier in terms of your stemmy, if they have widespread ST elevation in every single lead to the heart, and you're like, well, they can't have, they can't have a stemmy everywhere. Um Every vessel can't be blocked at the same time. Surely that would be incredibly bad luck. Um For a patient, it can't be like, why would all of the ST elevation be in every single lead? It's pericarditis. That's quite a, a typical ecg that we might see in an exam. Um My, one of my exam questions this year was uh like ast elevation, every single lead, click and pericarditis moving on easy mark. Um Lovely. So they're tachycardic, a wee bit pr depression as well. Um Their white cells will be raised, their CRP will be raised. Um Actually, you can, can get a troponin rise as well. And in real life, um quite often it is actually quite difficult to work out the difference between pericarditis and an acute Coronary syndrome. But in an exam questions, it's not in exam questions, they'll make it clear what it is. They'll be like, this patient has been virally for four days and now it's a sharp pain and like they're not, they're not going to lead you down. They're all right there. Um But in real life there actually can be um management at the end of the day. It's just inflammation of the heart. Um nsaids, aspirin, colchicine corticosteroids. Um If nsaids are contra, are contraindicated and beck triad is there just because I wanted to add it in here. Um I had add it in somewhere if an exam question talks about muffled heart sounds, a raised JVP and hypotension that's Becks triad and they have a tamponade. They have fluid around the heart that fluid needs removed as soon as possible. It's quite an acute emergency. They could die. Um OK, os stations, then what OS stations can come up related to cardiology. Um, history taking, they can have chest pain palpitations, they can be short of breath. Um And you kind of just have to take a history around that. Um, ask their past medical history, ask their family history if this person's came, coming in. Um, family history is gonna be so relevant. If they are having a heart attack or not, ask them about their drugs, ask them about their drug allergies. Um, uh, ask them if they smoke again. A massive one if they, um, in their social history. Um just go through a normal history. You, they all know how to do a history at this point. Um But it can be any of those presentations or really something else. Full cardiac examination, height for time normally. And an exam, they just go examine this person's precordium. So that's just the chest. You don't have to worry about the hands or the face or any of those signs um or the pulse or the BP or anything like that. So um examine the Precordium, examine the chest. Um Again, just learn that um Queens have a good dox of exactly what they want you to do online. So go and download the docs. Um It's on the Queen's Med Portal. Um It's exactly what they want you to do where they want you to put your stethoscope and what part of the stethoscope at all points. That's what I learned from my finals. They make you interpret an ECG um OSK stop um Are brilliant for ECG interpretation geeky matics. Um And what's that other one called ECG uh The I wrote it down somewhere for you. Oh, yes. Life in the fast lane. It's just a whole pile of example. ECG S. So it's really brilliant. They make you counsel on Warfarin or a Doac. I don't know if they can really, like, I suppose they theoretically can make you counsel on any cardiac medication. I can't really see it though and it's probably going to be warfarin or a doac in general. I would normally say drug counseling is more of 1/4 year and final year osk type of thing than a third year osk type of thing. But they can do it and they have done it in the past. So I would just have a wee look at some of the drugs that, of each specialty that they really could ask. Maybe Warfarin, maybe a Doac, they could also make you listen to an audio of a murmur. Actually listen to the chest of a person with a murmur. Um and interpret. Now that's a very final thing. Um I got the semi-finals this year. Um It was a child and then they were like, oh and here's their murmur and they gave you headphones and you put on the, the headphones. I know they died. I was like, oh, this is so hard. Um listen to the, the audio of the murmur um and work out what it is. So, tell them is it's systolic. Is it diastolic? Um And then come up with a differential and what you're gonna do about it. So, um yeah. Um they've done it in the past where they've brought in real people with aortic stenosis and you have to listen to their chest and you have to work out that they've got aortic stenosis, but that is final year. They will not do that in third year. They just won't. Um they're not gonna give you like they always say they leave the people who are five years when they will throw in people who actually have something wrong with them. Third year they just want you to make sure that you can actually do the stuff. Um Aips don't miss your easy marks. Um Give the intro with the consent of the hand washing. Um patients give you marks on your Aus be kind, just smile and you'll feel like you're dying inside, but just slap a smile on your face and be as kind as you possibly can be a that must be so difficult for you. Oh, I'm so sorry that's happening to you. Let's see if we can get you sorted out here now and then that's kind of um the patients will love that be the most confident version of yourself. Um And I tell myself this before every single ay sometimes before every single ay station in that minute that you have before you just go OK, smile on your face. Chin up, nod your head as if you know what you're doing and like there's no point in going into the ay station going. Hello. Um My name is Courtney Weir and I'm a final medical student and um you might feel like that inside, but there's no point in letting your voice go really, really quiet and um kind of fading away and not being confident in it. Just go in. Hello. It's lovely to meet you today. And my name is, even if you don't feel like it just be the most confident version of yourself that you can possibly muster up inside you. Um, clean your stethoscope. Easy Mark. I missed it in my cardiac exam in my finals. I came out of the station and went, oh, I didn't clean my stethoscope and I was gutted because I was like, that was the one mark I knew how to get. Um But um yeah, don't just clean your stethoscope. Easy mark mark for every single mark scheme. Why wouldn't you get it? Um Always discuss if you're talking about risk factors, um always discuss them as modifiable and nonmodifiable. Um, examiners will love that. They'll go, oh, what risk factors does this patient have? Ok. So this patient has both modifiable and non modifiable risk factors. The modifiable risk factors include the fact that the patient is obese, the patient is a smoker. Um The patient lives an unhealthy inactive lifestyle, whatever. Um the non, however, this patient also has a number of nonmodifiable risk factors. This patient has a family history of um cardiovascular disease and they, yeah, you know yourself um when summarizing, don't list the relevant negatives, there's no point in saying, oh, and they um don't have XY and Z they don't have this, that and the other um list the positives um list maybe relevant negatives. Um So for example, if in your brain, you're thinking. Ok. Um, this patient could have uh OK, let me think of something actually. Um Yeah. Ok. So you're in your brain, you're thinking, OK, this patient maybe does have a pericarditis and you're looking at their ECG say, actually there's absence of widespread um ST elevation throughout the leads, um which is swimming away from the diagnosis of pericarditis. Um That's a, that's a relevant negative. Um But there's no point in saying no, there's not this, there's not the other, there's not that and then you pro folks. Um I honestly, I don't know what happened there with the recording. It just totally everything just went black. Um But um thank you so much for coming and listening and if you've got any questions, feel free to email me, um my email address, I'll put it in the chat, um is C weir 24 at q.ac.uk um for any questions. And um I that was pretty much at the end of my presentation anyway, so it couldn't have happened at a better time. But yeah, I hope that was helpful. Um And if you've got any questions, don't be afraid to ask me. Um uh Yeah, I don't know what happened with the recording, but thank you.