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just a minute for everyone to sort of come in. Yeah. All right. It's reached a steady number. Um, so thank you so much, everyone for joining us this year. As we know, a lot of you might have come last year as well. And thank you so much for coming back for our exit teaching where we're going to be focusing on medicine surgery and also focusing on risky. But we're going to break it down to before P t one t two and then before I see, obviously we're gonna kick start with Cardiology are dates. Sorry. Could you go to the second page? I just want to see what the schedule is on the Yeah, So the schedule is on there, so we're starting on the ninth and we'll be hitting up to the 10th of November to make sure that we've covered everything in time for you to a COMPT exams. What we're going to cover here is you might find, like, if you come. If you come here to get, like, really detailed, picky information, you probably won't find that because we try to cater for everyone so that they can just go into the exam that you know the common information because common. It's common, remember? And that's what we're trying to get to in med school. So that's what we're going to be focused on, and it's going to be an SBA based. So today are teaching is going to be done by Thank you so much. Bye, doctor dot alien Naqvi, who is quite who's a budding cardiologist who started that imperial and then has worked in U. C. L and I will let him do. The rest of the introductions were so thankful to have him here. Oh, I'm sorry. Just before we start as well a few housekeeping rules. I don't think you can amuse yourself anyway, but please don't commute yourself. If you've got any questions relating to the power point itself, make sure you put it in the queue and a section as you'll see on the bottom bit. What I'll do is I'll ensure that we can answer the questions throughout, and also, if there's something we can't answer, we'll give Doctor next time to answer it. At the end. Any other technical questions like you have some wax and blah, blah blah. Make sure you ask them in the chart, um area. And I know you can't see who else is on the chart, and that's done deliberately so that you can focus entirely on this. And before you leave, we've got a feedback form that once you fill out, we can send you a certificate as well as sending you to sending you the power points. Because the power points have some key yield. Right at the end of the power point has he yield of investigations like just quick fire round of how to basically revise the conditions etcetera, which would be quite useful for you. Uh, please do come to all of our rest of our events because they're going to be great. And we've got lots of external and internal speakers to face it and let you get started. Great. Thank you very much for the introduction of beer. Yeah. So I'm Daniel. I'm currently doctor doing an F three. I studied the imperial and I did the AFP at you see LH on cardiovascular medicine. So I've got my email at the end of this power point. Um, so happy to answer any questions about, you know, just General F pass AFP, cardio whatever. But today we're going to do a session on the common conditions in cardiology. So this will be SBA based where the questions some will be easier than others and some will be a bit nature than others. But the actual concepts are quite general and we'll be talking about the high yield points that you actually need for your exams. So not about a lot of, like epidemiology and things like that, but the key buzz words and what you actually need to know from years 1 to 6. So these are the main topics, not in order. I will actually be covering today. So, like you can see, they're kind of general. And you probably heard of most of these, if not all of them before. But I'll tell you, tips and tricks just actually how to remember this for your exams. Okay, so we'll start off with an S p A. And I believe there is sorted out some polls, so you can actually physically answer this. So the first question is a 58 year old women Serena presented to a and B with severe bilateral pain in her hands. She has a background of sickle cell, for which she takes codeine and parasite more regularly. Her bowels haven't opened for three days. Over the last 12 hours, the pain has gotten worse. After she went out for an evening run on examination, she is tearful and in extreme discomfort and complaining of palpitations. She can't remember when we started. Here's the EKG, and there are some OBS and some bloods there for you. With the normal range is what is the next most appropriate step in management. I'll give you guys 30 seconds to a minute until you can answer that question and then we'll go through it. So, firstly, have a look at what the HCG actually shows, and then tip would be try and see what may be causing that. Okay, so I think that's long enough to have a look. Share the results, but essentially, most of you got it right. It is D. So what's actually happening in this case? So if we look through it, it's We've got a lady here who's complaining of palpitations, and she's got a background of sickle cell anemia. She's in severe pain and discomfort. After she went outside for a run you got to remember that it's winter and exercise and someone with sickle cell. The things that you have to look out for sickle cell are things like painful crises and chest crises. So this lady, the fact that she's having pain in her hands bilaterally mean she's having a painful crises. So that's one thing that you got a note now we actually can trigger these sorts of things, um, or actually works differently. If you haven't looked at the BCG, what does the EKG show? The EKG shows that she's got an irregular rhythm with no P weight. And what is that everyone should know That is atrial fibrillation. So what can actually cause atrial fibrillation in the? In this case, there's multiple, different causes that can cause it, Um, so the fact that her bowels and open for three days usually you'd expect that in the elderly patients for people who have sickle cell, the main cause of a F is severe pain, so severe pain in someone who's got a background of heart disease potentially can cause them to trigger into a F. So the management a of a F would be to control the rate and to actually manage the underlying cause. So for her it would be to manage the cause of the pain. So that would be the morphine and the Mobic. All is just in addition, in case you're worried about the bowels, but for her it's primarily pain. But let's talk about a F as a whole. So a f. I want you to remember it in two separate things, or two separate actual results. So the first one is fast A. F and you. This is what you'll see when you become F ones, and this is what you'll see to that you'll actually see on the ward's so fast. A. F is when you have an irregularly irregular rhythm, but with a rapid ventricular response. So sometimes you see it noted as a F with RVR, and that's basically you've got a F and you're going tachycardic, so that's a heart rate of above 100. Usually you're hitting around 100 30 140 with past a F, and that's what makes it an emergency, because you have to manage that. Otherwise, you can imagine the heart can't sustain that rate for too long before it goes into failure. So that's why fast A F is a big deal, and we're going to talk about how you can control that. A f so fast The air is what Serena the patient had. If you look back, you can take your time and calculate the rate there, but or even I've written it there. It's about 130 so she's gone into fast enough, so she needs immediate management. Now. Other people and this, particularly with the elderly. They have a F as just a general background condition. Um, these can be split into three different types. So first is paroxysmal, which basically means you go into a F and then it terminates and that's it. And then you can go back into a F and terminates, and it lasts less than seven days. 90% usually lasts less than 48 hours, but the official definition is less than seven days, so that's paroxysmal a fib, and you can usually see that noted as a small pea and then a f. Secondly, you've got persistent air, and that's when someone has an episode of air that last for over seven days. But it can terminate this last case is permanent, a F and permanent type of persistent A F. But basically it's refractory to all treatments in terms of drugs and party aversions and things like that. So you see this in 80 90 year olds, you're just you do any CT on the ward and you notice they're on a F, but they're going at a rate of around I don't know, 60 70 80 something within normal heart rate, and that's just normal for them. And they're not at risk of anything apart from strokes, so you've gotta anticoagulated them. But they just live in their life with an irregular heart rhythm, and that's how it is. So how do you actually manage all this? So with most cardiac conditions, if a patient is unstable, you jump straight to DC cardioversion, and there's no difference with that When we say someone's unstable or hemodynamically unstable were talking about the fact that either they're low GCS, they've got symptoms of the heart failure. They've got chest pain or their hypertensive, so they're in shock. So those are the four signs of hemodynamic instability. So in any heart condition, if someone's experiencing that, particularly with the arrhythmias. You go straight to DC cardioversion. What's DC cardioversion. You put the pads on and shock them, okay? And then they hopefully go back to normal rhythm. If they don't, then obviously you go to your seniors and see what else is going on from there. Otherwise, what you normally see as an F one on the ward is the case of Serena, and the first thing you're going to do is control it with rate control. Great control is beta blockers and calcium channel blockers. That's it. Typically, you can give some super low 2.5. Mix Lexapro. Five. Mix the super low and just see how that works. Give it a bit of time to work, and then hopefully the patient will the AFO terminate, and they'll go back to their normal rhythm. The third point in a F management is that you have to anticoagulate. Why? Because the whole reason that we're worried about is because patients with a F R a very high risk of having a stroke, and this is and it's worth noting that this is when the ATF terminates. So if you can imagine, the heart is the atria fibrillating so they're shaking, and you've got a lot of blood pooling in the atrial, particularly in the left atrium in this area called the left atrial Appendage. Now, when all the blood pools there, it creates a clot, and it doesn't move when the heart is fibrillating. But as soon as it goes back to normal rhythm and it gives a proper pump, that clot can shoot up into the brain and cause a stroke. So whilst the patients in the F, the stroke risk is actually not too bad. But you don't know if this patient's parents is more permanent. Whatever. And, for example, in the Serena case, you know that she's not a patient with normally who has a half has been triggered by her sick or cell crisis. So you need to anticoagulate before actually terminating the the F. And this is done with low molecular weight heparin. So you know the subcutaneous aspirin or enoxaparin or whatever, and then you consider long term anti coagulation based on dulcolax, and we'll talk about this shortly. Lastly, in order to manage a F with rapid ventricular response, you got to manage the underlying course. So, like with Serena, where you are managing the pain with morphine, you've got to see what the cause of the F is. The main ones that you'll see on the war was an F one are infection. So pneumonia. Sepsis. So you start antibiotics pain. So you start pain killers. Um, peas. Thyrotoxicosis surgery less common, But you can see them particularly. Actually, I should say, After surgery, you see it quite a lot and then hypovolemia. So when an elderly patient in particular is dry and dehydrated, they can go into a half, so you give him some fluids. Cardiac causes are rarer, but as you can see there they are there. But you obviously see the senior before actually managing those. So a F three treatments rate control Anti coagulation underlying course. That's it fast with long term if it's similar, but it's worth noting a few differences, so if a patient is in a F and you know the F started within 48 hours, you can cardiovert them. But if not, let's talk about what the management is. So parents is more you anticoagulated for the same reasons I said before to avoid stroke and use the chad vascular for that, and the other thing that you can do is use a pill in the pocket. So that's essentially a medication called flecainide or so too low. And there's different ones. And through your exams you don't need to know the specifics, particularly in med school. Um, but those control the rhythm, and you use a pill and pocket control for those who are particularly young and can tolerate these medications. Um, Flecainide is the one that you use, or you can use the sotalol if there's structural heart defects, and that's why patients need an echo before that. So that's the main management of paroxysmal, persistent or permanent A. F or I should say, persistent, persistent A. F. You use the 234 rule so 234, and basically means if the F has been ongoing for more than two days, I you can't cardiovert them. Then what you do is you put them in for an elective DC cardioversion in about four weeks' time, so you anticoagulated them for at least three weeks, and then you make do an elective DC cardioversion, and then you anticoagulated them on going for another four weeks, and you can give some metoprolol for symptom management if someone's having a F in the meantime, but that's essentially it permanent. You can't really treat. You can try some rate control, but the whole point is that they're just always an f. So not a big deal. But that's it. So great. Control Anti coagulation tree underlying cause for stay up for parrot says more. You can use a pill and pocket for persistent elective party version. Very easy people overcomplicate f but that that's all you need to know for a year. Just for time reasons. Let's move on to the next question. So you're the medical F one on call. You asked to see Harold, a 45 year old who's complaining of dizziness and lightheadedness on the ward, and he's being treated for a chest infection. He's a background of depression, for which he takes fluoxetine, and this is his admission. Easy GI. Notice his admission. EKG. The nurses have now repeated it, and it shows QRS complex. Um, it shows the Q r s 170 regular rhythm and polymorphic QRS complex is. So what is the first line management for this? The OBS are written over there. They all look reasonably normal, except for one which I hope is quite obvious. The poles up. Let's see what you think is going on here. This is a bit of a tricky question, and the tip for this question to think of is basically look at the admission BCG and see if there's any abnormality there and then compare it to the findings of the new E C G. That they repeated because there is something different. So there's a few things different. Okay, so let's have a look at the answer again. Most of you you were deciding between amiodarone or maxalt, and I could see why. Because you all have realized that a QRS of one seventies abroad. So this patient has gone into a broad, broad, complex tachycardia, a heart rate of 150 right? Regular regular Sorry, a regular rhythm. So you know it's not something like a f or VF. But the one thing that differentiates between the two differentials you've got to think of is that you've got polymorphic QRS complex and we'll talk about this in a second. So this patient has gone into what we say is torsades don't want, which is a type of V t, which is what I'm sure most of you were thinking of. And side note. Why did this patient actually go into that? Well, we know that they were on fluoxetine. I didn't just put that in for no reason. Fluoxetine can result in a prolonged QT. So you look at the admission BCG and he's got a prolonged QT. QT is measured from the start of the QRS complex to the end of the team wave and it the QT interval is corrected for male and female. And you can see it on the, uh the CD itself when you do the EKGs. I didn't give you a value, but you can physically see there that he's got a prolonged cuties. The fluoxetine interacts with a lot of antibiotics. Macrolite This guy's coming into the hospital, probably for an exacerbation of COPD or whatever it is. He's probably been started on an antibiotic And those antibiotics we had to fluoxetine, and that can actually exacerbate the Q. T. If you exacerbate a prolonged QT that can result in torsades. So a lot of people find arrhythmia is very confusing, but I think they're very easy to think of. You just break them down really clearly. So if we talk about tacky arrhythmias, what is attacked? The arrhythmia if your heart rate is above 100. So if you're tachycardic, you've got a taxi arrhythmia. Yeah, that's what you got to know. Then you just got to decide whether there abroad or narrow, complex. So you look at the QRS complex and see if it's brought or narrow. Let's say it's narrow if you've got a taxi arrhythmia. So someone who's tachycardic with narrow QRS complex is, but they're in a regular rhythm. Then your Sinus tacky okay? Or your sgpt Sinus. Tacky. I'm sure you guys have seen is literally just a normal. You see, GI, they're just going fast. Okay. S V t. The way you differentiate that from a Sinus tachycardia is that you don't have P waves or it's very difficult to see. They're essentially hidden within tachycardia. Okay, so tachycardia narrow, complex, regular rhythm, either Sinus tacky if they got P waves or SPT if they haven't got P waves. Easy. We've already talked about a F, but it's the same thing. Except there now, in a regular rhythm, but the Q R s are still narrow. Now we go on to the broad complexes. So if you've got a really wide QRS complex, you got to wonder whether it's regular or irregular, just like you did for the narrow ones. If it's regular, then you've got a ventricular tachycardia, and we'll show pictures of these in a second. Just so you guys have an understanding and VT. This question was tricky because it's torsades, which is basically a type of E t and you get I'll show you some pictures in the second. Different types of morphology with the QRS complex is, or if it's irregular and broad complex, you get a beer, which basically just looks like a squiggle that you can't tell what's going on side note. For probably the ones in the latest part of medical school, you may need to know how to differentiate between Bt and sgpt with bundle branch block, so if you can imagine bundle branch block, you get broad. QRS is, And if you've got a regular rhythm with a taxi arrhythmia with broad QRS, you're thinking VT. But technically it could also be an STD with bundle branch block, and I've written this thing called the paragard a criteria down below. Just for your reference, we won't go through all of it. But that's those are the indications for how you would differentiate between the two. Now there are some nice CCGs to look at. So the first one you can see we've got a taxi arrhythmia. So it's going fast. If you look at the rate, it's probably around 300. If you look between the Q R S s. So that's basically the QRS is you can you can tell it's going above 100 there. And can you see any P waves? Not really. You see some weird looking t wave after the Q r s. But that's really it. So this patient and sgpt the way you manage SPT the main thing you got to know is vagal maneuvers. And so that involves basically getting a syringe, filling it with some water, and then the patient actually blows into it, and that increases intrathoracic pressure. And that can actually reverse the sgpt. Um, that's one thing, or you can do a carotid massage so literally you just massage the carotid artery and that that could help if those don't work. So those are the things you do as an F one even before calling your senior. If those don't work, then you can try a drug called adenosine Adenosine. Um, you have 6. 12 and then 80 mg. So if the 6 mg doesn't work, then you tried 12 mg. 12 doesn't work, then try 18 mg, and those should hopefully try and reverse the sgpt now adenosine. The only buzzword thing to know for that is that a side effect of it is that patients feel a sense of impending doom, which is the phrases they're using a lot of exams and things. So the patient actually feels like they're dying so adenosine. The half life of it is like seconds. So you give the adenosine and the patient feels like they're about to die, so you have to warn them about that before they take it. But that's one thing to note for adenosine. So that's Sgts. You've got different types of sgts. But that's beyond the scope of this lecture. The second e. C G. Regular broad, complex tachycardia We know that can either be V T or two. Assad's do. The morphology of the C G of the QRS complex is look polymorphic or monomorphic. And all that means is, do they kind of look the same or are they expire in its spiraling about? They kind of look the same, right? But their broad. So they are different from SPT so. We know that patients and beauty, How do you manage VT? The thing to remember is amiodarone. Amiodarone is a type three anti arrhythmic, which basically means it works on both dedicated calcium channels and potassium channels. And the only things to note for amiodarone is that it's got loads of side effects. It's a very dirty drug. It's got iodine in it. So am I. Odor own. So you that's how you remember it can cause thyroid dysfunction because your thyroid response and react to different changes in iodine in your body. It can cause gray slated skin, which is something you hear. A lot of exams can cause liver function problems, tremor, seizures, pulmonary fibrosis and ironically, it can cause to Assad, which is what you see in the next BCG. And the only thing to note for to Assad is that the management differs and for some reason I'm not 100% sure why. I'm sure there's a really clever science behind it. It responds really well to magnesium sulfate. So magnesium sulfate you can use for a lot of conditions. But in cardiology, specifically to Assad's responds well to magnesium sulfate. And the last BCG you see here is broad complex. It's obviously tachycardic, and it kind of just looks like a really weird squiggle. Um, it's not really regular. Any of the QRS complex is if you can even call them that so you can actually see the patient was in V. T. If you look at the beginning of the CT Strip, but then they've gone into this smaller, squiggly pattern. So this patient has gone into the F. The f is non sustainable with life. And if you have the f, this patient needs CPR and full on cardioversion, you got to get the defibrillator pads on and you follow the LS protocol, which is this. I'm not going to go into it in detail just because it takes a bit of time. But I've left it here just for you guys to see. But the key message to know is if someone goes into V F or pulseless VT. So that's literally VT without a pulse. Then you start all these compressions and ALS management, Okay, but those are the main taki arrhythmias. Okay, let's go. On the other side of things. Halima, a 32 year old woman police woman, presents to the clinic as part of her medical to do as she has to do as part of our occupational health check up. She recently had the flu, but it's normally fit in well. She does, however, suffer from anxiety and complains of palpitations on occasion. But she manages this conservatively through stress management and reducing her caffeine intake. These are your observations or look reasonably normal. Do you have an EKG there? And the examination was totally normal. How do you manage the abnormality you see on the EKG? And again, no true questions, literally level. Look at the CD and see if there's anything abnormal. So start by having a look at the access, the rate, the rhythm and then look through each of the P waves. QRs complex is ST segment and T waves and see if there's anything that you can see okay, I can see most of you have answered correctly. So this patient has a first degree heart block and you can basically see that by looking at the PR interval. So normal PR has to be less than 200 milliseconds millimeters per second, brother. But this person, as you can see, has quite a broad QR PR interval. So it's bigger than one big square, basically. So the actual management for that as you watch and wait So this person is literally asymptomatic. She's coming for a medical. You've done an EKG and found a weird abnormality. It's not having any impact on her daily function, and her observations are all stable. So are you actually going to be like, Hey, do you want to insert a pacemaker and all of this? Not really. You're going to just see what happens. A lot of the population and many of you watching now probably have a first degree heart block, and it's not really a big deal, but let's talk about heart blocks. Well, let's talk about bradyarrhythmias now. You'd actually identify them first. So the same way you can identify tacky arrhythmias, you can have a look at and classify Bradyarrhythmias tacky was over 100 BPM. Brady is less than 60. If you have a patient going at less than 60 is their rhythm regular or is it irregular? If it's regular, you've got Sinus bradycardia. Loads of things can cause Sinus bradycardia, and I've written them all in there. And there's this nice acronym that you can use called for pneumonic that you can use called divisions. Um, that you can see there, but those are things that can cause bradycardia. Okay, and you treat the underlying cause for that, or if it's irregular, you can get a heart block. And the way F is irregularly irregular Heart block is regularly irregular, so you basically get a recurrent same pattern. But it's irregular, and we'll talk about that in a second. I've written here in that box the treatments for bradycardias and Bradyarrhythmias. So if someone is going really Braddy and they've got mobitz tattoo complete heart block sick Sinus syndrome, which is basically a problem with the Sinus sinoatrial node a f causing bradyarrhythmia so you can get past a F and really slower and drug resistant tacky arrhythmias, then you can start them on a pacemaker. If someone is bradycardic and less than 40 then you might consider atropine. And the main thing to note for atropine is that you have a max dose of 3 mg. For some reason, that's a really commonly tested thinning, thinning exams. So if you have someone going slow, you can start them on atropine. But you can only give up to three mics in 24 hours, so those are all well and good. But let's talk about why first degree heart block actually happen. So if you look at this diagram like I said, First degree Heart Block is a broad and QRS complex over 100 millimeters per second. Sorry, broadened PR interval. That happens because you got a partial blockage between the Sinoatrial node here and h a ventricular node. So basically it takes a bit of time for the electricity to reach the atrioventricular node. But not that big. A deal like I said, really doesn't really cause any symptoms. Most people live their whole lives with it and causes no problems when it starts to cause problems is when you get to second degree heart block. But 1st, 2nd degree heart block type one, also called Wenke back. So some people remember It's like a one c back because it's the first type of secondary heart block that's mobitz one. That's basically when you've got this partial blockage between the S, A. N and Avian, but then on occasion it causes a complete blockage, and the potential and the action potential can actually reach the IV in. So that's when you got this PR until it gets longer and it gets longer and it gets longer and then you have a dropped beat. So that's when this happens, the complete blockage. But then your heart gets back to normal again. Surprisingly, nothing really happens Because of this. People can live their whole lives with this and cause no problems. So again, you just watch and wait with that. Now, when really problems start is when you've got mobitz type two second degree. And like we said, this is an indication for pacemaking, and that's when the heart beats normally a V a n s a n T r a v a N s e and a V and everything's fine fixed PR interval, although it is prolonged. But it's a fixed PR interval. But then you start to drop complexes, and that causes this complete blockage that we talked about before. The reason why this is a big deal is because there's a high risk that this becomes third degree heart block. And when something becomes third degree heart block, which you can see here, that means there's no connection between the atria and the ventricles. If someone's got no connection between the atrium ventricles, each part of the heart is beating at a different rate. They're beating at their own rate. So as you can see in the last BCG, the P waves are all regular. But so are the QRS complex is. But just because the regular doesn't mean they're synchronous, so that means sometimes you have a a tree or beating against a closed valve or ventricle. Beating is a closed aortic valve or both of them, but at the same time, and your blood flow is basically non existent, and that can lead to a systole, and that can lead to death. So that's why it's important to get a pacemaker with second degree Mobitz two or a third degree heart block. But those are third degree heart, and those are hard blocks regularly irregular rhythms. Next question. 50 year old man Ali presents with crushing central crushing chest pain, which is now resolved. Chest pain started while Ali was no, and you didn't see that just minister. And while I was sitting on his sofa and watching TV, it lasted for one hour and radiate to the jaw. There was associated shortness of breath and diaphoresis, which basically means he was sweating a lot on arrival to and he his arms were stable, but he was clutching his sternum. E C G is shown below and he's got a drop of 38 which is raised normal. Top is below 14. I kind of gave the answer away, but answer the questions and see and see. See what? What you think it is. Okay, he was managed with dual anti platelet therapy. Yeah, I gave it away in it. I'm seeing all these all these answers, but either way you manage the patient with the dual antiplatelet therapy G t n morphine, and then reverted cardio and the coronary angio is what you used to have a look inside the arteries and see what's going on. So yeah, I gave the answer away, so we'll just get on with, um So this patient has a 90% stenosis of the led. What does that even mean? So if you look at the CCG, what are the abnormalities? So you've got a left axis deviation. Okay, big deal. A lot of people have that. You've got some T wave inversion in a V o. Okay, again, a sign of ischemia. But you've got to look at the Holy CG in the whole picture. But you have these really odd looking T waves, really from the one all the way to the four, which is the anterior territory, so they're inverted. And when you look at T waves, you always look at the second half to determine whether it's pathological or not. So these are what we call biphasic t waves. So they go up and then they get invert, and then they go down. There's one specific syndrome that you get a biphasic t waves in V two and the three and that syndrome is called well in syndrome. So you're looking at the sed of someone with Wellons. You may need to know that if you're in final yet? Well, in syndrome is critical stenosis of the lady, and you manage it as a. C s just for completion. The other options ballooning of the cardiac apex is takotsubo cardiomyopathy. So that's basically stress induced cardiomyopathy. And you get this ballooning picture of the edge of the heart and it's caused by, like, people call it heartbreak syndrome and things because people go through a breakup. I have a really stressful time, and it can cause a stress response. And you can see on the e c G Sorry on the echocardiogram where you've got this, uh, ballooned end of the heart stenosis. The less circumplex was just a distracter occlusion of the left anterior descending artery. Um, so an occlusion, you'd see a full blown stemi picture. Um, Wellons is treated as a stemi, but the patients not got complete occlusion, so there's still chance of re perfusion with the treatments and the angio, an occlusion of the left circumflex again. That's not that's the correct territory. Um, circumplex territory would be one a v e l b five c six. So although that was well, let's talk about a C s as a whole because you manage it the same. A C s is defined as a scheme year due to coronary artery occlusion. Ischemia means tissue. Death or infarction means tissue Death. Ischemia means that you're not getting any oxygen to your tissues. So there is still a chance of getting having some survival. Um, but a C s. You need to act fast. So how do you differentiate the different types of base? Yes, it's all a big umbrella pattern now. It used to be unstable angina and stemi non stemi. Now you manage it as a C s. So if you walk into an A and you see something and you see someone with chest pain and rage potentially racing shop, you see any changes, you don't label it. Yet you just say it's a C s until you can get the rest of the investigations. But, for example, person's purposes. Let's talk about how you would differentiate them. So firstly, check if there's ST Elevation on the BCG. If it is okay, that's obvious. You've got an ST elevation, am I? So that's the same. And with the stem me, what you see on the BCG is ST Elevation you can get new left bundle branch block, which is pathognomonic for ostomy as well, and you can get T wave inversion or ST Depression, which are just signs of ischemia. If there's no ST Elevation, then you check what the troponin is. If the troponin is raised, then you've got an end stemi. If it's not raised, you've got unstable angina. You can get some EKG changes on both, mainly an estimate. But the main thing that differentiate the two is the troponin, unstable angina you've got to remember or any a c s. The pain starts at rest. If it's on exertion, it's not a C s. It is still a cardiac. But A C S is by definition when you get ischemia and pain at rest. When you define ST Elevation, if it's more than one, many square in the limb leads, or more than two in the chest speeds. That's for ST elevations. So how do you actually investigate it? Like we said, you do a bunch of BCGs and you do a bunch of proponents, and the reason you do multiple E. C gs and proponents is because A C S is a dynamic condition and we know that by definition, because you see that it is a spectrum. So if someone comes in with chest pain and their clutching and the troponin is only like 16, 17, like tiny bit raised, you still want to check. Are they worsening? Or are they stable with this with this ischemia? If in an hour's time the troponin went up to 100 you know they're getting bad really quick, and the BCG might start to show some EKG changes like t wave inversion, ST depression, et cetera, and it may eventually blow into the stomach. So this is why you got to do dynamic BCGs and cereal proponents. If you suspect A. C s with anyone, you start the classic treatment of my back, which I'm sure you've all heard of. So morphine, which basically so painkillers oxygen was previously recommended. But now it's not unless the patient de saturating, but it's still part of the acronym, because if a patient is desaturing, you do start them on oxygen. Nitrates, nitrates, like GTM spray are vasodilators, and that will help with the symptoms acutely. And then the dual antiplatelet therapy is aspirin and clopidogrel. 300 beats okay, and that will stop people from getting worse. So that's what you'll see as an F one, and that's what you have to start people off. The rest is more senior, and that's based on that. You see GI findings. So if someone's gotta stemi, you send them straight to the Cath lab for a PCI. So that's percutaneously coronary intervention. And that's basically they get this little wire and put it through one of the femoral arteries or even a subclavian arteries and send it all the way through to the heart. And then they literally just break down the clock and put a balloon in and send it to the arteries. And that means there's no ischemia because there's no blockage anymore. So that's called re perfusion therapy. But for your exams PCI, that is the first line for me. If you are working in a hospital away from PCI Center, then you can do the fiber analysis. So basically, you just give them a medication like ultra place, and that breaks down clots. But the bleeding risk is crazy high, so PCI is the main way of managing en stem is you do medical management so that's your monitor. And then you give them a thing called Thunder Paradox, which is a blood thinner. And then you calculate the grace score. The gray score basically determines the chances of mortality in a patient with the current A C s that you're seeing. So they used troponin. They use background. They use heart rate ops, all of this stuff to determine the actual chances of mortality. If there are high risk patient, then you send them to the cath lab. If they're not, then you monitor on the ward. Unstable angina treatment is the same as the same. So don't think of it any different. So a C S is the main thing that you'll probably be seeing on the ward. Small note. Stable Angina is different to a C. S. Stable. Angina is when you have chest pain on exertion. So someone comes up to you in clinics like doctor. I'm having some chest pain and shortness of breath when I walk a mile. That may be a cardiac chest pain which might have a small blockage in one of your coronary arteries, but that's stable angina because it's not at rest. So this patient is imminently at risk of having an m I. But they still need to be managed quite a complex condition with a lot of different tests that you can do so I won't go through all of them. But you basically want to check how blocked their arteries are and stable. Angina. The management is basically you start them on an anti platelet aspirin to stop them from getting clots. Statins. Just because there are people with high cholesterol risk of cardiac disease, g t n because it's a basal dilating, it can help with the pain, and then beta blockers or calcium channel blocker is and then you can basically go onto these really complex meds like I SMN I've I've seen like Randall Ranolazine, but I won't go through all of that now, but it's written there just for your reference. But essentially all of these medications help with not coronary artery occlusion, but risks of ischemia when you're exerting yourself. Essentially next question. 39 year old lady Pria has some central chest pain pain, sharp and worse when she breathes in, started four days ago and has been worsening since it radiates to the left shoulder on examination. She's lying down in her bed and looks well, but a bit pale. She has normal obs, but on Auscultation, you know a soft scratching sound at her left sternal border. Her lung fields have good air entry bilaterally. And she's got a soft abdomen, which is the most Which of the following is the most specific PCG finding in this condition? No true questions on this one. Just work out what the You see, GI what the condition is and what you'd actually expect to see on the you see GI and notice the wording of the question which is the most specific finding. You may see more than one finding listed here on the EKG specific means. What finding? If you see it is most likely to point towards that diagnosis. Okay, give you another 10 seconds. Okay, So the most specific finding in a patient with pericarditis is PR depression. So this lady has pericarditis. She's got pleuritic chest pain that can radiate to the left shoulder. Which pericarditis you can have is quite a non specific finding. You can get that in a C S P s, but it radiates, um, worst one lying flat. She's got a pericardial rub, which you can hear on hospitalization, and a lot of you thought it was ST Elevation. So you get this classic widespread ST elevation pericarditis. But you can, so you do get that That is true. But in terms of the most specific finding by definition, If you CPR depression on your BCG, you got to think pericarditis people with pericarditis. It's something like 90. 95% of them have PR depression, where, as widespread ST Elevation is actually only in about 60 to 70%. So let's talk about pericarditis. All is is the inflammation of the pericardial sac, which is the sac that surrounds the heart, and it can be caused by different things. Primarily virus is the commonest one, which is especially common exams is Coxsackie virus. And then you get things like TB uremia trauma, which is a bit later, and you can get a post Emmy pericarditis. So in the exams, you get a question of a patient had an M. I two weeks ago, and now he's developed pleuritic chest pain. Worse when lying flat, Widespread ST Elevation PR depression. What is it? It's a condition called Restless syndrome, which is just post Emmy pericarditis. And then you have other things, like connective tissue malignancy, thyroid problems, which are much rarer. So, like I said, in terms of the BCG PR depression and widespread ST Elevation, As you can see, here are the most common findings PR depression You can see and lied to you. For example. It's quite clear there or in lead V six, and you get this weird sloping PR depression A V F ive been as well. All patients with pericarditis should get a transthoracic echo to work out if they've got any structural heart disease. And the way you manage it is with NSAIDs and culture seen so basically like any other information, you manage it with anti inflammatories. So a bit of ibuprofen does the trick, and then you've got to treat the underlying cause. So if you found this patient is TB positive start um, on TV, TV meds, and that will help with the pericarditis. The pericarditis is quite a simple condition and easy to spot on exams. But just remember, P R depression is the most specific finding. A lot of units are now putting that across because I think there was a paper recently that was identifying it. Next question. 54 year old male BJ presents today and you with some severe chest pain. He's nauseous and was diabetic. The pain was not exacerbate. It was not exacerbated by any movement or breathing. His investigation showed a raised D dimer, a raised troponin raised white cells raised neutrophils normal lymphocytes. But at the higher range, he's got a new early diastolic murmur with a wide pulse pressure. You notice capillary pulsations of the nail bed. On examination. He's got a widened mediastinum on his chest X ray and you see a CT scan there. How do you manage it again? A bit of a tricky question. And the way to go about this question is, I think a lot of you will get the diagnosis because I've given pretty much every single clue there is. But try and identify where that diagnosis has happened on the organ that you think is happening. The examination findings are quite clear if you're not sure what the diagnosis is. Okay, so you manage this patient with Labetalol. This is a patient who's got an aortic dissection. How can you tell that because firstly, if you start off by examination findings, diastolic murmur, white post pressure, you've got aortic regurgitation. That's your first trip. Capillary pulsations of the nail bed is called Quickie Sign, which is a sign of aortic regurg wide and mediastinum. Not much can cause that on the chest X ray. One thing to know is it's caused by aortic dissection. You look at this CT scan, you see this weird moon shape thing. That's where the dissection is in the aorta. And the key here is to work out whether it's in the ascending aorta or the descending aorta, and we'll come on to that. So what is an aortic dissection? It's a tear in the Tunica into more of the aorta. So one of the layers associated with a bunch of things, mainly more fans that you'll see in your exams. And it typically presents with central tearing chest pain radiating to the back. The signs are you've got these different blood pressures on both arms. No specific EKG changes, but aortic regurg is a very specific sign for your or I should say, aortic dissection, uh, is quite sensitive than the patients who have that end up having aortic regurgitation. You classify it in two ways. Type A if it affects the ascending aorta, so from the heart to the aortic card or type B, which is the descending so all the way down. And there's also a DeBakey classification, which splits into a few more findings. But in order for your your exams, you need to just determine if it's type A and type, because it's manage differently. How do you investigate someone you suspect has aortic dissection? You do a chest X ray, which shows they've got this wider mediastinum. Okay, that's usually caused by an aortic pathology or a cancer. And then you do a CT angio autograph, and that's when you see one of these. Here you've got a type A on the top image, which you can see. There's a moon shape on the vessel that's actually anterior, and that's the ascending aorta and type B. You see a moon shape thing on the vessel that's posterior, and that's Type B. And the reason it's important to note is because you manage them differently. People with aortic dissection are both in a lot of pain and also have a narrower Lumen, for your blood to go through. And this results in an increased BP. So the main stay of aortic dissection management is IV labetalol in order to manage the BP. The difference is, if you've got a type A dissection. So a dissection from the aortic almost from the aortic valve, actually all the way up to the aortic arch. That may need surgery. So you need to contact the cardio thoracic steam because that dissection can actually go and cause a tear in the aortic valve and the Sinus valsalva, and that can cause a lot of problems. So that's how to note there just for time purposes, we're going to move forward. I've got these tables about aortic regurg and some murmurs just for your reference, Um, but there's loads of signs you may need to know for your exams for aortic regurg. But I've written them there. A couple more questions. You are the surgical F one on a busy night shift and your call to review a patient Diana, 67 year old lady who's got a high news squat. She has a background of a s and she's had a tabby she's got severe Crohn's, which she's had an ill your pouch and anal anastomosis. Asthma and alcohol excess. She has a heavy smoker and presented four days ago with Abdul Pain and had surgery for small bowel obstruction. Two days ago it was uneventful, and now she's being monitored. Getting some fluid's getting Bt prophylaxis analgesia. She's a bit tachycardic a bit. Take a picnic. She's desaturated. Her BP and temperature look all right. On examination, she's got bilateral reduced air entry with some Kreps normal. How it sounds pretty much a normal abdomen apart from where the wound site is, and she's got some peripheral Adema up to the medicines. What would you expect to see on her chest X ray? So, in order to answer this question, have a think about her background. Have to think about what she's receiving POSTOP and think What? What of those may have caused the findings you see on examination, obviously, as an F one or F two. Or, to be honest, anything you will do a chest X ray in someone who's de saturating. So what are you kind of expecting to find what you'll find? I just promised a prominent pulmonary venous distention. So this person has gone in acute heart failure. The other findings behavior lymphadenopathy a sarcoid by basal dense consolidation. Is cove ID or any pneumonias? Widen mediastinum We talked about aortic dissection, and Erin pleural cavity is a pneumothorax. But this person has some prominent venous section because they've gone into acute heart failure secondary to getting a lot of fluids after her operation. So presenting complaint with acute heart failure, people come in and they're short of breath on exertion. They've got edema and they're fatigued. They're cyanotic, tachycardic and have a raised JVP because there's a lot of fluid in their veins and they've got a displaced apex beat because they get some cardiomegaly and the heart sound that you hear is a murmur called an S three gallop. And you can look into that. There's different types of Gallup rhythms, but basically here, an extra heart sound. And the main thing is, you hear crackles in the lungs because you basically got fluid leaking into the lung spaces. De Novo is when someone comes in as the first presentation. But the most common and communist thing that you see is decompensated heart failure. So that's people with no no heart failure that go into acute heart failure for a number of reasons, the main thing that you do is a chest X ray blood with the BNP, so brain natural peptide that can help identify if you've got any heart failure and an echo would be helpful to identify the ejection fraction. So that's essentially how hard the heart pumps. Those are the findings on chest X ray A B C D e. So you've got alveola battling. Shadowing is you've got these. Basically, it looks like a bat when people say that you've got these shadows around the high low region that can show venous distention be as curly beeline. So that's fluid in the not only just the fissures, but in the space in between the Alvesco line see as cardiomegaly. So that's if the heart is bigger than 50% of the X ray in a p a film d for, um, upper lobe diversion, which basically means you get this venous distention looking up, which is what this patient has, and he is for infusions, which this patient doesn't have too many, but you get planted costophrenic angles. How do you manage acute heart failure and you'll see this a lot as a new doctor as well. Uh, loop diuretics. So you give some IV furosemide morphine, but not really use that much nitrates because they're vasodilators they can actually help. But you only really use that if you've got concomitant heart failure oxygen because the person is saturating. You can give some noninvasive ventilation like CPAP if the condition is worsening because heart failure leads to acute type one respiratory failure. And if it gets really bad, then you got to contact I t you so you can use this L M N o p Q pneumonic to remember that. But the main thing is to offload them. So you start with the loop diuretics. Next question. So we've done acute heart failure. A 70 year old gentleman, Ahmed presented to heart failure clinic with worsening shortness of breath on exertion. He's got a background of n h Y A three heart failure and has been managed on ramipril and below, which is at maximum dose is four. He takes 40 mg p o furosemide daily in the mornings. He's got an s three gallop. His lung fields are pretty good, but he's got some basil donors. Abdomen is fine. Cards show some pitting edema, but minimal. He's still on persistent symptoms. Despite his having maximum medical therapy so far. What would you do next? And in order to answer this question, I have to think of what you do next in terms of not necessarily straightaway starting things, Or are there things that you need to do before you consider starting someone on medication? Or if not, what medication would you start? Okay, so you see this patient? He's got a known history of chronic heart failure. And we said that in the question stem. So how do you manage chronic heart failure? Well, the next step after bisoprolol and Ramipril, so an ace inhibitor and the beta blocker would be to start an aldosterone antagonist. But before you start the aldosterone antagonist, you've got to know what this patient potassium is because spironolactone, which is what you start, is the potassium sparing diuretic. So if the patients got a high potassium, then you may consider starting an alternative medication. So you got to check the using these first so chronic heart failure, it can be split using the New York New York Heart Association classification, but that you don't have to memorize this. But basically it just means the higher the number, the worse your heart failure. And that's all based on how it limits your daily function. So this person had, uh, an h Y a three heart failure, so it was quite bad. So how do you manage it? Everyone gets an ACE inhibitor and beta blocker, no matter what. Actually before I say that there's two types or there's actually there's hundreds of types of heart failure and heart cardiologists just love making different conditions. Uh, but the main thing you got to remember is that you get heart failure with reduced ejection fraction or heart failure with preserved ejection fraction. Hef. Ref versus have pet. Okay, forget about thinking about it's systolic diastolic For now. Just remember Jeffrey first hep so heavy rep is literally, as it says in the name your ejection fraction is low, that's it. And we've got treatment for hep hep f. We barely got any treatment sports, so you haven't You don't need to remember that as a med student in your exams, that's quite advanced. So treatment for hep a ref ace inhibitors be a blocker everyone gets if they still don't work, then spironolactone. But like we said, you got to check your potassium. If those still don't work or Optimus, then you've got to do specialist treatment. And I've listed some here. The main ones that I remember are the ones listed here. So if someone's got a F at the same time as heart failure, you start them on Digoxin. If someone's got a heart rate that's greater than 75 but an ejection fraction of less than 35 for protein, which is a a funny channel blocker and then entresto, um, which you'll start after an ace inhibitor washout period. Those are the main buzz words you got to remember. And that's only because it's got valsartan in, which is an ARB. So you wouldn't start an ace inhibitor and ARB together, and the rest aren't that big a deal. Um, if someone still got really bad heart failure despite all these meds, then you can consider giving them CRT, which is basically a biventricular pacemaker in addition to all of this. So those all help in terms of prognostic benefit for heart failure. You give people frusemide and loop diuretics to help with the symptoms, so someone's short of breath. You give them frusemide, but that has no impact on prognosis. It just helps symptoms. You should also offer people with chronic heart failure, the flu vaccine and pneumococcal vaccines. And that's because there's research showing that a lot of people come in with decompensated chronic heart failure secondary to infection. So if you prevent them from having a bad response to the infection, it helps the mortality of heart failure. Okay, I know we're running out of time, but this is the last question before the last final section. So you're seeing a patient Mr Quasi in a GP appointment. Here's a 56 year old Afro Caribbean Type two diabetic. He has come for, uh, hypertension review, which was previously managed with dietary modifications, and he stopped smoking. He's following his GPS instructions very closely and is keen to maintain a healthy BP, so he's essentially a good patient. He's got no drug allergies. His BP on ambulatory BP monitoring was 100 and 42/93 but he is asymptomatic How would you manage his hypertension if you think he's still got hypertension? And I know a lot of you would know the hypertension management, but I made it tricky with this guy just because there's quite a bit going on with him. So he's African. Ambien is a type two. Diabetic is of a certain age which may or may not be above the cutoff. Okay, so I think most of you just got it right. So you start them on lisinopril. And you might think why? I know people who are Afro Caribbean should be started on the Philippine. He's about 56 years old as well. But anyone with Type two diabetes you start on a second and we'll talk about that in a second. So first thing, how did you diagnose hypertension back in the day? It used to be easy. You just do one BP reasoning and check it out. But the research shows that you actually need to make sure that the patient is getting monitored at home. So getting ambulatory BP monitoring before making a diagnosis because of things like white coat syndrome and various other things, like walking to the clinic and cause a false raised high BP. So you need to have ambulatory BP monitoring. If you suspect hypertension. If a patient has BP is over 135. Sorry. Over 100 and 50/95 you started on treatment. It doesn't matter about anything else. You start them on treatment That's called Stage two hypertension. If it's 100 and 35/85 then you treat them if they're under 80 and they've got any of the following, which is diabetes end organ damage, cardiovascular disease, renal disease or accu risk of greater than 10%. And the reason you have to cut off of 80 is because when you're above 88 s inhibitors and all of these medications actually have effects of increasing the likelihood of things like falls, so it's actually risk benefit. It's probably not worth starting them on that, but that's when you treat. So these diagrams are from past mid, and they're literally the best, like there's nothing better than that. Just follow these guidelines, so if someone has diabetes, it doesn't matter if they're black. If they're 20 years old or 70 years old, then you start them on an ace inhibitor. That's the first step. If they're not diabetic and they're over 55 or there Afro Caribbean, then you start them on a calcium channel blocker first. If those don't work, then step to you. Basically, add the other one that still doesn't work. Then step three. You add on a diuretic the thiazide like diuretic, so that's like bendroflumethiazide. And then Step four. You check the potassium. If it's low. That means you can add on a potassium sparing diuretic like spironolactone. If it's high, then you consider a beta blocker or an alpha blocker does the main things to remember. Okay, an example. Usually test step one step forward. So those are the main SPS. But I want to. Before we finish. Just do a rapid fire BCG quiz, and these are the C. G s, which you may be able to recognize. They're not ones that we've gone through before, but because they're quite high yield. I just wanted to go through them very, very briefly, so there's no sort of poles for this, but have a look at these EKGs and see what you think. So This is the first TCG. I don't know if you can type in the chat if you want or whatever you get it. Or just consider the answer. I'll give you, like, 2030 seconds to see what you think of the cheap. Cheap. So have a look at this one. Spot diagnosis. Basically, Should we get some answers in the chart going? Yeah, Why not? If you can type in the chart, feel free to do so. Also. Sorry I haven't looked at the chat yet, but I understand we're going to do a proper like you. And after this, So yeah, feel free to type in the chat worries. Okay, so this is the first BCG you can see. They've got this sore tooth baseline, which is big birds word. And you probably recognize it. This is actual flow. And the way you recognize that is that just through this sort of baseline, you get a regular rhythm. But you check the baseline out and the management for it is similar to a f. It can be regular or irregular. Next EKG. What do you think of this? This is what they call is the great Mimicker's. So you might be wondering or worried about certain leads, but the fact that I have even told you that suggests that it might not be as serious of pathology. Sorry, guys. You should be able to try and type in the chat. Now, I don't think it was. Yeah, we've got some answers. Were rolling in a anyone else when I have to go. So yeah, we've got pericarditis or anterolateral m I. There's a good thoughts. Not either of them, though. Inferior, Am I? Not quite. But I see why you think that. So you guys are basically looking at the QRS complex is and the S T and the T waves, right? So this patient, I'm just going to talk to you while you guys answer and have a look. You can see they've got a bunch of widespread T wave inversion and you might be concerned, like John of looking at the one to V four and even, you know, some of the lateral leads as to where this potentially ST elevation is coming from. This patient has one specific finding that you won't see in a stemi and you won't see in any of the other answers like pericarditis whatnot and that these massively large QRS complex is so this patient has left ventricular hypertrophy, which isn't a dangerous condition on its own, because it's really a sign of an underlying pathology. But left ventricular hypertrophy, as it says in the name, is just a growth of the left ventricle and that can show specific CT findings. So you get widespread T wave inversion. You get early, benign re polarization, benign early repolarization, which can mimic ST Elevation. So even though this is going up here in the B one B T V three segments, the morphology of the ST segment is actually just not too bad, because when you have stem ease, you get flattening of the ST segment over here. If you look at the two and the three in particular kind of slopes up, which suggests it's not as scary and not as big a deal, and that could suggest benign early repolarization. And that's very common in the Afro Caribbean population. And you'll see that a lot as an F one, and it will scare you because you think the patient having a semi. But it's actually a normal variant. Um, but The main finding in LVH is these big QRS complex is and there's a certain criteria of above 35 millimeters or in terms of if you add, I think it was like me to and B c and D five or something. Um, but basically forget the specifics. You just got to remember that if you see these big QRS complex, is that almost overlapping? Then this patient's got dentures. Left ventricle. Okay, next question. Spot diagnosis. And again, not a trick question this one. Just a case of looking at what looks a bit different than the normal QRS. We've got one suggestion of the F, but you've got to remember VF is you remember VF It's that really small, weird squiggly rhythm that you'd see So it's irregular and you don't really see anything apart from a weird squid. Also, this is a bit more regular hypochelemia will come to Now people are talking about some bundle branch blocks which you're getting closer and we've got an answer. So over here, we've got a left bundle branch block. How do you actually differentiate between left and right or what is a bundle branch block? It requires a whole separate lecture. But the basics is you've got to remember that you've got these fibers in your heart that send action potential down to your ventricles ones on the left, one's on the right. If you've got a blockage of one, then that shows certain findings on the BCG. And in this case, you've got a blockage on the left bundle. The findings of left bundle, branch block or you get this big s wave in V one and be too okay. And then if I go back, you get this weird r M pattern RSR in V six and then in right bundle branch, you get the opposite. So some people use the term William Morrow to remember this. So you get a double, you should shape W and then em in left under. So, like W if for the V one l for a left bundle and then, um, for the end of William in V six and then tomorrow for right bundle. So you actually get the opposite. So M v one are meaning right bundle and then w and B six. But I find that a bit annoying to remember. So just remember where you see in our s our pattern. So that's like the weird bunny hop thing. If it's in the six, it's left bundle. If it's in the one, it's right bundle. But I think that's just an important. It's easy to remember because it's high yield. Next question again. No trick questions. Yeah, So people are coming in with the stem ease, and everyone realize this is a kind of big deal. Be specific with the territory you're looking at. So I'm getting some specific answers, which is good. So this patient, if you look at this, what is going on here? This is classic tombstone ing, Okay? And if the tombstones for the ST Elevation is in your anterior leads, then you've got an anterior. Am I over here? Over here. You've got them in the anterior leads and then some in the lateral leads as well. If you look here a tiny bit here, so you've got an anterolateral. My So this is this is what a stem it looks like. So if we go back and actually compare that to here, you see how the left ventricular hypertrophy ones are kind of like sloping up. If you look at the ones with the stemi. Look how flat be one is. That's pathological. That's a big deal. Look how flat V sixes before it goes into the T wave before, even so that that's what a Stemi looks like. And obviously the ST Elevation is massive. So that's what a stent is. This one's a bit tricky, and there's multiple pathologies going on. And then I got one more after this and then we're done. I've got a wolf, Parkinson White and the answers focus and white. Good guess it's a for those who don't know, it's a condition where you've got an accessory pathway that results in slurring of the QRS is because the action potential takes a bit more time. So you get this thing called a Delta Wave. This is not wolf Parkinson White. Someone's written a V N R T. That's the type of SPT By definition, you get tachycardia there. There's no tachycardia here. Got some bundle branch blocks written here. Good thinking. There's something more going on with this mobitz to Yeah, you're all getting there. You're getting there. No one's mentioned the exact diagnosis. This is third degree heart block. If you look at lead to. So the rhythm strip you look at the P waves. They're very regular in the way they go about things. If you look at the QRS complex is they're very regular in the way they actually go. But they're going at different rates. So by definition, that is third degree heart block. The good really interesting about the BCG and my cardio is so interesting is you can literally find out the exact pathology of this patient. So this patient's got a third degree heart block. Why? Because if you look closely, you've got some subtle ST elevation in lead to and a bit more obvious in lead three and A V F. So this patient had an inferior Am I Now the inferior am I is in the territory of the right coronary artery. What else does the right coronary artery supply the sinoatrial node? So by the fact that you've spotted this patient for an inferior my that's occluding the right coronary that's reducing the blood supply to the sinoatrial node, and that's resulting in your heart block as well. So just from one the C. D. You can literally find out what's going on with this patient and got to send them to the cath lab. Despite what we were talking about before in terms of pacemaking of things, you found out exactly what the cause is for this. So, yeah, this is third degree heart block secondary to an inferior my last CCG. Pretty much impossible, by the way, but I thought I'd put it in just for high yield purposes. But it's got a constellation of findings. So see what you think and try. Try to see what the findings are that you see, and then see if you can spot over all encompassing diagnosis. Okay, I've got an A F, but you can see some P waves. They're really tiny. If you look into need one, for example, right axis deviation is correct. That's one finding. Not a diagnosis, though. No atrial flutter. There's no sore tooth baseline, not V F because it's regular, not VT. Although I appreciate it's wide complex. Regular. Is it got the morphology of the V T segments? Not quite. So that's good thinking. So this if you look closely, we've got one form. We've got broad, complex QRS. We've got a large let's start with the one we've got our s our complex. So these weird bunny here QRS complex is and we've got a large s wave in v six. By definition, that is right, bundle branch block that we spoke about before. So you've got right bundle branch block, Let's move and look at Leeds one and lead three large s waving the one large Q wave or not, It's not that large, but you've got a bit of a Q wave and be lead three and you've got some T wave inversion. Indeed, three. If I said to you, you've got s one Q three t three. You got the answer. This is a patient who has got a massive piece, okay? And obviously, I wouldn't expect you to know that in the war is just from a PCG. But this just goes to show how e. C gs and how P, for example, can present very differently the most common common finding of pas on the C g. A Sinus tachycardia. After that, you've got things like right axis deviation, right bundle branch block. After that, you've got things like s one Q three, t three, which is just an exam finding, but because it's high yield, I thought I'd mention it, but that's what it would look like on the BCG. Thank you very much. These are some little slides made by the acid team as a sort of just some clinical features and investigations and management just for you to have a look at your own time. Thank you very much for listening and happy to take any questions. And here's the feedback link. Sorry for taking a lot of your time, but I hope it was a bit helpful. Thank you so much. That was really, really useful. Guys pleased with all the feed platform. That's where you go. And Doctor Maccabee, could you please return to some of the questions are in the, um, in the box? Yes. So there is, like, seven. Yeah. Okay. Got them. So, please, can you repeat the 234 rule for a f? So 234 rules. Just an easy way to remember the management of persistent A. So that would be two meaning if the patient has been in a F for more than two days. Three is if that is the case, then you start them on anti coagulation for at least three weeks, and then four is you'd arrange an elective cardioversion for four weeks from that from the time they started the anti coagulation. So that's the 234 to to Assad's was a regular, broad, complex, tacky thirties. EKG doesn't look very regular, I think, to Assad is a regular, broad, complex tachycardia. Correct. But you've got to remember the regular is in relation to how far the QRS is our between each other with the F, you can get them really close and then really, really close in the V T and to Assad's there at the they come regularly. Ptosis is different from V T because of the spiraling pattern there. Polymorphic. So the actual morphology of the PT is different. I hope that answers that question. How would a type B dissection cause the murmur could not have been a type A dissection involving both ascending and descending aorta. True type A deception. You're talking about DeBakey Type one, which is when it increase both sides. It can involve that the murmur isn't specific to Type B. It's quite specific to aortic dissection as a whole. The reason that question specifically, if you guys remember was type B because of the CT exam findings, you wouldn't expect to differentiate between those two based on just examination for hypertension. Is it 55 younger or completely under 55? Um, I think it's 55 or older. Sorry and younger. Yeah, I think it is. And it's the I think it's the one with, you know, the arrow and the equal sign, but just triple check that on the slides when you get that. But, um, yeah, in the exam, they won't be that mean to you to give you someone who is exactly 55. How do you know when to switch to interest out when the ACE inhibitor or I'll just during the protagonist fails? Exactly so not necessarily when it fails when they're not optimized, so the patients on a PSA inhibitor. So this is for chronic heart failure. If the patients on a PSA inhibitor beta blocker and you started them on aldosterone and they're still experiencing symptoms and they've still got edema and they've still got chronic heart failure that's not improving, then you'd consider starting them on the entresto before you start them on. Presto. You need to stop the ace inhibitor because Entresto has valsartan, which is an ARB. That's a high yield point. So you've got to have a washout, period hokum and LVH on BCG. So hokum for those who don't know is hypertrophic obstructive cardiomyopathy. It would have many similar findings as LVH on BCG. It's very difficult to differentiate between the two exactly. I'm sure there are some very niche differences, but again, as a med student specifically, and even as an F one f two, you wouldn't be expected to know them. So a good question. But you need to do an echo. So on an E c g. I couldn't tell you the answer. How much percentage diagnosis must there be until we see a characteristic stemi sign? So again, it varies per person. I think by definition you've got to have at least half of an inclusion. But some people like even in my clinical practice, I've seen people with echoes of 80% inclusion or maybe not 80 like about 70% inclusion, and you still haven't experienced any, um, stemi signs. They just go by and see me and the EKG changes are specific, and then you've got people who've got 50% inclusion, and they have stemi so again it really varies per per person, so there's no specific definition for that. In terms of a F management. Do you have to give low molecular weight heparin before rate control always give low molecular weight heparin in terms of before or after, um, give it before for the same reasons I explained before. The risk of stroke is high in a F when the atrial fibrillation is stopped. So if you're giving great control and you give a beta blocker, for example, and it can take up to 3 to 6 hours for the bisoprolol to work, then you want to make sure the patient is already anticoagulated. So give it before, if you had to choose one. In reality, you kind of prescribe them both at the same time. If the patient's not already on prophylactic enoxaparin or low molecular weight heparin, and that's all the questions I've got here. I hope that answered them. Let me know if they didn't and I'm happy to answer some more. Thank you so much. That was so good. I hope everyone else enjoyed it as much as I did. Any other questions? Feel free to add. We'll stay on here for another five minutes. Otherwise, thank you so much for attending everybody. Thank you. I know there was a lot to go through. Um, so I hope the speed was okay. I was going a bit faster. Got lots of thank you for coming in. No problem. Thank you so much. I think you can Really? No one else has asked any questions. Great. Thanks for having me. No worries. Thank you so much. Take care. Bye bye.