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Mhm. Mhm. Ok. Um I think we're loud now. Can everybody hear me if anybody wants to say yes or whatever in the, in the wechat, please? Yes, great. Ok, so hello. Uh we're gonna do uh an M CQ sort of um, session this evening. This is the first one. We, we've got several throughout the year, but this is the first one that we're gonna do this year. Um, and it's with, um, Sada Laxman who is, um, former, former president of the Society of, of um, Q Queens Cardio. So, and uh an F fy one doctor. Um, so she is gonna, um, lead the session and take, take us through it. Um I'm going to pop a wee poll in the chat every time she, um, presents a question and, um, please, if you don't mind, um, just voting and, um, whenever we get a certain number, we'll, um, we'll reveal the answer if that's ok. Um, if you have any questions or concerns or whatever, um, as we're going along, just put a wee message into the chat, but hopefully it should all be ok. And then at the end there, there will be in this um in this uh session, there will be a wee feedback form at the end if you wouldn't mind filling that out. I just all know at this stage if that's ok. So um sa over to you if you just wanna, I suppose, introduce yourself and then um crack on if that's ok. Yeah, no problem. Thanks so much Steven. Um My name is Sika, like uh Steven said, I'm a doctor. I'm an F one working in um Bolton and I was um a part of um cardio. So when I was in um Queens, so, um I'm happy to do some teaching on cardiology, anatomy and physiology and I'm also just gonna connect it clinically as well because I think that's a lot more high yield in terms of. Um and it's a lot more high yield, I think in terms of um thinking of your progress test and things like that. Um So just to start off, um I'm gonna cover some relevant anatomy and physiology and the main three things I'm gonna go over is acute Coronary syndrome af and heart failure. Um And then we're gonna cover, just look at some Ec GS as well. Um In terms of um Mc Qs, I've got a couple of random ones here and there as well just to see if um pe just to help with the revision as well. Um And just to, as a fy, I, I've mixed new slides and old slides and I couldn't find it for my old slides. So if the theme is off, that is why. Um So, yeah. Um, just to start off with a little bit of anatomy. So obviously on the left hand side, we've got a nice picture of the um, anatomy of the heart from a gross perspectives of your super superior Vena ca vena cava, where blood will come. Um Well, where the oxidated blood from the system will come through, going into the right atrium, right ventricle. Um and then uh going into your pulmonary arteries. Um And then you've got your uh what's it called um blood going back into, through the pulmonary veins into that is oxygenated, coming back into the left atrium, going into your left ventricles and then going out into the aorta to go into the system. Um You've also got your um electrical um uh anatomy as well where, where you've got your um sinoatrial node, which is your primary node that um starts the um cardiac cycle and the electrophysiology. Um the primary pacemaker of the heart essentially. Um And you've got the A node which is the secondary end which goes to your uh bundle branches as well as your purkinje vibes. Um in terms of your cardiac anatomy, I would say the more high yield things would be your coronary artery anatomy. Um And it's really, really useful to know because at risk to obviously your EC GS and um it relates to um acute coronary syndrome and it's most likely gonna be the one that you're gonna apply clinically a lot more. So, um your coronary arteries arise from aortic sinuses which are little um openings behind the aortic valve um flaps. So, um they branch off into the left side, on the right side. The basically the aortic sinus starts in the anterior surface of the heart. And that is why um majority of them fall around the anterior surface. Um The left coronary artery branches on the artery and that goes down the anterior um um goes all the way down the anterior aspect of the heart. Um The left coronary artery will continues to go um across the anterior surface and then it branches down to the left um marginal artery as well, which goes down the um anterior surface and close towards the um posterior surface. And then your left coronary artery continues on and then the bigger complex artery that runs a along the left posterior surface of the art of the heart. Um On the right side of things, you've got your right coronary artery which brings out your right marginal artery um and then also becomes the posterior interventricular artery. Um And that's on the right posterior side in there's an anatomical variation. So, in some people, in 20 to 25% of people, you've got your um posterior interventricular artery going on the left posterior side as well. Um coming off the left coronary artery. So that's an anatomical variation. The big ones to just keep in mind right coronary artery means right side and posterior um side of the heart, left coronary artery brings out the L AD and left circumflex. L AD is anterior and left circumflex is left um and like lateral aspect of the heart. Um Does that make sense so far? Any questions or comments or concerns if people are happy enough, I'll just keep going and if people have questions, I'll run through them. Um As we go, do you mind? Do you have your uh wee camera on? I've got my camera on. Can you not see my camera? No, no, we can't see it but no, if, if you can't get it working, don't worry at all. But um no, it's grand if you can't get it working, it just, it just looks great but, but it's fine. Come here. It doesn't. Oh Is it? I'm sorry about that. Um No, you can you car on. Yes. Yeah, you're crystal clear. Perfect. Um Sorry about that, but um we'll continue on for now. Um So I think this is a nice like 3d image of the heart. You can't see the atrium um because the um just to help visualize the where the arteries are. Um but you've got to see as you can see the left corner artery going into this left circumflex and it becomes leaving off the L AD and then the right coronary artery um with the right marginal artery coming down and then if you see here, it's becoming the posterior and turi artery down there. Um So I think it's just good to imagine that because it helps you actually understand how that correlates to ECG S which we'll talk about and um how that kind of develops into, um like how am I as well? Um The quick recap of the cardiac cycle, um You've probably gone over with this and you probably know this. Um But it's just good in terms of what happens you could be. Um So during your diastole, um you've got your ventricul filling up and you've got atrial cyst atria or pumping blood into the ventricles, you then have what's known as isovolume contractions. The way I like to think about it is when you're taking it basically doing a valsalva, you're kinda holding your breath. So basically, you've got this constant volu high volume and that's that when, once you take that deep breath out, it's a higher pressure. So that means the, the heart valves, the um aortic and pulmonary valves uh um open at a hi the blood at a higher pressure to push to the rest of the system. Then you've got what's known as your. So that's what we were talking about. Your ventricles are contracting, the valves are open and it's going um system and you've, then you've got isovolumetric contraction. So the ventricles relax and they refill with blood. And that's when the um the coronary arteries are filled with blood as well. And that's when they get the, the heart gets its own uh systemic circ uh systemic circulation. Um I like this image because it kind of look. So like we see the pressure in the atria, the pressure in and increases during the ejection phase during systole and comes back down. And then um you can also see how that correlates in A G as well. So, you've got um your P waves here which are organizations that f that atrial systole in that phase. And you've got that isovolumetric contraction are slowly coming up and you've um and in that increase in pressure and the outflow phase where um the ventricle acting and pushing the blood into, into the system. And then you've got your s where you've got that isometric vacation, um or ventricular as well. Um H um I was just gonna start cor correlating that clinically. Now, um we just as that was like a bit of a recap um in terms of your acute coronary syndrome. So your acu coronary syndrome is um separated into your predictable and your unpredictable pain. So the reason you have predictable pain is because in stable angina, you've got demand ischemia. Um which means that when your um heart and it's more blood needs more oxygenated um blood, um It's not able to dilate when you have unstable angina and you're starting to get that unpredictable pain. That's when you're starting to get supply ischemia. So, um, even when you're at rest, sometimes there's, there's no, because there's been of that vessel, you're not able to, um, get blood, um, get enough oxygen to rest of um the heart, um at rest as well as um during exertion. Um So usually what happens is you get um, plaque or atherosclerotic plaques. Um You've got your high risk um risk factors with hypercholesterolemia hypertension and all, all those things that cause that inflammation um in your vessels and that can increase your risk of this, um which we'll talk about again and um when that ruptures, that can cause further inflammatory processes, which um causes a thrombus. Um and that causes an occlusion here. You will start to get um E CG changes, but you don't get troponins. We'll talk about why you don't. Um But um you are getting ecg changes because you're not getting enough blood flow. And so the heart is not able to the heart, the heart is not able to um uh give adequate blood flow, essentially to um to the myocardium in terms of an end and a stemi, that's when you see an infarction is damage to healthy tissue. So, um you essentially the reason you, you that you have a difference between Anstey and stemmy is how infarction is. So you get either partial occlusion into the vessel which causes a subendocardial infarct um which is basically part of the um vessel wall um or part of the myocardium is um uh necrotic. And then in a stent, I mean, you've got a transmural mural infarct and goes um throughout the entire um uh throughout the entire myocardium. So, with an NSTEMI and a stemmy. So you've got elevated troponins again, we'll talk about why it's because you're getting actual damage to the myocardium and then you've got ecg changes as well. So you in your end sties, your inverted T waves and ST depression and then in your stem, you get your hyperacute T waves and your ST elevation. Um It's important to do between a type one and a type two M I. So like we talked about, you get vascular damage due to your high dose of things like hypertension and diabetes and hypercholesterolemia and smoking. Um And you get that uh atherosclerotic plaque that develops and then that ruptures and causes a thrombus which causes an actual occlusion. You can also get um inadequate blood flow and necrosis to da or damage to healthy tissue. Um when there's an ischemic imbalance, essentially between supply and demand of oxygen. So that um most commonly happens due to sepsis. So when you're septic, you'll become hypotensive and a tachycardic. So your heart is beating really, really fast. Um But it's not able to um it's not able to pump as much blood as it has the vo the hype because you're hypotensive and the volume of blood is a lot lower. So it's not able to meet that. Um that demand that your heart has essentially um other causes of that are anemia, arrhythmias, respiratory failure and hypertension. Um But I thought it was just good to cover this. Obviously, type one mis are more common in your exams and things, but it's just good to be aware of that as well. Um So, um again, this is something that we're um, is repeated quite a lot to us in terms of what acute coronary syndrome is, but it's really high yield. So I thought I'd cover it. Um, in terms of presentation, you get chest pain, um that can be on exertion in your stable angina or at rest, central crushing. It's, it's a lot of the times it can be described as dull or like a heaviness or a on the chest, someone sitting on the radiates to the left arm jaw and you also get dyspnea nausea and they get very sweaty and clammy. Um, in older people and in women, you can get um atypical presentations and atypical features. So, um, basically features of dyspnea, nausea and sweat, sweatiness without the chest pain. So, it's just important to, to keep that in mind as well. Risk factors we talked about. So, increasing age, male sex, family history, family history is really, really important as well. Um And then your modifiable risk factors, you've got smoking, um, sedentary lifestyle, obesity, diabetes. So it's, these are all things that can increase your risk of damage to vessel walls and also just hypertension which again causes further damage to vessel walls. Um So looking g so obviously, we talked about the um the anatomy of the coronary artery. So we talked about how the left coronary artery turns into the left circumflex when you go more lateral and it becomes LD when it's anterior and then your right coronary artery, um it falls mostly around the posterior side of the heart. And that relates to your, basically, when you're putting your E CG leads on the chest, you, your, your V one is going from the top right of your chest um until the six, which is going into your. So that's obviously going from more posterior or for more, more anterior, sorry um to more and then obviously, you've got your ground leads in your arms and your limbs um which um cover your more posterior and inferior side of the, of the heart. Um So that's why essentially you get um these, these E CG changes based on um based on the specific leads and why they relate to specific vessels. So um if you've got a thrombus in your L AD, that's the anterior side of the heart, you're gonna get change E CG changes in leads V one to V four. Whereas if it's more lateral, it could be the left circumflex artery and one to V six. So I've put three images here. Some people are more visual learners. Some people are more written and reading learners. So I've um put a mix of both. Um Apparently the audio is cutting off. Can Steven, is it the same for you or is there something I can do? No, my, my audio is fine for you. Sa there was um just some bits and pieces but for two seconds at a time there, but it hasn't happened in a wee while for me. So I think just carry on. I think you're fine. Ok. No worries. Let me know if there's any issues or anything. Um And I'll, obviously we'll send the slides as well if um if you need them and if you're uh if you want me to recover anything, um please feel free to put in the chat. Ok? Um So troponin soins, the, the structural um structural bound proteins and um during the um during um cardiac contra muscle contraction, it binds to calcium allowing for the contraction to actually happen. Um uh basically during um the du it al it sorry, um when it bound binds to calcium, it allows the Myosin head um to bind to actin allowing for a power stroke which essentially leads to contract. So, um they're really, really important in cardiac contraction. And so, or in muscular contraction and um because of that, they're found, um they're released in myocardial injury. And so that's why we test for them in um in a, in an MRI or in a CS. Um because there's a elevated levels um in terms of times of onset hours of onset and that basically peaks um at around 12 to 48 hours and then it takes about 4 to 10 days to resolve. Um That's why a lot of trust in terms of guidelines. Um I ask for serial troponins because that helps you get an idea of, ok, it's rising. That means this is um myocardial injury because some people just ha might baseline because they're just found in muscle and ways. Um lactate is a useful nonspecific marker of ischemia. It's um why a lot of people get blood thin um when they're um uh when there's like an unwell patient because if they're hypotensive or if they're um dehydrated, um that can cause an increased lac lactate and it's something that's helpful and um in uh an MRI as well cause it gives you an immediate indication that there's something go, there's something wrong here, especially for patients, more of an atypical presentation. Um So in your management of um acute coronary syndrome, um some of the thing is obviously pain morphine um is really, really useful in, in helping with the pain IV usually um you can give nitrates as well like a GTN spray, but just be cautious if they're hypotensive. Um you give oxygen, but only if their oxygen levels are less than 94%. The literature said that it's more harmful than helpful if their oxygen saturations are greater than 94%. And then you want to obviously treat what is causing this. Um This M I which is usually a thrombus. So you give aspirin 300 mg stat and usually another antiplatelet as well. So that can be clopidogrel or tag or it depends on the guidelines. Um So in terms of um a definitive treatment, you can get PCI for a stemi and for an uns, but it um uh it has to be within 12 hours of onset of the symptoms and it needs to be able to be delivered within um two hours. Yes. Um within 20 minutes of the um of the stemi or the symptoms. Um if criteria is not met, you can give fibrinolysis for a semi and with PC, you co you tend to count, calculate grade score, which is like the risk of six month risk of mo mortality. Uh you do within 72 hours if they're um low risk for in, in terms of their grace score, um or if there's no immediate PCI that they're gonna get, um you would also get Fondaparinux as well. Um in terms of secondary prevention, um a lot of people remember it as the, the um the four A s late. So that's aspirin which is like long it took or clopidogrel, sometimes prost as well as well as coming in beta blockers, atorvastatin um altogether. Um So I've got a question here if, um, there's gonna be a polar, the Q, um Q and A. Ok. So, um, these a 72 year old woman present with a one hour history of this and fatigue, um, she reports no chest pain. Uh, inspiration is not painful. She has a past medical history of type two diabetes and, um, a is a long term term smoker, chest is clear to auscultation, her BP, eye. Um, she's a bit tacky, um, oxygen saturations are 96 there. And ECG shows a broad complex t tachycardia consistent with a new onset left bundle branch block compared to a previous ECG. Um, what is your most appropriate next, um, investigation? Um So I'll give you guys a bit of time to answer this. This is something that I haven't covered in the, um, I, in explaining it because I just wanted to see if people had an idea of, um, what, um, what, what the answer might be. Um But then we'll talk about it a little bit more after, um, something that's really useful in MC Qs as well, just in general is to go through each, um, answer as well and just be like, OK, w why might it be this, why might it be this, what is this gonna actually, why investigate, what investigation is this actually gonna, um, help us with as well? Um So we'll go through give like a minute, we'll just uh leave it open for another 10 seconds and then we'll see what people say. All right. Sounds good. All right. Uh So majority of the people are right. So the, the most appropriate next, next is um a, a uh high sensitivity troponin. The main reason for that is this patient, in terms of ECG, we talked about um T wave inversion and we talked about ST elevation. Another thing is left bundle branch block is treated stemmy. Um Unless proven otherwise, I mentioned that ear cause I just wanted to see if people, I'm trying to get an idea of what people because um obviously everyone's at different levels, but that is something that's really in pain. So you always always wanna pair and E CG two previous C GS. Um And so if they've got that's being treated as a sty, so that's acute coronary syndrome. Um I mentioned previously, women and older people tend to present with uh uh A CS differently. And like when I say that, I also mean that practically, like in work I've had um had um like heart attacks and they've actually presented and they're like, actually I'm fine, I'm just a bit tired. I just have, but the main thing is that it's a sudden their baseline. Um and they, they suddenly disn suddenly they get really nice, sweaty clammy. Um So you could get, get questions like this. This is, I think from posted or one of them um definitely can get questions like this. So it's just important to think about in an acute setting. What is the best thing? So you've got BNP B MP is gonna um is usually measured for heart failure. So it could definitely a differential um in this because obviously she's got some dyspnea, she's got fatigue, but um usually what would happen is she'd also be a little bit, um She'd probably have low oxygen saturations. Um She might also have a history of heart failure. If not, they, they tell you that she's a bit fluid overloaded or she might have um some pitting edema and a better idea. Um In addition to that, it's not gonna change your management much if a patient's fluid overloaded, um acutely, you're going to treat the fluid overload whether they be in PS T or not. Um In terms of act, um Usually they desaturate and also you'd get chest pain with like is the answer. Observe and repeat the ECG in two hours you wouldn't really do. Um And then VQ scan is um sp ES in um patients who might be pregnant or are unable to tolerate a C TPA D and things like that. Um But well done. Majority got the answer right. Which is great. Um We got another one here. If anyone wants to give that a go as well, this one's a bit easier. Um I know I got a difficult one, but I thought it would just be interesting to get everyone thinking. So, just give it 20 seconds or so this time or 15 to 20 seconds or everybody wants to get their, their answers in ASAP, please. All right. Um So yes. So this question is, um, obviously this patient is having an Mr they've got um crushing, um radiating chest pain. Um And they've got ST elevation in leads 23 and aVF. So, um this is kind of like a two part question in terms of how you're answering. So they've got ST elevation in the first sense, which is giving you an idea that this is a stem ST elevation M I um and then leads 23 and aVF. So obviously, that is a little bit more of the tricky part is where is this happening? Um So we talked about it previously. So I'm just gonna go to the previous just so that we can kind of correlate, but 23 and eight. So sorry. Yeah, so 23 and aVF uh right Coronary artery lesion. And so if you think about it as like where the leads are located? 23 and are all in the posterior and inferior side is more of a um of the right coronary artery. Um I hope that makes sense. Um Keep going just for time. All right. So the next question again, we'll give you maybe about 20. We um continue on well done. Everyone's doing really well. Mhm All right. So um um so again, this is a type of two step question where you're thinking about two stages of the treatment. So we started with the acute treatment and then you're also going into what are you, you doing definitively for this clot? So this patient is also, yeah, it's got ST elevation um basically like this previous um like the last question and, and inferior M I. Um the main thing things to think about is in terms of OK, um acute management. So we talked about mona which is your morphine, um oxygen, uh nitrate and aspirin. So he's got aspirin already. They've given IV morphine. Um Now the, the next two things we want to look at um we talked about BP and oxygen, right? So his oxygen is less than 94%. So we're definitely giving him oxygen. So that rules out number one is, could we give him a nitrate? So his BP is running quite low. Um So you wouldn't give him a nitrate cause nitrates are very and so when um vessels dilate per BP. So we don't want his BP. Like we talked about in a type two M I when you're really high hypotensive that increases that um your um in the supply and demand of oxygen in your heart. Um So we'd want to avoid a nitrate. So that basically takes 3 to 5 out of the way as well. So you're giving oxygen and arranging fibrinolysis. The reason you're arranging fibrinolysis, this is 14 minutes with onset. So that's within 12 hours of onset, but with PC, two hour within two hours, um and it's not so 1, 60 minutes is more than two hours with that, you're not able to give PC and you're having a stemmy. So you're, we're gonna give them um fibrinolysis um and a cold but the, your progress is gonna be more clinical um questions and so um useful, like, look through both. Um So that is with that one. And then I think we've got one more, that's more like cardioversion, but it's like an E CG. This one's a little bit more difficult. So I'll give you some again, 20 seconds, but we'll talk through it because it's a bit of a team. OK. OK. So just in the interest of time, we're gonna go to answer. Um So the answer is arranged PC. So she's got retrosternal chest pain. She's got um she's vomited once and um this E CG obviously is an abnormal E CG. So the reason you're arranging for P uh PCI is because this E CG is um left bundle branch block. Um So obviously going into how to interpret an E CG is very, very um like it could be a whole other lecture, but I don't know if people remember the Mnemonic William Marrow where you have like R waves um in B1, the William. So the bifid kind of um tall uh wide um R waves in B6 gives you that William essentially in left bundle branch, as we said before, you're treating left bundle branch block as um a stemmy because this is new. Um This is a new change because all her previous EC GS are normal. Um So that's why you'd arrange um PCI IV max. So that's usually given in torsades de pointes. So that's broad spectrum tachycardia. It's very, very irregular, it kind of looks like the Arctic monkeys. Um am album if people know what that looks like. Um uh You wouldn't repeat the E CG in an hour cause they got they, if they had chest pain and um an acute change in an arrhythmia. So, in something like VT or um S VT, um but this is not that and then adenosine is used in S VT. Um and S VT is a narrow complex tachycardia. So it wouldn't be this. Um That was quite so well done, but um I just thought it would be useful to go through. Um Yeah, so now we're moving on to AF um which again is quite high yield. So we talked about the sinoatrial node as the primary pacemaker of the heart and that brings electrical activity into the A V node down the bundle, um ba down the bundle branches and up into um the walls of the ventricle through the purkinje fibers. Um So in terms of the pathophysiology of a, it's actually not really known what specifically causes it. So you can either get ectopic foci which is basically foci that um which is basically like the cardiac cycle gets ec sorry, the car, the heart gets electrical activity happening just randomly in between the cardiac cycle. And that causes really disorganized electrical activity and then also reentry circuits where um for the right cardiac um the pacemaker following nor at a normal pace. And then when it's going down the left side of, of the heart, it goes around and around and around, there's an extra um uh extra bit of electrical activity essentially um restarting. So, the essential thing is that you get disorganized electrical activity which causes a supraventricular tachyarrhythmia. So, supraventricular is basically above the ventricles in the atrium tachyrhythmia. It's uncoordinated. You get irregular and asynchronous um heartbeats and it's very, very fast. Usually you can also get slow. A but the main, more commonly you get is PSA um and this is kind of the different waves and uh basically, it's just a bit d it just looks very um chaotic in terms of TS and P waves because you can't really see P waves and the T waves are a bit um abnormal, too fast. You kind of miss it. Um The main thing to be aware of is when you get this really irregular synchronous heart, but you get stasis of blood, we'll talk specifically, um in a bit, but when you get stasis of blood, you have a clot and that obviously influences your management of a, in terms of types of af you've got basically, it comes and goes, self terminates more than two episodes before persistent af this basically means that it is not um self and it lasts longer than seven days and then permanent af is con you because it's continued because you can't cardio rhythm and you need to, to control their rate. Um And so the irregularity is a lot less of a concern than the rock. Um It cause an irregular heartbeat. If it's not causing them symptoms, it's usually a lot less of a concern than how fast and irregular it is essentially. So, it's both of those um concerning the most common is per um where, where it just comes and goes. Um and they have episodes here and there um persistent and permanent af is usually caused by. So um I have a pneumonic um with, you might remember, you might not find something that works for you. Um So you can cause um multi organ dysfunction when you get and you can get necrosis and electro instability, cardiac myocytes, mitral valve, like your atria are trying to push through um a pathological valve and that can cause stenos. I'm sorry, that can cause um irregularity because your um atria are trying to work harder than your ventricles and that can c um cause ectopic Folli. It can cause um that kind of abnormalities. And um the electrical physio is you're getting damage and necrosis of the cardio X LS. Um thyrotoxic rated to the ion currents of um the myocytes tension. So, atrial enlargement which um slow the slows the conduction because the themselves are just bigger and then part of the um are bigger surface area and then things like diet. So, sugar, caffeine alcohol, those all increase in effect. And um you see a risk of um um af complications. So we talked about flow to your brain to your heart um and to your legs. Um And then you can also get heart failure as well because um if your heart is going really fast and irregularly, it's gonna not be able to pump as well. Um Main one though is clots and you've got varicose triad which causes that. So, um that is low hyper, um which is basically when the blood is not flowing properly and or it's just static um hypercoagulability, um which is basically you're in a pos position, you're in a um kind of physiological or pathological state where you're more or at risk of clots. Um So that can be um sorry, it's just like completely gone th pregnant or being on like the um the combined oral contraceptive pill again, just puts you at more risk of clots and then endothelial injury because you've got more inflammatory processes going on. And that's gonna cause um platelet aggregation, that kind of inflam inflammatory process to cause a clot. Um Again, we've talked about the ECG findings. So you've got abnormal electrical activity which causes the tachycardia and this irregularly irregular rhythm, abnormal atrial depolarization because of those ectopic FKI because of those reentry circuits and that causes ab absent P waves. We talked about how P waves are in charge of atrial depolarization in that um ventricular filling phase. And that a uh so um diastole but atrial systole and you got r rapid and irregular impulses um that are going towards the A V node and the A V node are, is in charge of ventricular contraction. So that causes a very narrow CRS complex which is less than 100 and 20 centimeters and less than two squares um or two small squares. Um So that's what that looks like in terms of treatment, you can do rate control, which is um well, lifestyle advice, obviously, things like um reducing the cardiac um risk factors and also just things like diet and um and lifestyle in that way, um rate control is more common than rhythm control. Um in terms of um treatment because the rhythm is less, as I said, the rhythm is less concerning than the rate your indications for rhythm control as a first line is if it's a reversible cause af so some patients who um have sepsis or if they've got some sort of thyrotoxicosis, acute thyrotoxicosis. So, like hyperthyroid storm, um that's a reversible cause and so you can rhythm, control them. Um new onset af so if it's been less than 48 hours, you can um consider um cardioversion or um rhythm control af that's developed into heart failure and symptomatic af despite rate control, um in terms of your rhythm control, I have gone into it what it is. Yeah, we'll talk about that. Um And then control of um stroke risk is usually with a Doac or Warfarin. Um more commonly Doac and um you use your child's vas score to assess their coagulation risk and has blood to assess their bleeding risk. And you wanna balance the risk of bleeding with the risk of risk with the risk of clotting. Um and then make a decision as to how they're um treated for the most part patients will end up being on anticoagulation. Um In terms of rate control, your options are beta blockers. Um First line usually if they can't have beta blockers for other contraindications, things like asthma and stuff. Um you can do calcium channel blocker usually dilTIAZem. Um If one or two doesn't work, you can, you usually, you can combine them but it's important to not never combine um beta blocker with verapamil. Um because um verapamil is rate limiting and it can um risk of heart failure. Um Third line is digoxin not really used as much. It's quite a not um like a dirty drug just cause of all the side effects that can cause and it can get um toxic quite easily, but it's, it, it, it can be used. Um in terms of rhythm, rhythm control, you can do cardioversion um in terms of pharma pharmacological cardioversion, electrical cardioversion and long term rhythm control. So, um is usually used if in um acute fo af um in that kind of new onset, you can also do pharmacological con um cardioversion with fide or amiodarone. So, amiodarone is usually used if they've got some sort of structural heart disease, things like um heart failure or um or valvular disease and term rhythm control. Um The blockers and amiodarone or dronedarone can be used. Um But the more high yield ones to know would be your rate control and then electrical cardioversion and your pharmacological if you like um cardioversion. So flecainide, which is more your um in the pocket where they um suddenly get an episode of af and then um take their flo or amiodarone if they've got structural heart disease. Um I hope that makes sense and there's no questions running and chat. I don't think there is. Um But if there are questions, people are more than welcome to ask. Um So, Intercore, I've just put it here as to what the risk factors for um clotting. Um and stroke are. Um I think it's just a useful image to know what's included in the child's score if their score is zero. You don't need an, if their score is and they're a male. So they're not just scoring for their um for their sex. Um You'd consider an anticoagulation if they're scoring two and they're a woman. Um You consider anticoagulation um in some guidelines, it's warfarin for valvular af and do wax for nonvalvular af I think that might have, I don't know if that's changed. It's a bit unclear, but usually you'd choose one between the two. And more commonly dox are becoming more in fashion. Um So I've got another question here. Um uh It's related to af and um the treatment. So I was hoping if people wanted to answer them, I'll give everyone about maybe 20 seconds. All right. Um Just in the interest of time I'll continue on, but everyone's correct. So you would commence Apixaban. So this patient has um paroxysmal af so you want to anticoagulate them, um for the most part and in terms of what anticoagulation you'd use. Aspirin and clopidogrel are both um antiplatelets and um they've had already a single episode of paroxysmal af. Um So anytime they, after one episode basically of af you will start um uh coagulation cause that risk of clotting. Um If it's more than 48 hours is um quite high, you can refer to cardiology patients, but that isn't um the most important, essentially um treatment. The mo the first thing you wanna do is um anticoagulate them and then after that, we'll go on to kind of cardiology referrals and things like that. Um I've got another question here. People want to. All right, well done. So, yeah, this one's quite similar to the last one. You'd cut a child's vas score. Consider a doac um again, once a patient has an episode, you'd um start considering anticoagulation as the main thing. Another question here. Mhm. Um Turn one. Oh my God. All right. So a bit of a mix here of what the most appropriate next step is. This patient has sudden onset af um s um for about about six hours. Um and they're acutely in af essentially. So, um the main thing that you would do is DC cardioversion um in terms of the, the indications for that electrical cardioversion we spoke about um it's been less than 48 hours of onset. So we can start thinking about rhythm control. You would still think about long term anticoagulation. Um And you'd still consider um things like rate and rhythm control if um if they're still in af after the cardioversion. But first thing you want to do because it's af the most suitable next step is um your uh r your rhythm control. Um So that is why I po this question cause it's a bit um of a tricky one when you don't really know guidelines and to be fair, maybe at the end of this lecture, I'll just pull up the tachyarrhythmia guidelines, um cause they didn't cover them. But essentially, um, he's got new palpitations and he's still in af, and it's, um, in a short period of time, um, that in the tachyrhythmia guidelines as well, you would go for DC card. Um, if they, um, what's called, if they're symptomatic as well as, um, if it's just less than 48 hours of onset, um, you can also do things like bisoprolol as well. But it just um in terms of this question, he's the answer is, yeah. Next, we're gonna go into um our kind of side of things. So we're go coming towards the end of things. I know um it's common, so I really appreciate you um staying engaged. Um So in terms of um definition, so cardiac output is the volume of blood pumped into a chelation. And that's cal calculated by stroke volume, times heart rate, much volume of blood is pumped out of the left ventricle with a systolic contraction times how many times your heart is beating per minute? That is gonna be how many liter per minute minute um to the systemic circulation. Um Your enddiastolic volume is how much um blood is in the ventricles before the contraction. So how much is it filled essentially during diastole? Um And that's calculated by your um stroke volume, divided by your left ejection. Um fraction preload is essentially how much stretch you have in the ventricles before contraction and after load is how much pressure needed to pump blood during a contraction. So essentially, um I know, I don't know if people understood Frank Sterling laws and low key. I didn't really understand that until I had to teaching for this in fourth year. Um um but basically Frank Starling law is that when you have an increased, uh so basically, increase in um how much needs before contractions. So basically, the more you're stressing your heart, the more volume it's gonna help essentially. But the is that plateau pressure. So there's a limit to that cardiac muscle. So you've got a rubber band, the more and more and more and you stretch it, there's gonna be a limit to how much um you can stretch it, first of all and how much um volume that's gonna cause when it comes. Basically, the, the reason that this is relevant is that your limit to this cardiac muscle stress and heart failure. So you can have really, really high pressures and cardiac failure. But that plateaus at a, at a lower volume. And that is why you get in um your, your cardiac dysfunction in heart failure and you get um reduced um cardiac output and reduced ejection fraction. I hope that makes sense. In terms of the reason why you get fluid um changes in heart failure. It's related to your capillary dynamics. So you got change um hydrostatic pre pressures, increased pressures because your, your heart is trying to increase how much stroke volume and cardiac output. Um and to make at basically a norm at a normal cardiac stretching, essentially. So it's trying to pump um a normal stroke volume, cardiac output out to be pressures, which would be normal for um a healthy individual. So, and that causes um increase in hydrostatic pressures which pushes um fluid into the interstitium because the higher um because the pressure is higher in um the capillary itself, um basically pressure is gonna move from high pressure to low pressure. So that's why you're getting your fluid moving from inside the vessel to outside of the vessel, um your and osmotic um or um pressures uh moves uh basically fluid into the capillaries um and pressures that are um within the capillaries itself. So, the way I remember it is because hydrostatic pressure, it's kind of relates to fluid and colloid pressures is related to the capillary itself. I hope that makes sense. Let me know if it doesn't. Uh yeah, basically fluid's gonna leave the, the capillary because it's got such a high pressure inside the capillary um sense. Um In terms of the path that we talked about it, there's a limit to cardiac stretch and in heart failure, your um heart isn't able to pump or supply blood as well as it can as it as well as it normally can. So when you've got, you can split that into half, half and half path. So half puff is heart failure with preserved ejection fraction. So it's not able, able to fill as well. And so that stretch isn't as good as normal. And so you've got di diastolic dysfunction is basically it's not able to pump. Um So what we talked about with the Frank Starling law where it's not able to contract as well during the study. So increased pressure, you, you get volume overload and the way I think about it is volume is gonna overload into this. Um ba it's gonna back up into the system. If you got a top that's running through and you step on it, the top, the, the fluid is still running through, but it's gonna back up further, further down the pipes. So the reason in left heart failure, you're gonna get volume overload into your um lungs is because you've got, um your, you've got your blood, your oxygenated blood coming from your lungs essentially. So that's gonna be from your um pulmonary uh pulmonary veins. It's gonna back up uh from sorry from the left atrium, it's gonna back up to the pulmonary veins and then back into the lungs. Whereas with right sided um heart failure, you've got heart failure where um it's backing up into your vena cava, where it's going from coming from the system. In terms of causes of your heart failure. You've got ischemic heart disease where you're getting damage to cardiac myocytes, dilated cardiomyopathies, um or restrictive cardiopathy, uh myocarditis, things like arrhythmias as well. We talked about heart failure and so we talked about a and then things like um and disease as well can cause um heart fail. Um We talked about this as well. This is just a bit of a um nice summary of how that works and what symptoms basically get um in your left and right-sided, but basically you get fluid overload and that's gonna cause your symptoms. Um I'm not gonna go specifically into this. Um, but this, I think is just a nice um, overview of murmurs. It's more of a clinical um picture, but it's just a good to go over cause you can get MC QS relating to um like systolic and diastolic murmurs. Main things to know would be your pansystolic microgy murmur, um and your ejection systolic aortic stenosis murmur. Those are more common aortic stenosis is more related to your kind of um age relation and bicuspid valves and thing syndrome. And then mitral regurgitation is your ischemic heart disease and cardiomyo cardiomyopathy related things as well. Um But there can be other causes and it's just um, something that can be useful through, in terms of your investigations. You've got your um chest X ray which has um basically fluid um overload, which uh which, which shows fluid overload. So, um there's a nice Pneumonic ABCD E um in terms of looking through like unknowing what to find, um, look through what normal chest x-rays looks like and look through um what abnormal chest x rays look like and like radio pia is really good for that and shows you what things are. So um this is just a bit of a summary of what you get in a chest X ray. Um And then in terms of your management, the main things um is splitting into conservative medical and sur so conservative you wanna like refer to obviously cardiac specialist, counsel them heart failure, specialist nurses are really, really good and um helping with like lifestyle advice, you give them the yearly flu vaccine one off pneumococcal. Um just because they um they can be immu they can be immunocompromised as well. Um stopping smoking, exercise, lifestyle treatment and treat um comorbidities. Surgical can be valvular, replace replacement if they've got severe aortic dysfunction. So things like tabbies and stuff and then medical treatment, you can give ace inhibitors, beta blockers, aldosterone antagonists as well. Um uh And obviously you wanna give special get specialist input as well. Newer research is showing um the use of empagliflozin, which is a diabetic medication SGL T two inhibitor. Um that's also starting to be used in um in heart failure as well. Acute management is basically just stopping there, giving them oxygen and getting rid of the fluid. Um So if they're being given fluids, stop it, lift the bed up, um give them free smide, give them oxygen and a lot of the times patients will need ICU with, they might need vasopressors, inotropes and things like that. Um, daily weights, UK are also really useful daily weights because you make sure they're fluid overload. Daily use. These, you're giving them diuretics, you wanna check their renal function, check their potassium and then cardiology referral cause they're in charge of this. Um, so we're gonna go on to these CQ si think we'll do a couple. I don't know if you agree, Steven and then um, people can do the rest in their own time or if people wanna just kind of go through the rest of these MC QS. They're more than welcome cause I've got quite a few, just additional ones as well. But it's Yeah. Yeah, that's, that's a grand idea. Yeah. Well, maybe just do a couple of whatever, whatever ones you think. So. Um Just let me know when I'll do the poll. So I've launched poll number eight there. So, uh yeah, that's perfect. That's fine. Grand at all. Mhm. All right. So, um, well done in answering. So the answer for this one is annual and vaccine, which is correct. So the reason it's not, um, weight loss is because she's got ABM I of 24 she's got a healthy, um um, so obviously weight management and lifestyle advice is very important, but that's not the correct answer. Um, annual influenza we talked about is correct. It's a five yearly pneumococcal vaccine unless there's specific indications for things like CD or ace. Um uh um or um if they've got a SPL A splenectomy, um cardiac resynchronization is nothing you'd go for. This patient has chronic heart failure and um the GP can manage this. Um But they would still need referred to a specialist for additional um optimization of um of their pharmacological treatment and consideration of um surgical treatments as well. Um I think we'll go to the next question nine. Um and then um we can cut it down and people can try the other questions. Um So if we do question nine, Steven, then we can continue on. Yeah, that's question nine should be available now. Yeah, in terms of um whether the session is recorded, I'm not sure, but we can send the slides and if people have any questions, I'm happy to give um my email. Um and people are more than welcome to um send me an email if you need any help, whether it's for um help with cardiology or any other um kind of um revision. And um you're more than welcome to ask for just like advice and stuff on uni life. You, if you just wanna like to chat, I'm happy to help as well. So, um yeah, so we'll do this question and then we'll um, oh, sorry, I don't know if people saw that. That. All right. So we will start it down. Um, like we said, the pain is um in af um, so the reason you wouldn't um administer amio in rhythm control. You'd only give amiodarone in um what's it called in if they've got like structural heart disease and it doesn't really say there's no indication for her to have structural heart disease. It can also be used in VT, but it's not really, really in VT. Um atropine you'd be given if their um heart rate is quite slow. So, if they're bradycardic, um that's in the bradycardia algorithm, the reason you wouldn't give um flecainide is like we talked about is kind of that pill in the pocket thing in paroxysmal a rather than um uh an immediate cardioversion. Um So, basically with um with flecainide, this patient specifically is getting worsening af and worsening symptoms. Um So you don't want to give them kind of like a one off um like pill and see how they're doing. So we talked about how um in the treatment of P AF where um rate rhythm control is prioritized. This is um new af and it's also symptomatic and it's also lost in more than 48 hours. So, um you'd want to give them a um anticoagulation cause like I said, if they've had an episode of af for more than 48 hours, it's um high risk of developing a clot and then you'd schedule them for electrical cardioversion as well. Um So, um I think I mentioned before, if I didn't, basically electrical cardioversion is usually more prioritized than um medical cardio medi medical or pharmacological cardioversion because um it's more efficient and also it's just more guidelines and um research and literature support electric cardioversion in the treatment, flecainide and amiodarone were used as that pill in the pocket kind of of um pa treatment of paroxysmal um and to coagulate them before um you cardio rhythm because if you cardio rhythm and then a clot that has already developed spreads to their brain or to their lungs, that is also something great. So, um that's the reason for that. I hope that makes sense. I know it's quite a whistle stop store. Cardiology is so vast and it's so, um um just basically it's quite high yield as a topic because it's something we learn quite early. Um So I think it's just um good to kind of correlate why all these things happen and I hope that came across in more questions there and just a couple of bcgs as well to look through. Um But hope, um this was useful. I'm looking forward to getting some feedback to either make it better know what worked and what didn't work. Um And if anyone has any questions, I'm more than happy to answer. Yep, thanks. Um So, um sa has a wee um feedback form guys if you don't mind filling it in there. Um I see a just popped it into the chat and we should have a wee feedback form as well. Um So if you don't mind taking two minutes to perform and just filling it in that we really appreciate it by us all. Um And just um again, thanks sa for, for doing that. Uh And sa you um will make these slides available if that's all right with you. Um And people can go back and, and people can go back and look at the, the other content that you prepared, but we um really appreciate you, you, you taking your time, the time out of your day and organizing it all for us. We really appreciate that. So thank you for that. And is there any other, is there any other questions or anything or any final remarks you wanna make or anything or are you all good? Um I think the main thing with MC Qs is that you wanna look like if you don't really know what the question asking or what um the answer is kind of on the get go look, look through each of the answers and like use process of elimination and that can be quite helpful um with your MC Qs. Um Yeah, that's the main thing I'd say. Um Good luck if you need any like questions, I'm happy to get my email as well. Um If, if people want to kind of ask later on or Yeah, grand, yes, if anybody wants that's email, um Just let any of us know and the the, the Cardio Cardio Cardiology Society people and um we'll get her in contact with you if that's ok. Um but uh there's no other questions. No, nothing else to say. We'll, we'll leave it there. That's ok. Sa yeah, thank you so much, Steven. Uh No, thank you and we really appreciate it um and fill in the forms and um yeah, that's it. See you later. Really? See you. Thank you. Thanks.