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Uh Yes. Ok. I think this works better. Can everyone hear me? Ok, or? Yep, you're fine. Great. Ok. So this is the cardiology finals revision session. Um I've just put my, I'm currently an I MT in London at uh Saint Thomas's. Um I've put my email in there and feel free to email anything after or to be honest, like, uh I'll give my whatsapp as well at the end. Any questions at all to do with cardiology or anything to do with finals, just give me a shout. Um Yes. So let's get c it's basically, here's a kind of the gist the, the majority where the majority of the questions um in your finals, what they'll be on. Um So number one is a CS obviously because most relevant, probably one of the most relevant. Number two, a stable angina, probably less relevant. To be honest, it's mainly probably consultants and, and um reads who are sort of managing stable angina. Um maybe a bit in GP. But, you know, as a junior doctor on the wards, you're not, you're not really managing that too much. Um Well, not too often pericarditis. That's a common one. Of course heart failure. So both acute heart failure. So someone coming in um with acute heart failure and also the management of chronic heart failure that comes up. Yeah, definitely a lot. Um Then there's valvular heart disease, infective endocarditis, atrial fibrillation, that's probably the main arrhythmia and SVT S and then kind of a bit about pacemakers. So that's what you need to know for finals. So this is just a quick put your mind into cardiology mode. Um Yeah, kind of the biggest thing that I've learned from cardiology is that a CS is a, is a syndrome. It's a, it's a spectrum of disease rather sorry. Um So it goes all the way from this plaque eruption, you know, like um ST elevation where the whole heart muscle no longer um functions. And that's why you get this delayed conduction, you know, that's why you see it on the ECG. Um and it goes all the way from there to kind of no troponin rise. And um no, uh yes. So essentially no troponin rise and no um blocked uh uh no ECG changes, which would be kind of more of an unstable angina. Um But essentially it's still an acute Coronary syndrome that you need to be doing something for. And this is kind of a good reminder of all the things that you need to do that's don't focus too much on this. It's I think this is my biggest learning point from cardiology having done the job just recently as an I MT is the spectrum of disease. Um, and going, yeah, that's essentially it. Um, ok, we're gonna get started with questions now, I'm gonna give you about 40 seconds or so. Um, maybe a bit longer. Um, and yeah, just answering the pulse. Essentially any questions you can either save them to the end. There'll be a bit of time or, um, if they're quick ones or then feel free to ask straight after when we give the answers. All right, starting with the first one. I'll let you read them yourself. Uh Do you want me to still do the polls for you? Um, that would be really helpful if that's ok. Yeah. I don't know. I, oh, no. Oh Damn it. Yeah. No, that's, this is a, this is a warm up question. Um Is that ok if you can actually? Yeah, that's fine. I don't know if you can see in the poll section. I've queued up ones that are just choose an answer. ABCD. Oh, yeah. And I've just been, I've created like, oh, so I can do it. Yeah. Yeah. Yeah. Yeah. Um I'll create them so you can just do them as and when, and just delete them once that question is done? Ok. Got it. OK. That's coming up to a minute. So let's start this poll in that case. No. Yes. Yeah. Ok. So can you see the answer on that? Yeah, I can see it. So um I surprisingly it's a unanimous be. Mm. Ok. Oh, someone might work. Yeah. Ok. There's a percentage uh I see it was 100% because everyone got it right. Yeah. So this question does actually come up quite a bit um as you would expect but it's kind of which region is affected essentially which where is the heart attack um when you're seeing an ST elevation in these certain leads. So if you see the leads V one V two, technically, that's actually, I mean, I always think of it, think where your um ECG leads are. And remember all the vs are kind of your chest leads looking in at the heart. So they're like eyes looking in. So V one and V two are eyes looking in like where you put those in. Um So if you like point, if you like point at yourself, like that's where V one and V two is just point at yourself, kind of where the lead is um at that point. So any sort of cardiac, any sort of myocardial infarction at that point is going to show an ST elevation in V one V two for septum V three V four is anterior V five V six is where you put V five V six that's lateral. Um and VL. So VL, I remember left, so left arm, that's where that eye is looking. And essentially it's that lead. This is like one of those augmented leads, but it's that lead looking in from the left side essentially. And then AVR is in a specific region and then aVF so coming from the foot, um that's inferior and then leads two and three, those come up the way, look up the way as well and then leads one is lateral. So along is from the side again. Um because that looks in, I think it's, it's very similar to the augmented um VL essentially um any questions at all? If not, I'll move on. Yeah, this is a very common one. So do um Yeah. Do you know this? OK. Next question. Yeah. OK. And that's a minute. So it looks like 100%. I got that right again. So well done. Yeah. Valsalva to begin with. And then um does anyone want to message what the next um this, that was quite easy but what the next if that wasn't working, what you would next go to? OK. OK. I'll give you guys the answer. Um I'm assuming you knew that. But the next thing is adenosine. So the ne that you know the, the Yeah IV Adenosine. Exactly. Yeah. So, and this would, that's the sort of thing that makes people feel horrible like it's that sensation that your heart is stopping. Um And then what you do is you start, I believe, check the algorithm, but it's about, I think you start on 4 mg go up to eight and then up to 16, essentially you work out ade and if that's not working, then you're considering other methods. I think at that point DC cardioversion potentially. Um, um, they, they do it in a ranges of free, so it's free. 69, 12. 0, ok. Well, that's good. Good memory. Yeah, that, that makes sense. Thank you for tripping in. Um Yeah, so essentially going up, um, until it works. If the patient's hemodynamically unstable um ie BP is like low or dropping less than 90/60. Um then DC cardioversion um is what you do, of course. OK. Next up. Oh The Yeah, so essentially SVT narrow complex tachycardia. Um patients young, that's kind of quite a good um indicator that it's more, you know, like not a different arrhythmia. Um And so you're going down the narrow complex tachycardia algorithm um which is separate, of course to the broad complex and then, you know, you would give adenosine at that point. Um Yeah. And the other ones mentioned there broad complex tachycardia amiodarone, of course is first um unless the patient is hemodynamically unstable again, then it's DC cardio version atropine and adrenaline. Those who use bradycardia, I mean, atropine mainly for bradycardia. Um or, and then you want to be considering transvenous pacing which isn't often done. Um All right. Next question. Yeah. Yeah, that's coming up to one minute. I'll give you have 110 more seconds to answer. Mm OK. Um stop pulling. Yeah. So mixed answers here. This is quite a tricky one. So um it, yeah, it's, it's really quite tricky. Essentially. The answer is actually d so hypokalemia resulting in toads I II spelled that wrong. And that's literally not how you, I don't know how to say this word because II can't speak French but Toad Des I'm going to go with that. Um Yes. So essentially this patient has now it's this polymorphic ventricular tachycardia um that we're seeing and the way I think of it is um it tends to be a patient with a long, the reason why it's hypokalemia is in hypokalemia, hypo anything. That's the way I think of it hypocalcemia, hypokalemia. Um Those two specifically and I think hypomagnesemia and hypothermia, what you do is you get um the QT one might be long already but you get a much smaller T wave. So, you know that T wave to like flattens. Um And then in hypokalemia, essentially, you, you get a hyper uh a sort of that, that essentially flattens and it precipitates this sort of um sort of, if there is a prolonged QT as well, it might precipitate a um polymorphic ventricular tachycardia. And what you do is you treat with um magnesium. That's the treatment. OK. Right. Next. OK. OK. OK. Yeah. Well done. Yeah. So I'm gonna close that poll. I was gonna type to answer but I'll answer in a second. Um Polling. Yeah. So in this case, the most important thing, any sort of messing about with the heart essentially is going to cause some sort of inflammatory process and the pericardial sac. And in this case, after cabbage, it's not uncommon that patients have pericarditis. Um And what else? Yeah. So essentially that is just, it's just talking about pericarditis. So it's inflammation of the membrane that surrounds the heart. Importantly, differentiating it from myopericarditis is that in myopericarditis, the troponin goes up. So you would get a troponin rise. Um And that means the myocardium is affected quite a different sort of um usually different causes and things. Um uh So pericarditis, um usually idiopathic, I believe is an A one cause but second to that viral and then you get these sort of syndromes like after a Mr you might get dress syndrome. Um 2 to 3 weeks after sometimes if there's any risk at all of that, they might start someone on a culture scene to help. Um And after the cabbage, because you're physically ha you know, handling the heart essentially and the pericardium messing about with it. It's there's gonna be an inflammatory process and they might have a fever, but that's not present in this case. I'm just gonna quickly answer yes. So essentially it is answer. Sabina in regards to please, may you explain the association between PVT and hypokalemia, hypocalcemia, et cetera. So essentially all, all the hypos um because they are required, you know, in this whole um action potential, you know, the cardiac action potential. Um As soon as you get a lack of them, this is the way I think of it. Um I believe as soon as you get a lack of those, essentially, the QT starts to prolong in all of those. So that's the number one thing and then how torsade de pointes or, you know, PVT um poly ventricular tachycardia does actually form um or, or how it actually starts, I was reading about this um is that when that QT prolongs, it puts you much more at risk of to the point. And the reason for that is that the QT is so long that you're almost going to start the next um action potential um during that T wave if that makes sense. Um And there's this concept, I mean, this is probably in way too much detail. That's the most, that's the most important thing to remember, but how to explain that and maybe sometimes I need a better explanation to remember things is that when the QT prolongs and that T wave is so far, you know, like so far away, um like miles down, you can start to get another action potential on that. Um And when that does occur, that can kind of essentially mess up um start this sort of ventricular tachycardia, essentially, it's, it's called this R on T phenomenon. I mean, I think this is way too much in detail but have a read of it if you find it helpful. Um Yes. So, essentially flattened T wave um in, in these sorts of hypo electrolytes, hypokalemia, specifically flattened T wave, prolonged QT. And then all of a sudden you get this kind of like an action potential starting on that T wave. Um And you can imagine that kind of just literally puts the heart into like absolute chaos, essentially um causing this sort of ventricular tachycardia. The, yeah, the other one, I guess kind of, I saw quite a few people did answer hyperkalemia and actually, hyperkalemia, it can, I don't think to a at the point it causes more of um what can happen with hyperkalemia is you get tended T waves. Um And, and so it goes the other way. So essentially you start with 10 prolonged pr interval is number one, then you get a tented tr sorry, tented T wave. And then the way I think of that is um hold, imagine like an ECG strip is a string. And then so first like between your fingers, first kind of prolong the pr and then you tent the T waves. And you can imagine like it's like a floppy bridge essentially is how hyperkalaemia forms does. I hope that makes a bit more sense. Essentially, it's quite complex. But let me know if it doesn't make sense. I think slowed repolarisation is the probably the simplest like delayed repolarization is the simplest explanation Um All right. Next question. Five OK. 10 more seconds. OK. So stop pulling there. So a couple mixed answers. This is um it's, yeah, II think once you get the concept of this, it's actually quite a simple question. But I II me put it this way at medical school. I don't think I would have got it because I didn't quite understand um the basis of this. But essentially what this is, is a heart failure. The key out of this is it's a heart failure patient. I'll, I'll give you the answer. It's B Bisoprolol. Um The key here is that it's a heart failure patient. Um So diagnosed heart failure and in heart failure immediately when we know someone has heart failure. Um uh we look at the echo. So do they have a reduced ejection fraction or do they have preserved ejection fraction? Reduced ejection fraction? Less than 40%. So last echo, ejection fraction, 25% if it's reduced. So, in my first separation, is it reduced or is it preserved? And that's the only way that's the only thing you should be thinking in heart failure. Um In this case, it's reduced ejection fraction. So she needs to be on the four medicines of heart failure. Um that help with um prognosis essentially and we'll go into those in a second, but that's an ace inhibitor tick. She's on that. Um She needs to be on um spironolactone tick and the other one out of this is a beta blocker because that will help, you know, put less pressure on the heart, we'll go more. And the fourth one that I'll mention is the SGLT two. So that's dapagliflozin. So we'll go into this in more detail, I believe on the next few slides. But the other ones, no, because, I mean, ivabradine that's um used in stable Angina, you know, as like the third line or something. Bisoprolol. I mean, yes, that's right. Digoxin. No, because digoxin is used for rate control in atrial fibrillation. DilTIAZem. No, because that's used in stable Angina Atenolol. That's old school. It's not used in this case. Yeah. So essentially here this is the explanation. The patient's already taking some of the prognostic beneficial medicines, ace and aldosterone inhibitors spironolactone. In that case, the other addition is a beta blocker. Mhm. Yeah. Oh, that's OK. Oh, yeah. So in a second, I'll show you a table of kind of how to think about the heart failures in more detail. He peth versus he fre though. That's the two differentiators. Next question. So good question. I'll answer that. Um at the, when we go into the next. OK. Got it. 30 more on it. Maybe 10 more seconds. OK. OK. Yeah. So this question tests quite a few things. Um I guess the answer is a um statin ace inhibitor. Essentially the patient does have stage one hypertension because it's above 100 and 40/90. Um, and, um, they do have, remember, it's not just that, that means you have to start someone on an antihypertensive. They need to have one other risk factor in that table. That's the part. Always caught me out in this case as soon as they have a comorbidity, morbidity ie diabetes or the, the kind of the most subtle risk factor. One is the cardiovascular risk greater than 10%. Then you should be starting a, um, something to help control their BP. In this case, in a patient, um, greater than 55 um with diabetes, the first line would be um, ace inhibitor, essentially the way I think of this. Again, this question is, I mean, calcium channel blockers, their only use is to help with BP. Ace inhibitors have so many other benefits, you know, they, they help with the BP. They're used as we just saw in the ref you know, in the heart failure. Um, patients they use in, that's not for BP. That's to actually, you know, protect the heart actually by turning off. 00, yeah. That's a good way to think of it. Oh, yeah, young sweet. Yeah. Um, yeah. And um, essentially, um, yeah, essentially. So any, any um, any kind of other reasons so diabe diabetics, um, protect the kidneys, protect the heart. Anyone you're thinking I want to protect the heart. I want to protect the kidneys and the BP is a bit high. And ace is a great um choice. Essentially calcium channel, all I'm doing is helping the BP. So it's someone with just BP is essentially um I hope that makes sense. So that's it. I'm going to answer Yusuf's question. Um Is there any specific order you would start the heart failure drugs? So those four he ref drugs, I think that's what you're talking about. So, I mean, the one thing, heart failure, fur diuretics, that's to help immediately with the, you know, just get the fluid off. You need to think fursemide is only symptomatic. That's just an aside because I used to get confused. I was like, where does fursemide come into this? And bumetanide? Those are two diuretics, they help with symptoms only. They don't, they're not prognostic, they don't help the person live longer. The other four heart failure um medicines they do, they do this, you know, turn off the R system, they stop, you know, the the heart from being um essentially, they essentially remodel the heart. Um And I, I've literally seen someone comply with those poor medicines and come into heart failure clinic. And you know, that ejection fraction stayed the same for years. Basically having been on those someone non compliant with them, their ejection fraction will drop from, you know, like, I mean, it obviously depends, but from like 30 you know, 38% down to like 30%. Essentially in the case of like a few months. So they, they really, they do work essentially. Obviously, that's what the study showed. But so what old would you start those heart failure drugs in? Um technically all four at the same time. So, which is, it sounds mad. But on a very low dose, you could start all four, there's a few caveats to that. You know, the bisoprolol, you have to make sure the, the heart rate is not super low. So if the heart rate is less than 55 that's a contraindication. Um with um bisoprolol and the Ramipril because you can imagine they bring down BP a tiny bit. The the systolic BP has to be greater than 95 usually. Um and then dapagliflozin, the the the the third one, no real reason to not start it. Active infection is the main contraindication. Apart from that, no other real reason to not start it. And then the fourth one, the mra like as in moral called co antagonist or, you know, spironolactone or plain. The only thing remember is the potassium has to be I believe less than 4.5 is usually the cut off. But to answer your question, no, someone will get diagnosed with hep less than 40% injection fraction and will start them on all four of those medicines. Low dose. Um yeah, is is the simple answer. A cardiologist would. But then of course, a geriatrician may not because, you know, it's this classic argument. Like there's this whole thing of how do we manage cardiovascular disease in frailty um as well. And a geriatrician probably thinks more about that. Whereas a heart, a cardiologist thinks, oh, let me start them on all four and protect the heart. Uh Whereas a geriatrician might say that might, you know, make them have like debilitating postural hypotension and not be able to leave bed, but to answer your question all for you on a small dose and then go up on them as able. Um OK. So we went through that next question. P OK. Ok. Yeah. Ok. Yeah, I'm gonna close that there. Yeah, that was a good one. Well done everyone. Um So you also said IV Fursemide. So essentially this patient has very much the clinical symptoms and signs of heart failure. Uh Doesn't she? So kind of the classic, you know, bi basal creps? I'm sure it does say that. Yeah, bi basal creps um uh reduced air entry because her, her lungs are filled with uh got a lot of fluid in the bases. Um and well, pulmonary edema, bilateral pleural effusions and um yh a class two, I think um yeah, reduced exercise tolerance. Um And um off her baseline, essentially, she was able to walk a bit further. She's reporting very much orthopnea, um which is of orthopnea. I mean, as all symptoms are quite diagnostic but um as you know, obviously helpful, but orthopnea seems like quite, it's quite a good one to ask. I usually find like, less so P and D sometimes, but orthopnea, it definitely does happen. You know, the, how many pillows do you sleep with? Question? Um, and previous MRI. So, you know, it's probably ischemic, um, ischemic, heart related heart failure, one of her walls is probably just not working quite right. And as you all got the answer, fide exactly. So basically someone with pulmonary edema or any sort of fluid overload from a symptom point, as in any sort of fluid overload in heart failure, the most important thing is to get on top of their um they fluid overload essentially with furosemide. So get them to we all out. Um The only other things. Yeah, that's the main treatment I think I forgot. Was it like sog soggy something? I remember it was like an acronym. I forgot what that actually meant. But um sit them up, give them oxygen if they need aiming 94 to 98 not above. Um give them a diuretic sod sod off. That was it. Um Give them a um diuretic and then they wear it all out. That's the main things, to be honest. Yeah, I can't think. Yeah. And often actually, if you see a patient up who does have, you know, like pleural effusions, pulmonary edema, this sort of acute heart failure picture, it's, that also does help. Um because they, you know, you can see like are they, do they then have that where the water is no longer, you know, the upper lung part to breathe through. Um So the only other thing is oxygen and then sometimes, I mean, this is more complex but sometimes GTN is used and can help and then if there's any sort of respiratory failure, then CPAP can help because that pops open the alveoli, it's positive pressure and then there's other things, you know, they might need to go to ICU for these things. Um or um CCU uh do dobutamine um you know, to, to help the heart pump because um and keep that fluid going in the right compartment, not going out towards the lungs. All right. 15 more seconds. Mm. Ok. Yeah, that's yeah, well done. Um Most people or everyone. Uh Yes. So the key here is BD flows and that this is the side we're gonna go through. Um essentially in this case, ejection fraction. What do they have? Is it they have heart failure? Is it hef ref or is it hef pef um less than 40% greater than, is hef ref greater than 50%? Is hef pf 40 to 50? Let's not talk about that. Now, it's got another, it's, it's, it's something else mildly reduced. Um And the management is not, we don't need to talk about it. But um so essentially management of he, we spoke about those. So it's the four to reduce mortality. You know, um ace or Arne is um uh Entresto, you know, the super, I definitely don't say the that right. Entresto um beta blocker Mra SGL T two and then diuretics um ie fide if you need the he pe this was that, that, this is what this question was asking about. The only licensed drug now for you to reduce mortality is SGL T two. So da Gliflozin or Mlilo, but I think usually DPA is used. Um maybe it depends where um DPA or PE are the same drug, uh same class. Um And then um you might need diuretics to offload. So always think, do I need to offload them? Are they at their dry weight, like with fide or not? If they are, then I'm thinking prognostic medicines, heff these four heff. Just that one. That's the key of heart failure. Really? There's, there's nothing else that you need to know too much. Um Yeah, you, you don't need an echo. Technically. Um I mean, I think an echo is helpful but clinical signs, um maybe you actually to formally diagnose heart failure, you probably should have an echo. But clinical signs, you know that peripheral edema fluid in the chest um is um that and then abrase BN P particularly, you know, greater than 400 or greater than 2000 depending on how quick you want to get the echo and then you do need an echo. Sorry, that is the guideline, an echo showing kind of any sort of dysfunction. So that sort of diastolic dysfunction, like the heart's not resting properly or it's not quite pumping properly. Like systolic function, any dysfunction on a on an echo is with signs and symptoms is diagnostic. Heart fail. Ok. Next one. Ok. Yeah. Mhm. Ok. Five more seconds. Right. So, yeah, just about right. So the answer was b so continue atorvastatin and repeat LFT S within 4 to 6 weeks. Um The reason is yes, the patient has developed elevated transaminases. Um But these are within three times the upper range. Sorry, I didn't actually give the range there of normal. Um And then it says that there is three times the maximum normal range, not three times above the patient's baseline result. Therefore, it's acceptable to continue the atorvastatin and then monitor the LFTs um with a repeat test in 4 to 6 weeks. If the level had been greater than three times the upper range, then stopping atorvastatin and repeating LFTs would have been an appropriate, there's no need for an ultrasound and changing a statin um can play a role if the statin is not tolerated. But um ie you know, pain and muscle cramps and things, but this is not the case so far. Yeah, that's one of those. Just. No, no, unfortunately, things, right. Oh God. Can you see that? Ok. Hopefully they, they do have the option to make it full screen for themselves as well. Oh, good. OK. This is quite a tricky one. Wait, so give me one second. I'm just gonna ask, sorry about that. Um Yeah, so this is quite a tough one. So the um essentially the key here is it's a patient with clearly infective endocarditis. So they definitely fulfilled Duke's criteria, you know, positive blood cultures and fevers and I think they had a new, a new murmur. I'm pretty sure does, it does say that. Yeah, a new murmur. Her. So those three. and the key here, OK. It's oo over, it's aortic, it's an aortic valve. Um It's infected with um infect Arditti, it's got the vegetation on it. Um And we've got them on treatment. Um Basically, the key here is all the bloods are strep bovis. Yes. At some point, the patient will need a colonoscopy because that's the one associated with colorectal cancer. Um But the key, the most important next step. And this is quite complex is that and, and this is why a every patient with aortic valve infective endocarditis needs a daily ecg that prolongs pr it's irritating the sinoatrial node. Um I believe. Oh no, sorry, the AV node um it's irritating and causing essentially a first degree heart block. Um which at that point, you know, it's eating away into sort of the myocardium and essentially, or there's an aortic root abscess. So the answer is d refer to cardiothoracic surgeons. Um And yeah, essentially, yeah, two positive major um criteria and then minor ones, all of those. And then despite starting antibiotics, the ECG shows prolonged pr which may be reflective, an enlarging aortic abscess, sorry, disrupting the A V node. Um which is an indication to refer to cardiothoracic surgeons. That's quite a tough one, but there's a lot of knowledge that comes out of that. I think um that you can learn. So kind of um yeah, other surgical indications, any sort of heart failure, uncontrolled infections. So kind of not getting on top of things and then um pulmonary prevention of embolism. So what happens is they shoot off the septic emboli um you know, from the aortic valve, like all those little vegetations, like shoot off everywhere, so into the brain. Um So it kind of, it's like a stroke picture essentially but off like septic emboli rather than um thrombo emboli. Um And it can go where, where else everywhere essentially. That's why you get spinal hemorrhages. That's what that is, you know, the little micro emboli depositing, then these osis nodes. Um Yeah, which II have seen actually so quite cool to see. Um No, not for the, not for the person though, obviously. Um And uh yes, that's essentially it. Next one. Got you. Yeah. 10 more seconds. OK. So this one is one of those just knowing unfortunately how to treat warfarin um or higher in Rs. Um The answer is D so give F FP stop vit K stop Warfarin. So just remember it's really that major bleed criteria. So um stop Warfarin give IV VK. Um And you give, sorry, sorry, not F FP, sorry. As in my answer copied over the wrong thing. Um Prothrombin complex, not F FP, only if that's not available and then if it's a minor bleed, then you're just stopping and giving a bit of Vitamin K And then you just keep repeating the inr um quite often and then if there's no bleeding, then you're still giving oral vit you're giving oral Vitamin K and then keep repeating the inr and then you can restart when it's less than five. And then if it's minor bleeding, a tiny bit of Vitamin K and then if the inr is just a tiny bit up, um then you can just um withhold for a couple of days. OK. This is quite a quick one. Oh, sorry. The question isn't actually to complete elevates first. Um When there's a myocardial um in ischemia, 10 more seconds. OK. All right. Yeah. OK. This one, the key here is the answer is c so it's actually myoglobin. Um This is probably a more of a postgraduate question. Um But essentially the, the, what you should know out of this is that um so, so the troponin starts to rise, you can see a rise at six hours is, is the key really. Um And so anything that's, that's the key question. So, if someone comes in and their chest pain has just started, then their troponin might, you might not actually catch that significant of a raise, but that's why we do repeat. So we'll do a troponin at like three hours, then we'll do one at six hours, then we'll do 16 hours after that. So 12 hours even, um, as in, and you can see this trend that it goes up and up and up to, you know, like, and if it raises that's, that's the thing. If it goes up by a certain amount, then that's much more worrying or, or even if it's coming down, then you might be catching the tail end of something. Um But you, there's room to kind of miss in the first, you know, hour or two. And sometimes that's just relevant. Um Not, not often to be honest now, like, I mean, catching the trend is, is the key but you don't like in a semi, if you see the ST elevation they're going in for an a coronary angiogram, they're not, you're not waiting for that troponin to come back. Um Because hopefully you've got them there within that two hour window so that it's kind of relevant for that, you know, the whole guideline about um presentation and things kind of getting people into the P CPC as soon as possible. Don't wait on the troponin. I mean, irrespective if you saw ST other vision, you wouldn't wait on the troponin. But yeah. Um so myoglobin is the first to go up. Um So which of the following drugs? Oh, we kind of did speak about that. I'm not going to do that as a poll. So that was a um ace inhibitor. And OK, I think this is the sec the last question, potentially. Yeah. 10 more seconds. Yeah. Ok. Yeah. So the answer be the majority of you got it. So, anticoagulation should be continued for at least four weeks. Postcardioversion. Um And it should be, they should be on it for four, sometimes six weeks. Um before um you know, before you uh cardiovert, put it back, put the heart back into sinus rhythm because that's the risk of throwing off a clot. Um And even kind of, it's obviously really important. So even kind of one missed dose and things of like a DOAC would be within that sort of um here it says three week. So, um well, they've had it for three weeks. So four or six weeks, six weeks, I believe is the guideline in most places. Um So I realized it's 12. So I'm just gonna, I mean, you can screenshot this so you can answer yourself later. Um And this is just a good guideline kind of explaining when you intervene and when you don't with um sort of like, is it with Angina essentially? Oh My goodness. Too many questions, screenshot this one as well. Um Patient on maximum does what would you next recommend? So it's about kind of like the next what you're next intervening with. And then um the answer was C so calcium channel. But then which one to use? Because I used to always get this question wrong. You know, like which ones you're not, you're not allowed to use with bisoprolol is what that's showing? Yeah, thank you. I hope you screenshot. Well, at the end, any questions at all, I think the key really is what we spoke about. The very start. So kind of a CS heart failure. Those are the main two. a tiny bit on stable Angina. Oh Yeah, this a general question. What stressed you for preparing for finals worked well and with sight, what would you have done differently while preparing for exams? Um So um I would say um it went too fast. Oh yeah, you've got it there. Um So for preparing, I think the most important thing is um I mean, honestly, I think it's really, it's, it's gonna sound ridiculous but kind of really knowing like um I think what many different or however best you learn, like read and watch many different resources on those big presentations because you really need to understand kind of the big presentations rather than, you know, like heart failure and A CS rather than just kind of like, I think I honestly roughly knew them, um knew about them, but I didn't really understand them. And I think for the sake watching a youtube video um as in like four different youtube videos and really understanding like a cs or really understanding heart failure then like, that's the most important thing, the big presentations. Um and then apart from that, then do past paper questions. But don't, I'm very guilty of getting into the route of doing past paper questions and not understanding um as in like, you know, like not being bothered to read up about it after that makes sense. So like take a break, watch your youtube videos or read online how best you learn and then go back to it but really understand like what, what's happening with heart failure? Like why do we use these things? Like what we like, what is a CS, you know, like, II don't think it took me a while to really actually get my head around how it's like the spectrum, you know, like and like why STEMI versus end? Like what are those two? And like, yeah, I hope that's helpful. Could you show the second to last question briefly again? Yeah. Um You do not, if you're happy to send the slides to me by email, I can add them a slide deck. So they have them after. But if you use these continuously, you don't have to do that obviously as your work. Yeah. Yeah. Um I hope that you got the screenshots there um seconds last, but we'll send them anyway. Yeah. Um, oh, I'm, I'm glad. Yeah, cardiology. I really did not. Um, to be honest, understand it enough coming out of medical school, like, in all honesty. And I think the key things, I think that's the key things is what I mean, arrhythmia is still really tough but he things. Acs, um, heart failure, unstable angina. Oh, no, sorry, stable angina. You know, that whole algorithm of like beta blocker, calcium channel blocker. I mean, it's usually a reg or a consultant in clinic who's making those decisions. I don't, we will ask them, I think maybe one or two questions I remember, but they're quite like, I think just know the first, like the second line if anything, you know, like the beyond Bisoprolol basically. Um and then arrhythmias, it's usually atrial fibrillation. So that rate control versus rhythm and then like fast and so on. Um Those are the main cardiology questions to be honest, like, yeah, hope that was helpful. Any questions or I'll put my feel free to whatsapp Me as well. I mean, whatever's easier. Um or email, it's up to you. Yep. Um I'll repost the feedback form as well. Just remember to fill it out as well guys. And if you didn't get the chance, um you go back to the top but further up the chat, you can find the one from the previous session and any other disappears. There are, yeah, one of the finals actually. And uh, I think they have them in a few weeks. So the start of February or end of January or something. They got Oscar? Oh, ok. Oh, my God. I find oy, so scary. I literally, II can't lie, not to scare everyone. But I literally, II thought I was like, oh, it'll be ok. You know, like we're all in this together. Literally go, oh, it's just like there's nothing to prepare, they're just so as in to prepare you for the, it's just, that's just so scary. But if it's, if it's hot, I'm just gonna say it the classic. It's gonna be like you, no one is gonna hate you. I mean, obviously if there's hope like scars and stuff is it um as in maybe that might be something as in it might just be like you need to identify it's a cabbage or something, but it's aortic stenosis. If it's a murmur, I'm going to say that probably. Yeah. Yeah. As in especially, I mean, even I've seen Pas which is like the one, you know, like in four years after finishing medical school roughly. Um and that one like it's actually there's been like other things but it seemed to be like mitral regurg or aortic stenosis like, yeah, which maybe Tricuspid um Yeah, just uh feel free to write any more questions guys if you have any just before I finish up. Um Just before we do finish. So obviously, thanks for coming Um Once the slides are sent over, I'll put them up to the slide deck. And if you filled out, I'll get the use me to send out the feedback form via email that you can do that way and you should have access and obviously we're running a session tomorrow as well. So it's obstetrics, gynecology and respiratory. So it's a bit bigger. Um Yeah, and if you do find these useful next year, you'll be in the same boat. Uh, feel free to let me know if you want to potentially help out next year. It's not a definite, obviously you don't know what your vote is or anything. It'll be like next year. Um It'll just be, someone will send you a message and you can say yes or no, I'm busy or whatever. Cool. Well, yeah, I'm going to head back. Um and yeah, see you, I'll send you the slides, Adam. Perfect. Thank you. Yeah, it starts at one tomorrow, one until about 10 past four, whatever. Thank you. All right. I am. Hopefully seeing most of you tomorrow, if not, best of luck with your exams. Um Hopefully it ran quite smoothly. Um I looked at some of the feedback for the question for the previous one. I'll try and make it a bit quicker for tomorrow, but I didn't really run the questions in this session. So, um we'll see how it goes. It, it varies a lot. Um It does go right in front of you when you add that pull too quickly on. Um Yeah, that's fine. Uh You're free to go. Hopefully we'll see you tomorrow. I'll add those slides as soon as again. Thanks for coming guys. See you tomorrow.