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Ok, so I think I'm starting you guys off. Can you all hear me? Ok. Er Cash, I might need you to read out anything that gets put in the chat because for some reason I didn't see James's message that came up. Um, so I don't know if I have access to it but um but yeah, if you just read out anything that lovely. So hi guys, I'm gonna teach you a little bit about EC GS. Um we're gonna go over some cool stuff and some less core stuff but the less core stuff that kind of helps you understand a bit more about the E CGI think is useful in terms of just if you get something plonked in front of you and your ay um you'll be able and you don't know what the hell you're looking at. Um, it might help in just allowing you to unpick it and think about it a bit more in terms of what's going on electric, electrically in the heart. Um, so we'll get started. Um, so I always start with just a simple approach to every E CG this if you do this for any of your EC GS, um, you'll look like, you know what you're doing, uh, with the examiner. Um, and generally, um, it's like it just covers all the bases. If you interpret an E CG and you cover all this stuff, it'll be fine. Um, so it's R RP WQ ST and if you just repeat that it kind of rhymes um, to yourself, you can, you can drill that into your head pretty quick. Um, so we start off with the rate. Um, can anyone tell me what's classified as Tachycardia and what's classified as Bradycardia in terms of BPM? Have we got anything in the chat? Yeah, they're saying 100 is tacky. 100 is tacky. Very good. And Brady, someone said less than 60 is Brady. Yeah, very good. Er, and then rhythm, um, there's two different options that most people go for, I think, which is, you can do 300 then divided by the number of large boxes between which is, is good. Um, but I find that sort of quicker and faster way is to just count the rhythm strip across the bottom. Um, so you just look at lead to count the number of QR s complex as you can see and times that by six cos it's a 12th strip. Um, that way if they've got an irregular rhythm, you'll be able to calculate the rate much more easily. Um, yeah, in terms of rhythm, you just want to look at the Q RSS, you can get a piece of paper, um draw over each RR and then just move it along. See if the space between gets wider or shorter. That's always a good way of doing it. Er, then you move on to P so just are there P waves? Can you see P waves? Is this person in sinus rhythm or not? Um And that's um you know, immediately giving you a good idea about how their Atria are doing. Um Then the QR S so we'll go over bundle branch block. But if you're in doubt, a wide QR s means impaired conduction through the ventricles. Um And if you're not sure if it's a left bundle branch block or a right bundle branch block, you can still see if the QR S is wide and that's, you know, better than nothing if you're not sure. Um You can just say I can see that the QR S is wide and this means there's impaired conduction through the ventricles and look like, you know, a little bit more about what you're talking about. Uh, one that's often missed is Q waves. So deep Q waves mean an old M I might have happened. Um So you'll see that as a very deeper inflection at the start of the QR S complex. Um And that, yeah, generally means someone's had an old infarct. Uh And then obviously is there ST elevation is there ST depression? Er, and is there any T wave inversion? Uh And those are both sort of signs of ischemia, which we'll go over later. Um So there's looking at this, this is lead a VR or VR is what they put it as here, this is T wave inversion. Who thinks this is normal? Who thinks this is abnormal? No, no response yet? Someone said normal. Oh, a few people have said normal. Is it a person that said abnormal? Ok. So a couple of people set up normal? That's good. That's good. So then um I, I'm glad I put this slide in. So this is actually normal. Um So in a VR it's always um inverted and often it's inverted in V one as well. Occasionally it is in V two and in some ethnicities, even V three and V four. So if I go back to the last slide, you can see the VR there up in the sort of middle top left um is, is, is inverted and that's, that's perfectly normal. So if you see that, don't say it's an ischemic change cos um the examiner will mark you down potentially. Er So moving on to axis deviation, er, does anyone have a technique for axis deviation? Um I would normally open this up to the floor but I know you guys can't talk. Er, so I'll just quickly run through it then. Er, so I normally use the thumbs technique. It's nice and simple. I'm a simple minded person. Um, it's simply that, um, two thumbs up is normal, you hold your left thumb and your right, er, thumb like this. And then if they're pointing towards each other, um, then you've got the right thumb is pointing up. So that's right axis deviation. And then if they're pointing away from each other, then the left thumb is pointing up. So that's left axis deviation. So, um, if you look here you can see. So sort of one and two in the very left picture are sort of pointing towards each other. So that's a bit of er right axis deviation, they're pointing away from each other in um the other picture. So that's left the middle picture. So that's left axis deviation and they're both pointing up in er the right picture. So that's er just normal. And then, oh yeah, in terms of what that normally means. So uh left axis deviation is a conduction abnormality and right axis deviation is normally right ventricular hypertrophy. Uh So go on to conduction problems. So basically, it's always good when you're looking at E CG to think about how the conduction's moving through the heart. So the impulse starts in the sino atrial node at the top of the atria, spreads through the atria gets to the A V node and then spreads down the bundle of his into the bundle branches and then up and around the ventricles and that causes the ventricles to contract. So, er if someone could answer this for me. So what part of the E CG measures the time taken for spread of depolarization from the SA node to the ventricular muscle. There's a bit of a clue on the images. I've had some people saying pr two indeed, yes. So the time between that P wave starting and the QR s beginning is that, that the whole process is the electricity moving from the top of the Atria down through to the A V node. Um, so that's the pr interval. How long should it be? Not got any responses on that, which I think is fine. Yeah. No, no, no one really remembers these intervals and stuff. Um, so don't worry, we've got less than five so small squares or naught 0.12 to naught 0.2. Very good. Yeah. So 200 generally five small squares just to keep it simple. Um, so obviously with this one it's, it's prolonged, er, in the bottom right here. Does anyone want to hazard a guess at what kind of block we're seeing here? Haven't got any response. Yeah, that's fine. Uh, someone's saying first degree, first degree. Yeah, very good. So, uh, first degree heart block is the nice and easy one. it is just pr intervals prolonged. So it's just, you know, when you're looking at, um, a first degree block or any sort of heart block, any sort of arrhythmia patient, um, just have a look and see, have a look at the pr if it's prolonged, you can say they've got a first degree block. Oh, I've finally got the chat available. Fantastic. That's gonna make my life a lot easier. Um, ok. So what are the causes? Um, so on, on its own? It's actually fine. You don't need to do anything about a first degree block. But think about how the patients come in if you're seeing this E CG and they, they're in hospital for a reason. Um It could be significant if they got digoxin toxicity, rheumatic fever, ischemic heart disease or electrolyte disturbance. So like all EC GS, you've gotta take it with the history with the examination, what you're seeing with the patient. Um And I think I've already answered that, but in terms of what you do nothing unless the patient has a history suggesting they've got a heart, they've had a heart attack or they've got acute rheumatic fever. So if they take, if they're coming in with chest pain and you're seeing that first degree block, then you may need to think about repeating the E CG in a bit just in case anything's going on. Um And similarly with acute rheumatic, if you think this might be rheumatic fever, then uh treat it accordingly. So secondary lot, there's three main sort of types you can classify it into. Um and this is when we're starting to get a bit more worrying. Uh cos it does mean that they've got a good bit of heart disease going on. Uh, and it often can be a Herald sign for M I. Um, it might be the sort of one of the early signs you see. Um, so does wanna hazard a guess, um, in terms of which three of the forms this one is and if it needs any treatment, so, Eric's written Mobitz type one and there's a bit more of a clue for anyone else that's not too sure yet. So he's right. Uh So you can see the pr interval is getting longer and longer and longer until eventually you get AP wave and the ventricles just aren't responding. So that P wave has tried to spread through the atria and it just hasn't gotten to the A V node and therefore hasn't caused the QR S complex. Um And this is, yeah, so Venky back or Mobitz type one and on its own, there's no need to treat. So this one, so they wanna either identify it straight up or to describe what they're seeing. OK. So I'll, I'll carry on then. Er, so this one is er Mobitz type two. So two PS for every TRS. Uh So I think what you're actually seeing there ursula is the er, it's the T wave and then AP wave. So we've got P wave Q RST wave, P wave, Q RST wave, P wave, Q RST wave, P wave nothing. And then another P wave but the pr tool doesn't sort of prolong, it's pretty constant. Um, so this one is, uh Mobitz type two, um, and it sometimes needs, er, treatment but only if it's like causing symptoms. So if this person's coming in with syncope, um, or, you know, other sort of worrying signs, um, then they might need, um, might need treatment. Uh, and then this one, does anyone want to hazard a guest for this one? So for speeds sake, I'll, I'll, I'll carry on. But, uh, this one is, um, a 21 block. So you can see there's the arrows point out each of the P waves. You got ap wave at wave, ap wave nothing. P wave, Q RST wave, P wave nothing and so on and so forth. Um And yeah, this one always needs treatment. Um, either temporary or permanent pacing. Um, especially if they, if they're going a bit slow and a bit. Braddy cos they're gonna start fainting. Um So that's not good. So that's a 21 block. And this one here, anyone wanna give us a go for this one. So this one is complete block. Yes, very good test. Um So you've got, you can see the P waves are actually regular. They're happening at a regular interval. The time between those arrows that are pointing them out is, is regular. Uh And the Q RSS are also regular. It's the same amount of time happening between them, but they're happening independently of, um, of each other. Er, and James. Yeah. So I can see what you're saying. 31. but actually this is, this is complete block and the way you can tell the difference is because the Q RSS are being regular, the P waves are being regular. Um, it's, and it's not like there's any, there, if, if it's a 31 block, there should be like P wave, P wave, P wave QR S and the QR S will be very shortly after the P wave. Whereas this one, you can see there's some P waves that are kind of happening almost within the QR S like there's one P wave there that's hit in the first QR S, it's just completely hidden and that means that it's the Q RSS aren't being caused by those P waves. They're just happening on their own. And the ventricles basically aren't getting any input from the Atria at all. So they're just set to their own usual rhythm. Um So yeah, if you, if you're not too sure if it's a 21 block or a 31 block or a complete heart block, just have a thing is the, is it that the Q RSS are happening straight after the P wave cos then that means that they're related and they're being, the Q RSS are being triggered and if they're not, or there's P waves happening within QR S complexes, then it's a complete block. Um So, yeah. So the atrial contraction is normal. Nothing's been conducted to the ventricles. So they're just completely independent. Um, and it normally means that they've got a fibrotic conducting system, um, which is the common causes of all sorts of arrhythmias in old people. So, af, is fibrosis in old people, third degree block. It's all fibrotic. How do we treat it? Very good. Yeah. So we, we need to pace these people, um, because it's normally um a good idea cos they'll be running slow, cos their Q RSS will be beating at the standard rate is about 30 bpm. That's just naturally. If the ventricles don't get any input, that's how fast they'll be, which is obviously too slow to do anything. They might be all right, sitting in a chair. But as soon as they get up and try and do anything, they're just gonna collapse because their ventricles are not gonna be pumping enough blood to their brain and they'll, they'll have a syncope. So bradycardia, let's, let's go over that. So, um you start off with your A two E approach. Obviously, if you've got a bradycardic patient, you've been bleeped to go and see someone um and usual to identify and treat reversible causes. Uh The main reversible causes we see in patients are drugs and electrolyte abnormalities. Can anyone tell me any drugs or electrolyte issues that might cause bradycardia. There's loads of drugs we give patients that make their hearts go slow sometimes they have too much. Very good. Yeah. So beta blockers are the, are the big one. but you could have a rate limiting calcium channel blocker like verapamil that can, that, that slows us down. And then in terms of electrolytes, there's three electrolytes that cardiologists love to test every cardiology ward. They're always doing these three electrolytes on their patients because they want to make sure they're uh repleting these electrolytes. Anyone want to hazard a guess. Has anyone been on the cardiology ward recently? Well done Aron. Er, well done. Who's so, yeah, calcium's a big one. potassium's a big one and magnesium. Um, so, um, all of those, if they're low you can get a brandy. Um, and then in terms of, um, once you've treated those reversible causes, then you go on to thinking about, am I gonna treat this? Am I not? Am I just gonna observe them? So, things that make you treat are if they've got any life threatening signs or they're, they've got risk factors for racist. So they are just sort of going completely stopped. Um, what sort of life threatening signss might be suggesting to us that they're going so slow that they're not perfusing and he guesses. Yeah. So we've got some good ones coming up. Um, so basically it's, yeah, it's all the ones where if blood's not getting to where it go it needs to go. These are the things you're gonna see So if it's just systemically not going, your blood pressure's gonna drop and you're gonna be shocked if it's not getting to your brain, you're gonna have syncope and you're gonna faint if it's not getting to the coronary arteries after getting out of the aorta and they're right there, they're gonna have myocardial ischemia. So they're gonna describe heart attack symptoms. So they're gonna have that cardiac sounding chest pain. Um And similarly, um, if they're beating so slow they're getting backed up, they might be showing signs of heart failure. Um, cos obviously, if their heart's not pumping that blood out, it's just gonna back up. So they're gonna get breathlessness, they're gonna have pulmonary edema. Um, all those kind of things. So if you see those signs you need to treat, um, and then you also need to check for the asystolic risk factors. I won't go over them for time purposes, but it's uh, mainly blocks or, you know, ventricular pauses. Um, there's one, only one drug you need to remember for Bradycardia in the acute scenario and I've given you a big clue on the right hand side. Can anyone tell me which drug we give for Bradycardia to speed up the heart? Very good. Yeah. So it's atropine, er, which comes from this, er, plant deadly nightshade. Um, back in medieval times, people used to put deadly nightshade on their eyes to dilate their pupils and it made, they thought it made it look them look more attractive and it's the same mechanism that causes the pupil dilation, that causes their, the heart to speed up, which is basically the, er, deadly nightshade is a parasympathetic antagonist. So it's knocking out your rest and digest system, which means your fight and flight system is the only thing that's working. And obviously when we've got our fight or flight system activated, our pupils dilate similarly, your heart rate goes up. So um so yeah, that's um how I remember it. Um So yeah, HP 500 mcg IV and that should sort them out. Um So yeah, in summary, so you do a two E check for the life threatening signs or asystole and if they have either of them uh treat with atropine, if they don't have either, you can, you can observe them and just make sure um they're all right. Uh What happens if atrium doesn't work and they're still going too slow? What can we do next? Uh Good thought Aron with adrenaline. Um But actually we just go to transcutaneous pacing. So you put the pads on like you're gonna defibrillate them and yeah, you just start doing shocks. It's not very nice. So it's obviously a last resort. Um but it just means that you can get them to have some cardiac output, um adrenaline and um isoprenaline infusions, all those kind of things you can do before you do transcutaneous spacing, but I've left them out of this talk just because you're not gonna be doing that as an F one that's gonna be like, you know, a bit more of the, the ITU or cardiologists will be considering doing that. Um, the only one you'd want to start would be, um, atropine potentially. Uh, ok. So moving on, uh, this, does anyone want to suggest what's happening in this E CG? So, yeah, I see what you s, you mean Eric about the, the um T waves and them being a bit big. Um But they're actually not too bad, they're not super tented. Er and they're not all over the place. Um So yeah, there, there's not actually hyperkalaemia here. Look more at the Q RSS and see what you think there, w what are we, are we thinking that the conduction through the ventricles is OK? Is it, is it wide or is it narrow? Yes. So we got bundle branch block. Lovely. They're all coming through now. Um So yeah, so this is a left bundle branch block. Um And you can tell that with uh the William or Wilhelm technique. Um So I think Wilhelm's a little bit better than William Cos as you can see, this is a classic left bundle branch block E CG and V one does not look like a W it looks like a V. Um whereas the MS quite classic in the V six. So generally when you see a bundle branch block, it makes interpreting the rest of the ECG impossible. Um, so don't, don't sort of start over interpreting it, especially if you're in an OSK scenario. If you see a bon the branch block, just say I can see on the branch block. Um, so that means that I'm not gonna be able to interpret, um, some of the other features on this ECG cos it makes everything a bit unreliable. Um, is it worrying is left on the branch block if you see it worrying? Yes. So, yeah, it is, it is worrying, er, cos, it always indicates disease but especially if it's new, it's a possible, mm. I, I'll speed up a bit cos I think we're going a bit slow. Well, I'm going a bit slow so this one's right behind the right block. So again, you've got the M and the, er, in V one and the sort of W shape and V six, this one's not as bad. So, um, the reason it sort of looks, the way it does with the QR S is, is because excitation slowed through one side of the heart. So you're seeing the QR S start in the left ventricle and then start in the right ventricle. So there's kind of like two R waves. Um, and it's not as worrying sometimes it means there's a, an atrial septal defect. So if in a pediatric case, maybe, um, you'd, you'd want to have a think about that. Um, so we do worry about right behind the branch block when there's also left axis deviation. And that's because more than one of the three main, er, conducting routes through the heart has been knocked out. So, um, it's bifascicular block. So you can see in the first image we've got a normal axis, all three of the conductions, uh, conduction circuits are working fine. Right. One, the branch block, it still sort of stays the same, the overall conduction through the heart follows that same arrow route. But if the left one gets knocked out, um, then, then there's only one part of the heart that's still conducting properly, you get this big swing to the left axis. And if the pr intervals prolong two, that's a trifascicular block. Um And you need to sort these patients out because basically their heart's not, is, is completely fibrosed, they're not conducting properly. Um And uh they're probably gonna need pacing. So moving on to arrhythmias. So this one is a nice normal respiratory sinus arrhythmia, you see it a lot in healthy people. So you can see there's ap wave, there's a QR S, there's at wave, they're all nice and normal. The pr intervals, not prolonged, they're always regular. It's just that the time between the Q RSS is sort of getting longer and then it's getting shorter and then it's getting longer and that's them breathing in and out. Um And it's totally normal. You normally see it in very athletic people or younger patients. Um, but it's really, you know, if you, if you see this just don't panic, you can say it's an arrhythmia cos it is. Um, but it's, it's not anything to worry about um escape rhythms, er, when your heart is being crap basically. Um, er, it's beautiful how the heart works because we've evolved so that if one bit of it gets knocked out, the next bit of it is able to take over. And it's designed in a way that the first point um of failure is set to beat faster than the next point. Because obviously, if, if your A V node or your atrial muscle was set to uh to beat faster than your SA node, you just have arrhythmias straight away. Um So from, from the get go, so your SA node's set to be at 70 then if that doesn't work, your atrial, just waits until it hits the 50 bpm point and then it will just trigger on its own same with the A V node. And then the ventricles, like I said earlier, beat at 13 actually. So it just means that if the SA node gets knocked out somewhere in the atrial muscle will take over and start its own conduction circuit and that will eventually go through the rest and um get to the A V node and then get to the ventricles and so on. Um So anyone want to hazard a guess at what we're seeing here. So we've got a nice normal P wave at the start, a nice QR S and then at wave and then a slightly dodgy P wave I would say, and a QR s and then at wave, and this is exactly what I was talking about earlier. So basically, this is atrial escape. So the P wave, the sino atrial atrial node has been doing a crap job and it hasn't set off AP wave. So you've got this weird P wave now that is actually the Atria somewhere else in the Atria has gone. Well, I'm not getting a signal, so I'm just gonna kick off the circuit cos otherwise we're not gonna get beating. Um So that's why it's a weird shaped er P wave, er cos it's, it's originating somewhere other than the SA node. Um And then that's then kicked the heart back into normal rhythm more or less. Um And then you get some normal P waves, normal cr normal T waves afterwards. OK. So in this one, we aren't seeing any P waves at all. Um And then, but we're still getting a narrow complex. So that means that what's happened is that the SA node hasn't fired, nothing's happened in the atrial muscle to trigger an impulse and it's actually gotten to the A V node and the A V nodes gone. Well, I'm just gonna beat on my own then. So there's no P wave at all. But then there's still a normal QR S. So, you know that the, er, if the beat started in the ventricles it would be a wide QR S but because it's narrow, you know, it still happened supraventricular but because there's no P wave, we know it's must be in the A V node and that's sort of showing you how you can identify where in the heart the problem is, or where the impulse is starting based on what you see on the E CG. Um So it's his junctional escape. It's like a atrial escape, but it's the A V node um where it's kicking off. Uh So this one here don't wanna say where they think the impulse is coming from. So basically, there's a big wide QR S. Um So yeah, it's coming from the ventricles. Um So this is ventricular escape, often it happens in complete heart block cos obviously, nothing's getting through. So the ventricles are starting on their own. Um So it's just kicking in doing its own thing. But you always, when the ventricles are doing their own thing, you've got this wide abnormal QR S. Um And that's why it happens in complete heart blocks. And you can see here you've got just these P waves, they're constantly trying to get through to, to the ventricles, but there's clearly a block happening somewhere probably in the A V node and then the ventricles are just going well, I'm not hearing anything from, from the, er, Atria, so I'm just gonna do my own thing and you've got these big wide abnormal Q RSS. Uh, so for the BSN S units, this is a Harry Whit slide, it's in mint green. So I don't expect you to remember this. Er, but this is one just to keep an eye out for. This is these big we weird wide Q RSS are often the sign that someone's just gone into a heart attack, they've just gone into an M I, it's called an accelerated idioventricular rhythm. Um So there's, you can see there's three normal beats and then this big weird ventricular rhythm starts and then these abnormal T waves. So it's not hyperkalaemia. Um It's just simply that they've got this widened QR S that's then causing this weird repolarisation. Uh So extrasystoles very similar. Um but they just occur early rather than late. So some part of the, of the heart muscle kicking off early, er they all follow the same pattern as their escape variants. So this one big wide QR S. So this is a ventricular extrasystole. Um And that's how we know it's, it's ventricular because it's got an abnormal QR S, they're very common, generally not a problem um when they are a problem is here. So this is called the R on T phenomenon. So it's when you're getting a ventricular extrasystole whilst the rest of the heart is repolarise. So, d during the T wave, there's a QR S complex that happens inside it. And if that happens, the person can go into um into ventricular fibrillation. So they'll have an arrest. Uh So if you see that on an ECG, that's, that's worrying and you need to keep an eye on that patient and escalate. So, uh this one, you, again, we can work out which one of these is atrial, which one of these is junctional. So the one on the left, you can see there's no obvious P waves. Um So, but the Q RSS are narrow. So we know that this isn't a ventricular tachycardia because the QR S complexes are narrow, they're not a wide QR S, but it's also not happening in the Atria. So it has to be in the junction between the two. So it's a junctional tachycardia. Um So the A V node is, is to blame on that one. And then this one, you've got a nice normal sinus rhythm and then a dodgy P wave. So somewhere in the atria kicked off early and then that's sent them into a tachycardia. So that part of the heart is just kicked off and is now firing and then causing them to have a um an S VT. Um So how do we manage S PT S? Then you all want to hazard a guess and what, what we can do first before we give any medications. That's a hint. Yeah. So, Valsalva maneuver is a good one. so just your vagal maneuvers. So, blowing on a syringe, heading an ice bath. But the usual ones are vals, Salma valsalva or carotid sinus massage. Um, we'll talk about that in a bit. Step two is adenosine, um, try to avoid it unless, um, you absolutely have to cos the patients feel like they're dying. It's really horrible, um, experience for them. But if, if you know the vagal maneuvers haven't worked and you're certain this is an S VT and not just a dodgy af, um, then you do adenosine and Maria's jumped the gun with the doses. She's al way ahead. Uh, so, yeah, 6 1218. Nice and easy. Just moving up in sixes. Um, and then step three, anyone want to hazard a guest there if adenosine doesn't work and doesn't slow them down so we can use Ril or beta blocker. So, the same sort of thing. Er, yeah. So, yeah, so that's, that's it. We start with six. We see if that brings them under control. If that doesn't work, we give them 12 and then we just keep upping it basically until they hit 18. And then if that doesn't work, then we add on the usual stuff we use for af um, so if it was an irregular uh tachy card, you'd go straight to wrap them on beta blocker, er, and then step four, shock them. Um, obviously you don't really want to shock a conscious person. So you're gonna need to sedate them, er, or anesthetize them. Uh, but that's the last resort. Um, crossing sinus massage is really good because it can improve or abolish a supra ventricular arrhythmia, but it doesn't do anything for ventricular arrhythmias. So, as long as it's safe, you can do this if you're not sure if they're having a ventricular rhythm or an S VT, er, because a, a va ventricular arrhythmia won't respond whereas an SVT will, what's the reason for not doing a cross sinus massage in a patient? Why do we tend to avoid them unless, um unless we're certain that they're safe to do it on? Yeah. So, um in terms of bre, yeah. So, um if they got stenosed carotid arteries, they might have a bit of clot sitting there and then if you're rubbing on it, you're just gonna send it firing off and give them a stroke. So tend not to do them. Um, but they are really useful if, if, if they're done safely. Uh what does this rhythm show? Where, where is the dodgy conduction happening in the heart? Is this in the atria? Is this in the, er, a V node? Is it in the sa node? Is it in the ventricles? Yes. Yes. So it's a ventricular tachycardia and you know that because again, the chia are wide. Um So we know that's where it's starting. So you got B broad QR S can't see any discernible P waves or T waves. How do we manage this one? How is it different from S VT? So, yeah, it is a shockable rhythm but if they're conscious you're not gonna wanna shock them. Uh So we can do some drug management of this one if they're, if it's a conscious patient with a, with a ventricular tachycardia. Um and we go with amiodarone instead of adenosine. So a adenosine doesn't work on ventricular rhythms, cos the ventricles don't care about how much adenosine you put into someone. Uh they do their own thing. Er but amiodarone is um a lot more powerful but it is quite a dirty drug. Um So you need to use it with caution. I'm just gonna quickly grab a phone charger cos I'm using my hotspot and it's dying. Bear with me. Thanks hospital Wi Fi. So, yeah, this, I'll just put this in as well. Cos I, you're not gonna get this on your exams. It would be horrible if your med school does this, they're very mean and very horrible. Um But basically you can have a broad QR S tachycardia and it's not a ventricular tachycardia, it could be af with a bundle branch block. Um in which case you'd treat it as if it was fast af um rather than um than a VT. And similarly, if they've got torsades de pointes, which you often see in um antipsychotics. Um So that's where it, it's VT but it gets smaller and then it gets wider and then it gets smaller. Um, with that you give magnesium, that's normally the first line. Ok. So this rhythm, what does this show? Every one of you should be able to get this pretty quick. It's one of the most common dodgy EC GS. We see. So it's af uh, yeah, so should be nice and easy. Um, so af management depends on if it's less than seven days, more than seven days or more than seven days. And you've tried to give them drugs and it hasn't worked. So, Parox is more persistent or permanent. Uh The main principles are, do we wanna rate, control them? Do we want to rhythm, control them? And do we wanna give them anticoagulation? Um And when you're thinking about rate or rhythm control, you've got to think is their heart normal or abnormal, normal, younger patient, abnormal, older patient with fibrosed conducting system. How long have they been in AF cos if it's less than 48 hours, then it's probably safer to knock them back into a normal rhythm. Whereas if it's been longer, they might have formed a clot and if you then knock them back into rhythm. Oh yeah, not very good point there from cash. Um So yeah, that's something to bear in mind. Um So yeah, and then also checking if they have life threatening features um and that all depend that all affect your management and what you go for first. Um so gone through this already. So, yeah, these are the things we use for rhythm control. So younger patients, we can give them flecainide, which is a pill, they just carry around a pill in the pocket is what they often and call the treatment. And then as soon as they feel the palpitations come on, then they've got this paroxysm my off, they take the flecainide and sort them out. That's not gonna be any good for someone who's got um a fibroid conducting system. Um If they've got an abnormal heart and it's very dodgy, you can give them a amiodarone um rate control. So beta blocker is usually your first line um or if they're asthmatic and therefore you can't give them a beta blocker. It's not a good idea. You can start with a calcium channel blocker like Rapam. Um And then if they've got heart failure, digoxin is good cos that also increases the contractility. So you're overcoming that heart failure and also controlling their rate at the same time. So it's double bubble very good. Um And then obviously, so when we've decided rate or rhythm control, we then also have to think, do we anticoagulate them? So we do chads VSC for that. Um And those are the features you can get that on MD CAL pretty easy. Um But it's good to keep these in your mind, but they're generally like the cardiovascular risk factors that we all know about. Um So that, you know, if you're, if you're having to do it on the spot in an exam or something, just have a think about those. Um And if they score more than two, you're put in them on an anticoagulant. Ok. So which option is best for this patient? He's 28 years old. He suddenly developed sudden onset palpitations two hours ago. Normally fit and well and he's not hypotensive or got any life threatening features. So for this one, the best thing to give is flecainide because he's nice and young, not got any problems. Um So that's the best option. It's been less than 48 hours. So he won't have had time to form any clots. Um And his BP is ok. So you don't need to shock him. Ok. Ok. This 184 year old woman from the nursing home, four day history of shortness of breath, heart rate's fast BPS. 100 and 54/92 examinations, otherwise unremarkable and she's got osteoporosis and asthma. So for this one, we're gonna give them verapamil and that's because you would go for a beta blocker, obviously, first line in this sort of patient, but because she's got asthma, verapamil is a slightly better choice. Um But they've, she's gonna have an old fibrosed heart. She's got four day history of her symptoms. So it's been possibly over 48 hours. She's been in af um, so we don't, we don't wanna do rhythm control, rate control is the best option. Er, similarly for this one, if we're, er, anticoagulated or not, so the last person would have scored, I think zero for their chance of act. This lady already scores a point because she's a woman already scores two points cos she's 84 so she's already on a three. So we're gonna be starting her on an anticoagulant. Um, this one here is atrial flutter um very similar to af but you've got this very classic sore tooth appearance. Um uh And it's basically because um the A V node is, is struggling to keep up with the, with the atria. Um and you can often spot it if uh if they're going fast by using ac carotid sinus massage. Um This one is VFIB um So obviously big emergency. Um you probably gonna be dealing with the patient anyway before you spot this on an E CG. Uh But yeah, so in some for arrhythmias, if they're going slow, speed them up, speeding them up atropine, that doesn't work pacing if they're going fast, slowing down. If it's a supraventricular, then adenosine if it's a ventricular amiodarone, if it's af um just your af treatment. So beta blockers, calcium channel blockers, um amiodarone if they're, if they're really bad with digoxin. If HP doesn't work, we're pacing them and the two arrhythmias that won't be affected by crossing sinus massage are ventricular arrhythmias and af so moving on to ischemic EC GS. So uh in ischemic ec GS, what do we see you wanna hazard any guesses? What are the sort of three things we look for in patients where we're worried about an M I. So we're looking at T wave inversion ST elevation or ST depression. Um So yeah, you can see those there. Um So ischemia infarction. So ST depression is ischemia, but you gotta be careful about reciprocity. So if you see an ST depression, start looking for ST elevation cos sometimes you'll see ST depression as a reciprocal change in a semi. Um So don't get too bogged down um in focusing on one part of the ECG look everywhere around in case there's something else that's more worrying T wave inversion again, is ischemia on its own. Er if you see T wave inversion and deep Q waves though, it's an old infarction, an ST innervation that's a proper infarction, the whole heart, the whole of the heart's affected. Um So just thinking about territories. So I know this is really tough for some people. Um and it freaks people out trying to work out territories and all that sort of stuff. I think the best way to think about it is where the position is on the E CG er on the E CG leads. So if we're thinking about the an the the V one to V six, you've gotta think V one and V two are right at the front, they're the septal leads. V three and V four are at the front just overly the front of the heart. And then as we move round to the side, we're going more laterally, which is where you get V five and V six. Um, inferior leads are always easy. Just think of them as the boots in the bottom left corner. So it's like a little boot shaped bit here. So if you see ST elevation here, it's an inferior M I, if you see it in V five and V six, all the high lateral leads. So that's one and a VL, that's AAA lateral M I um V one V two septal V three V four anterior. Um and then you can link that to, oh, there we go. Um to sort of the vessels. So you can think about what vessels are affected. So I like to remember it as this. There's only three, you need to really remember um for the purposes of finals. Er that's er in terms of the arteries that supply the heart, there's loads, but the three main ones are the RCA, the left circumflex and the left anterior descending. Um So the RCA, if you look at the diagram on the top, right, swings round and goes underneath the bottom and supplies the bottom of the heart. So in inferior eyes, the RCA, er the left circumflex supplies the lateral wall cos it comes around the outside. So that's why you see it in the lateral leads and then the left anterior descending obviously supplies the anterior leads. So, anterior, it's la lateral, left circumflex, inferior RCA. So just these last few slides and then I'm finished. So um we've got anterior lateral or inferior. Who's saying what on this one? And you wanna hazard a guess? Is this an anterior stemi a lateral semi or an inferior? Very good. So it's an inferior. So yeah, the boot is affected. So 23 and a VF. Um So that is that one? How about this one? Very good. Yeah, so you can see that it's, it's really quite high in V two V three V four. So there's a little bit of lateral extension as well cos there's a bit of V five there. Um So yeah, that's a, that's an anterior M I with a little bit of lateral extension. This one. So yeah, this one's lateral. So you can see it especially in the high lateral leads. So one and a VL and the reason they're called high laterals is because they supply a higher bit of the heart and you can see reciprocal changes in the opposite side of the heart. So the inferior leads. So high laterals, you've got an A stemi and then you got se depression in the boot down here. So 23 and aVF um if you guys can see that. So that's, that's what I mean about reciprocal changes and then this one's a bit of a tricky one. So there's ST depression in the anterior leads, but I can't see any ST elevation anywhere. This is one you don't wanna miss out. It'd be a bit naughty of them to give it to you in the finals. But in practice when you're working next year and you see this don't think. Oh no, this is an end Demi this could be a posterior M I. So what we're actually seeing is reciprocal changes in the anterior leads because the infarction is happening at the back of the heart. So, in this scenario, we take all the chest leads off and put them around the back and you can see on this next slide here, they've got, they've taken that off. So you've got 78 and nine and you can see there's ST elevation in the leads, they've stuck on the back of the chest. So they've actually got a posterior M I now that's systemic. Um So, yeah, so that, that's the criteria for the stemming. Uh So it has to be at at least two leads or if they've got left bundle branch block, that can also be the criteria for a semi, so, eric, so reciprocal changes. So generally, like, obviously, if it's, if it's ST elevation, that's, that's the pathological lead. Um And then, and then you look for reciprocal changes. Um But yeah, if, if, if all you're seeing is, is er ST depression it might just be ischemia, er, and that might be the pathological leads. But you've just got to check basically cos you just don't wanna identify something and think that's the pathological thing. But actually it's, it's a, it's a reciprocal. Um, so, yeah, I just wanted to also point out one meal is all you need for a stemi. So, you know, ii know it looks tiny compared to like a massive sty but it still is a stemi and still needs um treating. That's why it's important to do serial ec GS. Um So if you're in doubt and it's just a tiny, little bit of ST elevation do it again in 20 minutes, half an hour and it might have progressed. Um So stemi management, I'm sure you guys all know this. But yeah, morphine oxygen nitrates aspirin. Um and obviously clopidogrel or Tabl or one of those other ones, cos we always do dual antiplatelet therapy, antiemetics if they're feeling sick, prompt PCI, if possible in under two hours long term, these are the ones we give and that's just managing all the cardiovascular risk factors basically. Um So that they don't have one again. So we're, we're taking down their hypertension, treating any hyperlipidemia, taking the pressure off the heart with beta blockers and calcium channel blockers. So it's not working as hard um enemy. So you'll have ischemic changes on the E CG. So how do we um what do we need to identify what we do next with en ente and unstable Angina. What's the, the blood test we need, so that one's cereal troponins. So we need cereal because if the TRS rise, then we know something actively is happening. If, if there's no rise, then it's either unstable Angina or that drop rise in the setting of no E CG changes might be one of these other things on the right. There's loads of stuff that can cause rise drops that isn't cardiac. Um So with an Nstemi, you're not sending them straight for PCR, you're ringing up the cardiology team and going, do you want to do an angio on this person? And we use the gray score to kind of work out who's at high risk of um of m morbidity or mortality and how quickly they need a an angiography. But then the management is very similar. Um How often are you doing serial troponin? So, Charlotte, so um trot wise, even if it's small um is, is good enough really to then give cardiology a ring um especially if you've got ischemic changes. Um You don't need to repeat them really. Um Unless, unless you're concerned or, or you've been instructed to do so. Um uh So yeah, um in terms of anticoagulants, so if they're not going for angio straight away, so they're not having any invasive procedures where they're at risk of bleeding. We give them Fonda paranox. Um and then you only need to do angiography and revascular if they've got high risk features. So if they've got heart failure, if they're hemodynamically unstable, if they've got arrhythmias or their chest pains, not responding to um to treatment with GTN, then that's um that's a bad sign and they probably need, they're more likely to need an angio unstable angina, you can be a bit more gentle with. So if they've not got a tr rise, but they've got this ischemic E CG, they're going aggressive. There's actually less evidence that helps the patient. So we start them on the usual drugs. So dual antiplatelet therapy and symptomatic relief, then we start them on anti anginal meds. So beta blockers, calcium channel blockers, slow the heart down, give it more time to fill more time to pump blood out, more time to then perfuse those coronary arteries. GTN as they need it to dilate those coronary vessels, get more blood flowing through them and then cardiovascular risk reduction to prevent it from turning into a full blown heart attack. And again, I need to do angiography plus minus revascularization in, in the lab. If they've got high risk features and that's me done. I will let you take over cash, sorry for overrun, slightly. Hope you guys found that useful. Um I'm just responding to the S TRS questions. Give me a second. So basically, if you're um if you're like mid your suspicion is kind of like uh you're not, you're not definitely sure if it's like an A CS usually do it like an hour or if, if it's not that suspicious, 3 to 4. But if you're like, really, really not suspicious, but you want to be on the safe side, you'll do a six hour time but always just, just double check that with like your own cardio reg cause that's just what I've done for the past year. Um And also having done cardiology. Um But yeah, so my section um Ryan's gonna make me up little slight. So do you want to just control it because then I will take a while? Yeah, sure. No problem. I'll um I'll turn off my camera so I'm not a distraction, no worries. Um OK, so for my bit, we're going to go through like the conditions, the key conditions that the key conditions um for UK MLA finals and even for A and V. So we're gonna start off with heart failure. I'm sure you guys by now know very well what heart failure is, but we now categorize it with he ref and half pf so he ref based on the e on your ESC guidelines is having LVF of less than 40% and half PF is preserved when it's more than 50%. Anything in between is mildly raised, basically, anything can cause heart failure. Um It's any chronic condition really and the way to think about it with any condition when you're trying to, when you've been asked about causes and stuff, always break it down in terms of either the A Vitamin C pneumonic or break it down based on the um specialty. So I've put the first line as any cardiac condition, chronic lung disease. The next one, any high output states volume overload. Um obesity and stuff like et cetera and then drug induced and toxins are the last one that's just way easier to like break it down when you're answering questions. So the slide on the top right shows the symptoms and signs of heart failure. We're not gonna go through that right now. But what I found that is very key in he, in trying to figure out if it's heart failure or any other cause of breathlessness is these two, these two questions, paroxysmal nocturnal dyspnea and cardiac asthma. Can anyone in the chart tell me what P ND is? No takers? Ok. So paroxysmal not, oh yes, waking up at night gasping for at night. So basically P and D is when they get either coughing fits, when they lie flat, when they try to sleep or they just wake up gasping for breath. That's because they're supine. And all the um all the peripheral edema is just going up and back flowing cause congestion. So just wake up breathless. That's P and D cardiac asthma is similar concept, but it's affecting the lungs. So there's increased pressure in the bronchial arteries. And so the symptoms kind of mimic asthma where they have breathlessness and they also have a wheeze and they just start coughing. So that's two key questions to always ask in history when it's a breathlessness picture. Um And then the classification for um symptoms for heart failure is the N yh A. Um I've just put this diagram because it's very important and you come up in five of us where they like kind of just ask you what is, and you've been asked to explain it, but I'm not gonna go through that due to time. Next slide, Ryan. OK. Sorry. A bit of a crackly mic. I don't know if that's the same for everyone else. Is that right? Yeah. D do you wanna try turning it off and on again? Is it better now? Yeah, it's a bit better. OK. Let me know if it's any different later on. Um, but basically when I go through the path of physio, oh, what's going on? OK. So half rough and half puff. Why is the, is it just me or the slides are not very, they're quite blurry. Yeah, they've gone blurry. Do you want me to try and present what slide number is it? I think it's 129. OK. Sorry, guys just bear with us for a little. Yeah, it's back on. Yeah. Sorry. It's probably a problem with my network or something. Half and half, half. They, they're similar but they've got different pathologies. So half R is when the contraction is abnormal. So the left side, the, the left ventricle, the systolic function is not very good. And that because of the pumping function, not being good, does decreased cardiac output. Hef puff is when there's poor stretching or relaxation of the ventricles. And that because it's less filling, there's more pressure in the ventricles and that decreases cardiac output. Previously, the terms left and right heart failure is being used. It's still being used really, but it's, it shouldn't really be used because it's not really left and right heart failure anymore. Um Left heart failure used to be used just to say that it's because of raised aortic pressure and right heart failure is used to be used because of raised pulmonary pressure. But in the end, we should be using he ref and he ef to kind of classify heart failure. The other term that's not very used now is congestive heart failure. Just cause that term actually means accumulation like salt and water retention. So that's a very old like textbook kind of term. But now I think based on ESC guidelines, we're moving towards half and half E so you'll see more when you're on the wards. Um If someone's had heart failure for a long time, in older notes, it will be written as CCF but then in newer um notes will be written as he fre or hep next slide, right? So I've got an E CG up. Um I know we've done lots of EC GS today. Um, but I'm gonna put a pull up now, um, and just name the findings or select the findings that you can see. I can't really see the poor responses tess can you, um, so where it says chat and you can have messages up, you can also have the poll up. Oh yeah. Yeah, I see one. Yeah. Yeah. Yeah. Ok. So. Oh, ok. We were split on the 3rd and 4th option and just because of time, I'm gonna stop you guys there, but most of you have answered the third option, which is right. So next slide. So basically it shows left ventricular hypertrophy because if you see the leads um V four to V six, the S and R waves are kind of clashing together. There's actually a criteria for that. Does anyone know the criteria? I'll be quite impressed actually, if you, if you remember it right? That's fine. So it's called a Sole Leon criteria. You guys can Google that later on. But basically, if it, it's just the summation of the R NS wave, if they're above a certain value, then it's left ventricle hypertrophy. But just by looking at it, if it's looking like that, then it's L VH when it's the S waves are deep and the R waves are really tall and there's T wave inversions in V 45 and six with ST depression. And then um there's bi P mitral P mitral is basically, when you've got the M waveform on the P waves, does anyone know what that means? Having that wave F? OK. So that waveform basically means, so P wave is the mark of it shows atrial depolarization, right? So when you've got a broader P wave, that basically means it's taking longer for the signal to pass through. So when you've got the M morphology or if it's bigger and broader, that basically means that the left atrium is bigger. So having a larger left atrium and having the ST depression and T wave inversion, which is a sign of left ventricular strain and having LVH is another, putting it all together, it looks like the left side of the heart is significantly impacted. And this is one of the EC GS that you can see if someone's got HEF ref next slide. So investigation wise. So fluid status assessment is more in your examination. But um when I, the reason why I've put it there is because you need strict input output, charting, you know, your body weight, cardiologic lo body weight um and ECG S can always, it can be normal. Um I'm not saying like every single heart failure, ECG would have the signs that we went through earlier, but having um a normal ECG is completely fine. If they've got left ventricle hypertrophy and left bundle branch block, then it's a sign that's happening on the left side. If they've got RV strain. So that means you, you look, it'll be right bundle branch block or um having an R wave on deep R wave on B1. That's a sign that it's, they've got RV strain. So that means it's like a clue. That's right. Heart failure and P mitral, like we said earlier, it's left atrial enlargement. You get an echo and um bloods as you can see. So BNP is the marker that we use for heart failure. There's BNP and there's NT Pro BNP. Does anyone know the difference between BNP and NT pro BNP? OK. So anti Pro BNP, they're both the same but it's just the composition of the um blood test itself. BNP has a shorter halflife than anti pro B NPI. Think anti Pro BNP is like 100 and 20 minutes and BNP is like 20 minutes. So if you do, if you do anti, if you use anti Pro BNP, the value will be really raised. But you must make sure that when you repeat the value, it's you're repeating anti Pro BNP and not BNP, you shouldn't do BNP and then repeat it with NT Pro BNP because the values won't be the same. Anti Pro BNP will always give you a higher value because it's got a, it's accumulation over a longer period of time. Um B MPS are a bit questionable because um a lot of things can cause it to be raised. Any chronic condition. You will have a raised BNP, but it doesn't signify that someone's got heart failure. It's only if it's like significantly raised and um they've got symptoms, then you take it into account. There is a lot of conditions that can cause to raise BNP. Um And chest X ray that's very important. Does anyone know I meant by A to E on the chest x-ray bit? Right. So that's the one that I used for chest X ray findings for um heart failure. So it's ABCD ea being alveolar edema. Nice. OK. Alveolar edema. So you've got the bad wing appearance B being curly bee lines rightfully said uh where you get the horizontal lines at the base C being cardiomegaly. So more than 50% of the width of the thorax, D being dilated upper lobes and e being effusion. Great. So that's all you, that's what you can see on that chest X ray. Next slide. So management of acute heart failure, you get off oxygen target sets above 94% loop diuretic. So that'd be Furo oh Furosemide. Um and then vasodilator. So GTN infusion is normally started if someone's come in with a flash pulmonary edema and they're um in hypertensive crisis. So their systolic BP is like 190 or 200. Um and then they could be considered if they're a candidate for CPAP and they're in type one respiratory failure, you would start CPAP on them as well. Um And then there are other things that you could consider at the time. So, inotropes and vasopressin, um the reason why you give inotropes and vasopressor is to increase their mean arterial pressure. Um inotropes increase contractility. So it increases cardiac output vasopressor, they vasoconstrict. So that inherently increases your map. Um intraaortic balloon is that's quite interesting as well. That's when you um percutaneously put um a catheter and place a balloon in the descending aorta and this is a temporary measure. So you put it in there and it kind of um dilates and kind of closes depending on systole and diastole. So when it's diastole, it inflates to keep the aorta patent. So that increases perfusion. But in systole, it collapses. So that keeps the resistance that keeps the, maintains the afterload. So that in that way you're in, you're keeping the map raised and then you would do secondary prevention, which will come to when we cover chronic heart failure next slide, right? So we've got another question. I'll just send the pole now, right. So which of the following drugs reduces mortality in patients with heart failure? Nice. Most of you have gone for the right option. So it is the SEC. It's B the second option. Um Ramipril depa spiro and Bisoprolol. There are a few more drugs which will cover that also increases mortality. But out of the options, B is the right one. Furosemide is always a trick one. It does not do anything for mortality. It only improves symptom um option A Sacyr Valsartan is another drug that improves mortality. But the reason why that one is wrong is because aglycin and digoxin doesn't. Um next slide. So management of chronic heart failure, um it's ace and beta blocker. A mineralocorticoid antagonist or aldosterone antagonist S DLT two furosemide and B bumetanide. So, um the first three options are what standard medications that you always start for anyone with heart failure. It's because they improve mortality as we went through with the question just now. Um I can't, I don't really know like any. Um there's a movement towards using bumetanide because it helps with gut edema. It's way, it's way better at that than furosemide. Uh And then there's other specialist stuff like ivabradine, um digoxin hydrALAZINE and cardiac resynchronization. Um Digoxin is specifically licensed for heart failure when someone's got af it's because it acts as an inotrope for patients with af and heart failure. Um hydrALAZINE and nitrate, it's a vasodilator. So, and that is also another drug that improves mortality. Um but that's only started by a specialist team. Uh cardiac resynchronization or ci T is a device. It's basically a pacemaker where you've got two leads in the ventricle. So it's biventricular and it acts as the pumping function. It basically supplements the pumping function um for someone with heart failure and it's got a very specific criteria where it's, you need to have broad QR S complexes uh in the ecg and you need to have obviously heart failure. And then there's the other things that are non pharmacological like exercise, training and smoking cessation. And then with any, um just like CO PD, um you would offer them annual influenza vaccine and a one off pneumococcal next slide. So we're gonna quickly brush upon valvular heart disease. Um The only thing, yes, you do, Maria, um Tess would explain later on at the end. Um So we're gonna cover valvular heart disease really quickly. Um The only bit that I'm not gonna cover is aortic regurg because that's um that's the only, the only thing that you, that's the thing that you see in aortic dissection and ie um and I don't really see the need of covering it for this session next slide. So for any valvular heart disease or any heart disease in general, the workup is ecg a transthoracic echo chest X ray and plus minus transesophageal echocardiogram. Next slide. So we're gonna start with mitral stenosis um with all valvular heart disease. Their symptoms are pretty much basically the same. They've got dysnea, they've got chest pain, they've got um syncopal episodes and they kind of have constitutional symptoms of lethargy um and um weakness. But with mitral stenosis, um the signs of the key with any valvular disease, actually, the signs of the key. So you get me mela flush, it basically like it looks like they've got blush on the cheeks and it's also called the butterfly rash. I think they've got, they're either in af or they've got um A and then they've also got the a tapping apex beat, which is basically like if you place your hand on the apex area, you can feel like a quick tap. It's also called a heave. Um And then the other things is that they've got low volume pulse or they've got a loud s one, the murmur is a middiastolic murmur. The way I remember it is that is that I always remember aortic stenosis A S so that will be systolic. So if aortic stenosis is systolic mitral stenosis will be diastolic and because MSM starts, it's called M, right. Um So for MS, it would be M for mid, so middiastolic murmur, that's how I've always remembered it. Um It's also got an opening snap next slide. So with MS, if they've got af you immediately, just start them on anticoagulation and it, the licensed anticoagulant is warfarin that talks about Doac but it's not licensed yet. If they're asymptomatic, you don't do anything, you just do um regular echoes for them just to monitor the symptoms, uh monitor the progression of the valve. If they're symptomatic, you can either put a balloon or they can have surgery where you basically cut it open or replace the valve. Next slide. So then we're gonna move on to Mr um where they would have a displaced apex beat and they'll have a soft s one. So the most common cause is um a post Mr complication which is papillary, muscle rupture or mitral valve pro uh prolapse. And with Mr, you'll get a pansystolic murmur radiating to the axilla or a holosystolic murmur. Next slide. So with Mr, because there's so much backflow to the atria, the aim of treatment is to increase their cardiac output and to do that, you, you, you can either you've got a few options. Basically, you've got nitrates diuretics and you've got inotropes and the like we spoke about earlier in heart failure, you've also got the intraaortic balloon pump that can be done temporarily. Most patients with Mr, especially if they've got really bad, Mr, they would already have heart failure. So they'll be started on heart failure meds and the treat the definitive treatment for that would be repair or replacement. Next slide. So the next one would be aortic stenosis. And in aortic stenosis, you would have a heaving apex just like MS. You have a slow rising pulse, a narrow pulse pressure and a soft S two. The most common cause for aortic stenosis is calcification. In older people, you've also got um the other, the other causes like congenital bisbid valve because aortic valves are tricuspid, you get an ESM murmur that's relating to the carotids and apex. Next slide. So, if they're asymptomatic, you just observe if they're asymptomatic and the valve gradient is more than 40 they've got like some L VSD you would do, you would consider surgery most of the time they will go for surgery. If they're symptomatic, it'll be either a valve replacement or it'll be a tay. So when to decide what surgical AVR is when the patient's a young patient and they've got good performance status and the TV is used for when they're an older patient and they are not fit for surgery. Surgical AVI R last a lot longer. I think they last for like 20 years, Tavi, they last for like about 6 to 10 years. So that's why you use it more in older people. The other option is balloon. Balloons are normally done in Children and in adults who are not even fit for a tabby, but they need something to kind of prolong life just for the time being. So that's an option for them. It's basically like in the image where you can see the catheter being placed to keep it open next slide. So we're gonna cover ie for the next 10 minutes. Um Infective endocarditis. I'm sure you guys know what that is. Um inflammation or infection of the endocardium. There's many, many, many different pathogens that can cause it um be it bacterial or fungal. Um So there is a few, so you, I like to break it down based on the valve and based on what, how they got it. So if it's native valve, um if they're an IVD, if they've got a prosthetic valve, they've got a device or there's a suspicion of an autoimmune condition. So native, you just got to remember like memorize this for because like this is a very common past med question and MLA question where they kind of will elude you, they give you a scenario and you just have kind of to show like which is the most like likely pathogen. So it makes valve, um it's like staph aureus, um group Verda and strep IVD. S again, staph aureus strap gram negative Veli and they most likely have like a mixture of pathogens as well. Prosthetic valve. Um If early basically means if it's within a year of the prospective wall being placed, that's what early means late is a uh beyond a year. So early, it's staph a of all coagulate negative stuff. If it's late, it basically can be the same of it can be any other pathogen. And then you've got a device rated endocarditis which pacemaker, endocarditis and autoimmune endocarditis. Next slide. So, just briefly on the path of physio, how actually IE happens. Um So your where the valves sit in the heart, that's the site where there's the most turbulent flow. So when you've got bacteremia, that's that bit of the valve that's most that's got in contact and the most turbulent flow, they are at risk of having um valvular endothelial damage, basically. So, due to that damage, you get your clotting cascade starting there, they get, you get fibrin over there and you get collagen being built up and platelets being built up to um basically form a fibrin clot. And because you've got that there, it's like a pro thrombotic situation. Um That's it, that bit develops into a vegetation and then the bigger it gets, that's how IE starts. Basically, you've got a vegetative there. That's basically it, next slide. So acute. So ie there's many different presentations to ie, not everyone comes in from the get go within a few days of symptoms. Um Acute I es whenever, when they come in within less than six weeks of symptoms, subacute is when it's six weeks to three months and chronic is when it's more than three months, those with chronic uh or subacute, they don't typically have these normal symptoms of ie that is a fever, tachycardia. Um Either having like the per the um peripheral stigmata or the any um condition because um when you've got vegetations, these vegetations can lodge off and basically be an emboli and they can go anywhere, they can cause a stroke, they can go to any of your peripheral um vasculature and cause a septic joint or an a or ischemic limb and it can basically go to any organ and cause an infarct. Um So that's a very common presentation as well where they come in because of a septic emboli phenomenon. So, um the other signs as uh listed on the slide. It all depends on how they present. So that's, uh, you have to really do a thorough clinical examination to rule out everything. Does anyone know what the, um, fundoscopy image on the right shows nice. So, yeah, it's raw spots and basically it's when you've got hemorrhages, um, around the, um, optic disc, um, next slide. So, investigations ie would always do three sets of blood cultures taken at 30 minute intervals even though I don't think we do that in real life. But we should, um, and you'll get an up to date echo. But regardless you would discuss with micro and start empirical treatment, you don't really wait for the all the three sets of blood cultures. You wanna, especially with the septic, you just wanna treat them. Um ECG can be normal, but it depends on where exactly the vegetation is. So it, it, the ECG is very useful to kind of kind of guess where the vegetation is. So if they've got a prolonged pr interval, you know, that's kind of coming from the Atria. Um And then they could basically have any ECG changes, they can even have heart block. Um, blood wise, you would do your box standard FB C and RP ESR, if you're suspecting an autoimmune condition, you would add complement ana and rheumatoid factor, you would do an uh you would do t as well because you want to rule out if they've got um hepatic congestion because a lot of times when people come in septic and you're suspecting it's ie e um they can have um raised alp because of pulmonary congestion, that's affecting the liver as well. Um For definitive diagnosis of ie it's always a transesophageal echocardiogram because that's the only way you can properly visualize the vegetation. Um You can see it on the arrow on the top, right. That's an a vegetation in the aortic valve. Um if the TE is negative, but you've got a really strong suspicion, you would get that repeated within 5 to 7 days time because sometimes the vegetation is too small that you can't really see it. Um And then there's other fun tests um that you can do um cardiac CT is normally when the patient is not really fit enough for a toe, but you just need something to visualize it. Then you can do a cardiac CT and MRI is done. Uh You, it's typically MRI head because you want to see the, um if they've got any um septic emboli in the brain, if they've, especially if they've got meningism and they've got symptoms of low GC, uh reduced G CS or anything like that. Pet CT or spect that's usually done um later on if you want to um really assess if they've got any disseminated infection. Um But that's not really done as common. Well, I've only seen it done like once or twice, but that's done if someone has been really septic and they've gotten better. But you need to rule out um you need to basically check the whole body to see if they've got any deep rooted infection anywhere else next slide. So, um yeah, so the criteria to diagnose IE is the modified, modified dukes criteria, put the clip out there cause I think it's quite, quite cute. Um Basically, the criteria is if it's two major, one major, two minor, sorry, one major, three minor and five minor. So um bacteremia. So it's like you can see the bacteria at the bottom, right? And they've got either positive echo or a new murmur. Um And then minor criteria is when they are either an IVD. So you can see the syringe, they've got a fever which is the boiling thing, vascular phenomenon, which is the vessels, um immune phenomena. The immune is the moon immune um and bacterium. If I'm an atypical organism, I think that's supposed to be the, I don't know what it's supposed to be. But anyway, next slide, I think that should be. Oh OK. Management. Um So mm sometimes they come in septic, sometimes they don't but always start with sepsis. Six. and antibiotics most of the time is empirical. So you, you start based on your hospital guidelines and then you discuss your micro um in treatment for infective endocarditis is always MDT guided. Every trust would have um a link to a specialist endocarditis team. So in it would be the endocarditis team in Brighton. Um, you would always start them on. I mean, everyone gets started on BT prophylaxis, but it's most important for people with IE because IE, as I said earlier is a prothrombotic condition. They're very, they're high risk of getting any form of clot and strokes. So, indications for surgery is if they've got heart failure, they're in shock. Um, and you can't control the infection so they're getting complications, they're getting abscesses, they're getting aneurysms or if it's a fungal condition and, or if they're at high risk of an emboli forming or emboli being dislodged and they've got a massive vegetation. Basically. Don't worry too much about indications of surgery. Just know if they're really septic, they're probably gonna get, you just need surgery to get the, get rid of the vegetations next slide. Oh, that should be it also. Um, to add, if it's like pacemaker endocarditis, you just wanna get it out. Like with anything of an IE if they're IVD S, you just wanna take out the infec the vegetation. If it's native valve, you wanna take out and replace the valve prosthesis, take out the prosthesis and let it heal, just take it out. That's all. But yeah, we're done with my section. If anyone's got any questions, you can just pop it down. Um Yeah, we'll upload the slides, um, in the catch up content section. Thank you so much.