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So as I was just saying to the guys from Craig Van here, um Obviously, this is for both final year and third year, but it's kind of aimed more at the final years. Um So it's not a complete basics of ECG S, but I think in surgery you've already had a bit of talks on ECG S anyway, so hopefully, we don't need to do a complete basics one. Um So I'm gonna skip through some of the stuff that's on this, concentrate a little bit on cardiac axis and rhythm recognition and then we'll go through some ecgs to hopefully sort of put that together. Um And see if it brings out any other questions that you have. Um And just if you have any questions, feel free to unmute yourselves and shout out as we go along. I don't mind questions as we're going, you know, OK. So we're not necessarily gonna go through all of this, to be honest. Um We'll just flick ahead to the bits I think might be most useful. So if we think about um the rhythm recognition initially, has anybody seen this before? This sort of way of doing rhythm recognition. Yeah, your final years have. So, it, that's sort of the way that you would get taught in, um, resuscitation courses. But I think it's quite nice. It's sort of fairly, fairly logical, I think. Um, so the first question asks, is, is there any electrical activity present? Um, and really by electrical activity we're meaning, are there any cure complexes present? Is there anything that could, um, cause ventricular activity? If you only have P waves, you're only gonna have atrial activity and that's not enough to generate a cardiac output because your ventricles aren't working. So electrical activity in this instance means are there any curious complexes? Um And if there are it then asks, are they regular or irregular? And from that, we can decide what the best way of working out the heart rate is we want to know is the cure with normal or prolonged. And then we look at the atrial activity and decide how it's related to ventricular activity. So as I say, we'll go through some of those bits, just remember like all our investigations in medicine and surgery and everything. Um You never take an investigation, result in isolation, you always take it in context with the patient. And that's very, you know, very important for ECG S because for the same ECG you can have a very different patient. And an example of that would be um somebody in VT so ventricular tachycardia. Um I remember being called to the pre op assessment clinic years ago by one of our ECG physiologists. Um so the patient was getting an ECG done a week before they were coming in for, let's say it's prostate surgery and they were on VT in VT and on their E CG as they walked off the street completely asymptomatic. And I got this call. Can somebody come down from the ward quickly? Um But results were completely normal. He had no chest pain, he had no shortness of breath. He had no worrying signs and he actually then reverted to sinus rhythm while I was with him. And we didn't need to do anything. But that same ECG could equally have been shown on a patient in CC who had had a heart attack two days ago and had got up to use the toilet and had a cardiac arrest and could be a pulseless VT. So same ECG very different outcomes potentially. Um So never take the ECG in isolation is what I'm trying to say. Ok, so the first question is, is it regular or irregular? You'd think that would be a really easy question to answer. But actually sometimes when the heart rate is really quick or really slow, it can be quite difficult to eyeball it. Um But you know, to take your piece of paper and mark off your two successive hour waves and slide it along because if you can't, if it looks regular, it might not be if it looks irregular, it probably is. All right. Um If it's irregularly irregular, it's probably a but not definitely, but just keep that in the back of your head as being unlikely diagnosis because then you can sort of work through the rest and see if it all matches up what's a ventricular rate. Um, so hopefully we all know that normal is between 60 100. To be honest, in cardiology, we don't get terribly excited by 50 to 60 unless the patient's unwell or there are types of heart block on it. Um Where the, the GP world when I see patients with heart rates at 40 or 50 they're obviously much more worried because they don't see it all the time. Um But 60 to 100 is our normal. How do we work out the heart rate on an ECG any volunteers for how to work it out? What's on the screen? So that works really well. If it's regular, you can kind the or like what do you call it? The pins? Yeah, in like a certain time frame, I mean, yeah. So if we took this example or maybe check the previous one, if you look at an ECG, um All ECG paper has some sort of mark every three seconds. All right, it might be a little triangle like you're seeing in this example. It might be a wee notch or a wee line down at the bottom, but it'll be some sort of marking if you look closely. Um So in a standardly calibrated ecg, um, a three second block is 15 squares. Um, it doesn't really matter what time block you take, but six seconds is a nice easy math. So if you work out what the heart rate is in six seconds, you only have to multiply by 10 to get the heart rate in a minute. Uh If you're standing in a ward round, when your brain's gone to mush, then that's something easy to work out. Um So for the sake of argument, if we say there's a wee notch here, my papers not long enough to give us a full six seconds, but let's say it's here just to make it easy. So if we count the number of complexes in that six seconds, it's gonna be 12345789, 10. So a heart rate of about 100. Um And we can see it looks irregularly irregular. So you think it's probably af we don't know for sure until we further analyze it, but that's high up on our list. OK. Um The next question then is about the QR S width. Does anybody? Oh, I was about to ask you what the normal Qs with is, but it's up on the screen. So it's there for you. Um So less than naught 0.10 technically is a normal QR S but on our measurements, um it's easier to look at three small squares, which is naught 0.12. And if it's a bundle branch block, it has to be more than naught 0.12 to be a bundle branch block. Um If it was naught 0.11 technically, that's still starting to enlarge, but it doesn't meet the criteria for bundle branch block. Why is the width of the c complex important? Um Well, it can give us a bit of an idea of where that complex has originated from. So if the CS complex is narrow, it tells us that that has originated from the AV node or higher up. Um So it could have come from the sinus node in the atria. It could have come from somewhere in the atria, not the sinus node or it could have come from the AV node. But if it's broad, we can't say for sure if it's come from any of those places, if it's broad, it could have come from the ventricle or it may have a bundle branch block in it. So it may have originated in a normal place, but then taken longer to get through the normal conducting system. If you think about your ventricle contracting, um it's kind of a key to our cardiac output. So the ventricular contraction should be very quick and very efficient. Um So our CS complex is narrow to give us that good oomph and to give us a good cardiac output once her Qs complex starts to broaden, it may not be such an effective contraction. Um And also if you think about how it's getting through and why it's quick. So our, our sinus node sends out the impulse that goes down through your atria down through the A V node. Where does it go next? Once it's gone through the A V node bundle of his and then purkinje fibers so that all transmits really, really quickly. So if for some reason, one of our bundles is blocked, it has to go down the other bundle and then spread through the ventricle in an abnormal fashion, which takes longer than usual. So that's why a bubble branch blocker cures complex is wide or if it's originated from within the ventricle itself, it's not going through those normal pathways at all. So that's why it's wide if you've got like a ventricular ectopic beat or VT or VF something that's originated from within the ventricle. Um So knowing whether it's normal or prolonged can help us to decide where it's most likely to originate from. OK. Um So that's just what we've talked about. And then it asks, is atrial activity present. Um So really, we're asking, is that AP wave, is it the normal sinus node? Is it some other sort of atrial wave um like a flutter wave or a fibrillation wave or you can get other types of atrial waves um that aren't P waves um get other types of atrial tachy, which maybe you guys would be more aware of. But in third year, you're probably not really aware of the atrial tachy side of things and sort of try and keep it reasonably straightforward for third year. Um, but certainly flutter waves, fibrillation waves, sinus beats are the three big ones that you've been looking for initially. Um And if we can see any of those, we then want to know how they're related to the ventricular activity. So, is there an atrial wave for every PR S complex or is there more than one atrial wave for every C complex or less than one atrial wave for every CS complex? Um What's the, if it's ap wave, what's the pr interval? Like it's the same every time does it change? Um Is there any pattern to it? Is there not? So we're just gonna go through a few examples which will hopefully sort of pull that together a little bit. Sometimes it's hard to know if there is any arial activity present there or not. Um So if you have an ECG that is quite fast, um the atrial waves can get hidden and the C as complexes and T waves depending on what the atrial activity is. So it can be difficult to know what the atrial activity is or if there is any atrial activity. Um So sometimes if we can slow the heart rate down, that then gives us a bit more of an idea of, of what the underlying rhythm could be in terms of the Atria. Obviously, it tells us up there about, we can slow up with adenosine. But there are other things that we can do before we go straight for adenosine. Does anybody know anything that they can do to slow the heart rate down a bagel? Um Or not. No, not, well, it through the vagal nerve. So, um because I'm busy agreeing with you. Um So a vagal maneuver um simplest one to do if you're in a hospital setting is to take a 20 M syringe and tell the patient to blow the plunger out. And by doing that, they automatically generate a valsalva maneuver um which is much easier than sort of starting to explain to them that they, they want the feeling of bearing down or pushing out a baby or being constipated or whatever. Um So Valsalva maneuver initially, if that doesn't work, then were you starting to say about no, no something um easier, but you're sort of in the neck area. Yeah, massage. Um So sinus is a baroreceptor if you press on it, um it can slow conduction through the vagal nerve and slow um the conduction through the, the IV node. So it doesn't have any effect on what is happening in the atria. The atria continue on as they are, but um not all of the complexes will get through the IV no to the ventricles. So, the ventricular activation will be much, much slower. And then you can see hopefully what's going on between the success of R waves. What the atrial activity is. So chronic sinus massage. Um Obviously having a listen with the carotids first to make sure there's no bruise. Um and asking the patient have they had a stroke before. Um because you, you don't really want to do it to somebody who, who had a stroke and then if those don't work or, or contraindicated thing you can think about adenosine. Um Has anybody seen adenosine used? I'm sure you haven't for that purpose. That was not by any chance. No, I was just gonna say there was somebody that had it today. Um And on my elective in the summer, I just struggle to say they were clearly that or I couldn't figure out what it was because they couldn't get enough space. So, and do you remember how the patient felt? Yes, because I wrote about it in my, because they always say they said to him and the patient was warn about it. You could physically see like the blood draining from his face like it was and he started to panic even though he'd been told, he, he told it's gonna feel like you're gonna die for like a couple of seconds and you're gonna see yourself flat, but you are gonna come back. But he was like, yeah, and you could see his eye widen it was wild. If you look at the top example and the bottom example. Um So if we look at the top, I've got to come back to what you're saying. Um If we look at the top example, we can see that a pure complex is present, they look regular eyeballing it if we look at the heart rate. Um Well, actually let's do our two squares between um success of airwaves because it's easier than me counting all those number of cure complexes with the mouse. Um two big squaress of the 300 100 and fiftyish so fast heart rate. Um And our curss complex is narrow. Uh So we know it's come from the IV node or higher, higher. Um Can we see any atrial activity present in here? Does anybody want to put their hand up if they can see ap wave? And if anybody in Daisy Hill thinks you see, you give me a wee thumbs up. Ok. What about um can you see any other form of atrial activity? Anybody want to say? Yes. No. Um What about, would you say? You're not sure if you can see atrial activity or not? Yes. I'm getting lots of nos from Craig Daisy Hill. Would you agree that you can't comment if there's atrial activity there or not? Hopefully they're all still this one. Um So this patient, we're not sure what's going on. We wanna slow down the rhythm so that we can see So either they've had their fetal maneuver or their carotid sinus massage or else their adenosine. But let's say they've had adenosine. So they've gone from a heart rate of 100 and 50 here to a heart rate of, there's three seconds, six seconds, two complexes. So a heart rate of 20. So if you go from a heart rate of 100 and 50 to a heart rate and 20 in like a split second, you can see why your patient felt really, really, really rubbish and why you could see the blood draining from their face and they probably dropped their BP a bit. Um I don't usually tell them that they're going to feel like they're gonna die because I think that's a bit scary, but I do say you're gonna feel really, really rubbish, but it's only gonna last for a few seconds. You're gonna feel horrible, but it's honestly, it's not going to stay. Um, so yeah, it's still not very pleasant even if they're expecting it. Um, but it doesn't last a anything that's got a really short half life. So most drugs when we're giving them IV, it's a, it's a gentle push or not even push, just a gentle going over it, you know, like a minute or two adenosine. You have your adenosine drawn up, you have your flush drawn up, you've got a three way tap and it's literally squirt squirt. Um, because you want it in and acting before it wears off again. Um, so at least, even though we know they've gone from a heart rate of 100 and 50 to 20 it's either going to convert to sinus rhythm or it's gonna bounce back up again. It's not going to stay down at 20 because the anything wears off so fast. So now that we've slowed down this, um, ventricular activation, we've got a better idea of seeing what's going on in the atria. So, can anybody see P waves, can anybody see any other form of atrial activity? I'm always getting confused between flutters and, and what else? And whether they, whether that would be a true thing or flu? Yeah, you're right. And I would agree sometimes in the real world it is harder to say they're not as really obvious pushed over humps that they, it's trying to work out. Are they symmetrical or are they not symmetrical? Um, sometimes the rate of the atrial activity, if you're thinking it might be flutter, gives it away a little bit because flutter waves are really, really fast. And if you've got a 2 to 2 to 1 conduction, um, you're gonna have two flutter waves for every CRS, the CS rate is probably gonna be around about 100 and 30 100 and 40. Um, so if the flutter waves, if you're expecting flutter waves don't seem to match in with that, then it may not be flutter. Um, so the flutter wave is always regular. Flutter waves should always be regular. Yeah. Um And you know, if we look here, they definitely look like they've been pushed to the left hand side of the screen or the room. Um, they're not symmetrical, you know, little humps the way P waves would be. Um that's sort of AAA pretty classic saw tooth rhythm that you would get a flutter. Um And if you give adenosine, um it will slow flutter down, it will, it will slowly cure us activation of flutter. So it will make the flutter waves obvious. If you give adenosine in sinus rhythm, it's not gonna do that. It's not going to make you see lots of sinus beats and it probably won't really have any effect if it was a sinus tachy. All right, if you give adenosine and it's actually an underlying SVT which we use to um describe either an AV reentry tachycardia or an AV nodal reentry tachycardia. Um So that's sort of when we talk about S VT, it's very specific for those two types of rhythms. Um Pardon me, if you give it anything for an SVT, then it should convert it. All right, might not convert it on the first dose. So if it doesn't have any effect, then you give a bit more and you give a bit more until you get an effect or you're pretty sure that it is just sinus. OK, happy enough with that and move on to the next slide. So then we want to know about atrial activity and how it's related to the ventricular activity. And as I say, those are some of the things that we're looking out for. So we've got CS complex is present, they're nice and regular PS width. Sorry pr S rate is normal. Um It's about 80 BPM or so. Um CS width is narrow. So we know that it's originated from the IV node or higher up the conduction pathway. Um Can we see any atrial activity? So can we see P waves, flutter waves or any other types like atrial fibrillation? So if you know, what do you think somebody put their money where he is? He is. Yeah. So nice, symmetrical little humps before the PS complex and they're definitely symmetric. Last time they don't look like they've been pulled, pushed over to that left hand side of the screen or the room. Um Is there ap wave for every PR S complex? Yeah. Is there a cure complex following every P wave? Yeah. What about the pr intervals? Does anybody remember what a normal pr interval is? I said? Yes, it is. Do you remember what the normal is? So between three and five small squares and each small square is not 0.4 seconds, so up to 200 would be normal. Um So that is what about 10 small squares roughly? Uh so definitely prolonged as you say. Um is it the same every time? Yeah. So in this example, the sinus node is working perfectly. It fires off the impulse gets down through the Atria. No problem. And then it slowly gets through the A V node, sorry, it gets down to the A V node. And then it's very slowly uh passed through the AV node, which is what's making the pr interval prolonged. But the AV node lets the P wave through every time. It just does it very slowly every time. So that's first degree heart block and first degree heart block is not uncommon. And we see a lot of it in cardiology because we see a lot of patients that have heart disease and previous infarcts. But also we see a lot of patients on antiarrhythmics and beta blockers and that can give us or some of you may well have first-degree heart block overnight when you're in bed, particularly if you're relatively fit. Um when your vagal tone is higher when you're fit or when you're sleeping. Um It's much more common to see first degree heart block, to see sinus brady to see drop beats. Um And it's just part of the vagal response. All right. So we don't get terribly excited about first degree heart block unless the patient has a history of blackouts or you've seen other types of heart block on other EC GS. Um So it said symptom lead or medication lead. So if we look at the top example, again, we've got pure complexes present. Do they look regular? No. Um So we need to get a piece of paper out to see if that RR interval is the same or different to these ones. But certainly that RR interval there is prolonged. Um If we look at her heart rate, there's our six seconds. So 1234567. So the heart rate overall per minute is fine at 70. Um And our curious with um I gotta say it's two small squares to keep it easy because it would complicate things. So what about our P wave or, or sorry, our atrial activity have we got AP wave? We do again, our nice symmetrical little hump. Have we got AP wave before every PR S complex? So hang on, we've definitely got AP wave before all the CS. There's AP SPC spsp SPS. So every CS does have AP wave before it, but every P wave doesn't have a QR S complex after it. OK. So yeah, there are drop beats and then if we look at the pr interval, so if we take this one to start with, so that pr interval is um let's call it 44 small squares just over four small squares. So just coming in upper end of normal. And then if we look at this one, it's um more like five small squares. And this one is I maybe that's actually more than five this one's about seven, this one's maybe eight, this one's longer again, um nine maybe. And then we've got AP wave with no care complex. So pr interval is increasing, increasing, increasing and then you get a dropped beat. So again, the sinus node is working fine because the P waves are grand. It's getting down through the atria. No problem when it gets to the IV node. The first time it gets through the AV node with no bother. But then every subsequent time it takes a little bit longer to get through the AV node until this P wave here gets to the IV node and doesn't get through at all. All right. And this is an example of second degree block. Robert Swan. And I remember as a student learning that Robert Swan was a little bit wonky and therefore the other name for it is back. Um I've remember it that way ever since. Uh so second degree block moment Swan or you back again, we don't get too excited about it unless there are symptoms associated with it. Or again, if we see any higher degree of block. Um, but in itself, it tends to be relatively well tolerated. Um I certainly would be looking at their medication, looking for any underlying cause and removing anything that might be contributing towards it. But if there are no contributing factors and if they weren't giving any symptoms, then we got that you don't get too worried if we look at the bottom example, we've got QS complexes present and the cura complexes um are regular but they're very slow. So again, I'm just gonna sort of take that as being a wee notch and there six seconds, it's not quite six, but it's nearly. So there's 333 complexes and um, that makes the heart rate of 30. So that's low. So, already alarm bells are going off in my head. How's my patient? Are they tolerating this or not? We then look and see um about our QR S width. So 234, so slightly elevated. Um So it could be some sort of block there or it could be um that's originated from ventricle. So now we need to look at the atrial activity. So have we got P waves present or any other form of atrial activity? She said not want to you at all? Yeah. Yeah. Yes, a few. Yeah. Yeah. OK. So nice symmetrical little P have we got ap wave before? Every curious Yeah, we do. Have we cut a CS complex following every pee. No. So there's ap there's nothing P CSP, nothing. That's just a bit of artifact P CSP, nothing P CS, et cetera, et cetera. So this time round again, the sinus node is working fine again, it's getting down through the atria just fine and then it gets to the A V node and the first time it gets to the A V node, no bother gets through. Second time. It gets to the A V node doesn't get through. So you don't get any ventricular contraction and then it resets and it's fine. It goes back to normal again and then the next one doesn't get conducted and it's a bit like the AV node is being a bouncer in a nightclub and it's going, you can get in, you can't, you can get in, you can't, you can get in actually. Do you know what we're getting fill up? Now, none of the rest of these is getting in. So all of a sudden then you go from every other P wave being conducted to no P waves being conducted and P wave P wave P wave, which is basically P wave in because you have no ventricular activation at all and therefore no cardiac output. So second degree block mos two is a much higher risk type of heart block and can deteriorate into either P wave late or if you're lucky, maybe a complete heart block because the, the pacemaker ventricular pacemaker will kick in. So when we see third degree block, we're very much looking to see how is our patient? Have they got symptoms? What are the reversible causes? Do we need to be thinking about a pacemaker even if they're not symptomatic? Do we need to be thinking about a pacemaker? And then this one, so again, we've got cures complexes. They're nice and regular what's her heart rate like? Again, it's really slow. So, again, if we sort of take that as being six seconds to hear. So, excuse me, again, her heart rate is about 30 BPM. Complexes are broad. So, um, what's that? Five small squares? Um, have we got any atrial activity? Yeah. And what sort of a activity have we got? Nice, three symmetrical PIS, is there ap wave immediately before every CS complex? No, there is one over here. But you know that that's very long. That's that P wave hasn't caused that purees complex to happen. And that P wave hasn't caused that cure complex to happen. It just randomly is sitting a bit before it. Um So there's not AP wave before every CS complex and there isn't a cure s complex following every P wave. Our CS complexes are nice and regular. If we look at our P waves, there's ap that's ap buried in there. P wave, that's ap wave buried in there. P wave. That's the P wave buried in there. P wave P wave P wave. So the P waves are nice and regular as well. So the sinus node again is working just grand sinus node sends off the impulse that goes down through the Adrian just fine gets the A V node and nothing happens and nothing happens and nothing happens. And then the ventricle goes oh no, I better do something. And the ventricular pacemaker kicks in because the sinus node isn't our only pacemaker. We've got a pacemaker in the IV node and we've got a pacemaker in the ventricle there as our get rid of the free card as our backup plan. So usually the IV no pacemaker will kick in first because it paces a bit more quickly. So it paces um 40 to 50 BPM. And remember we said that the size of the CS complex helps us to work out where it's been um generated from. So if it's generated, if, if the AV node is giving AV node pacemaker is working because it's situated in the V node, it's gonna give you a narrow complex QR s where this is a broad complex P. So this is originated within the ventricle itself. So this is a ventricular pacemaker kicking in which we also know because it's pacing at 30 to 40 BPM, 30 in this case. So ventricular pacemaker is lower. The A V node pacemaker is a little bit faster. The ventricular pacemaker, the cures complexes are broad, the IV pacemaker, the complexes are narrow. All right. Um So does that make sense? All right. Yeah. Um Going back to what we were talking about just at the start before we sort of set up the zoom bit. Does that is that sort of what you've learned already? Does it help or does it help you um that sort of stuff that we get and, and all Yeah. Yeah. So hopefully that will then make it a little bit easier. Um, ok, all we do there's no clock on the trip, quarter past 4, 15 minutes. Right. Let's get, get moving on quickly. Um, if we do very briefly about Axis, but if it doesn't make sense, we'll maybe not dwell on it too much so we can get a few, a few EC GS at the end. Um, so I think what we're talking about axis, the first thing to say is when we're looking at a 12 lead ECG and you look at the QS complexes, you can see some QS complexes are what we would say, predominantly positive. So they've got a big R wave and a very small um S wave and Q wave. So more like this sort of a picture or they can be predominantly negative where you've got either TQ or S wave and a very small air wave or there can be kind of somewhere in the middle of it biphasic. And when we think about our electrodes um on our body, when we're doing an E CG, um we're thinking when we do a cardiac axis, um just like a I Daisy Hill. Can you see? Let me see if I stand somewhere, I don't know where the camera is or is the camera off now because I've got the powerpoint on. That's what it is, isn't it? OK. Might not work unless I go out of the thing, but I'm not gonna bother doing that. Um If you imagine that your heart sits in your chest more in the vertical plane than the horizontal plane. So most of the wave of depolarization is gonna go down towards your feet rather than out towards the room. Um And when we've got our leads put on, we've got all our electrodes and we've got four on the limb leads. So they're gonna be the ones we use for access primarily. Um But when we look at our 12 lead ecg, we've got six limb lead electrode or 66 limb leads. So our four electrodes give us six leads on the ECG. Um And that is because some of the electrodes are bipolar and some are unipolar. So they get information from different ways and the way I think of it is really, really basic because I haven't done physiology or physics for a very long time. Um So basically our wrist electrodes on our left wrist and our right wrist, they pick up any information the, the bipolar bit picks up any information going between those two electrodes. So if we stand like this man is standing with our arms up in the air, any any information, any wave of depolarization that's going in, that horizontal plane will be picked up by lead one, any information that's going in the plane between our left wrist and our feet will be lead three. So we can plot the sonograph So there's lead one, there's lead three and then any information going from our right wrist to our feet will go in this direction, which is lead to you. But then our limb leads electrodes are also unipolar. And the way I think of that is they're picking up any information going from the heart out to the electrode. So our right wrist electrode will pick any information going out towards our right wrist. And we can plot that on our graph as well. Our left limb electrode will pick up any of the information going from the heart to the left wrist over here. VL. And then aVF will pick up any information going from the heart down to the feet in that vertical plane. So down here and we do have 2 ft electrodes, we've got one on each ankle, but one of them's on earth. So that's why you only get six instead of more than six. Now, I think the best way to think about axis is actually work through some examples. So just remember some of her TS complexes are prominently negative, which means that they're going away from that lead. Some are predominantly positive, which means they're going towards that lead and some of them are neither positive nor negative, which means that they're going at right angles to that particular lead. OK. So if we look at the ECG and we're looking just at the limb leads, not the chest leads is lead one positive or negative, positive. Yeah, lead, two positive lead, three positive AVR negative aVL. Yeah, neither by face, neither positive nor negative. So we're in the middle because it's sort of half and half and then aVF positive. So what we want to do is think about where our biphasic lead is and that's usually the smallest um complex also. What are the limb leads generally? So that's VL. So we know our overall wave of depolarization is going at 90 degrees to VL. So it's either going to go up, we don't have an electrode exactly at minus 120. So we look at AVR as being our closest representation of that. So it's either gonna go towards VR or else towards lead two. So if we look on our ECG and AVR and lead 21 of them should be positive, one should be negative and it's a positive one that the electrode that the wave of depolarization is going towards. So our positive one is lead two. So overall, overall wave of depolarization is going towards lead two, which is normal, our normal axis lies between minus 30 plus 90. And um and that makes sense if we think about the way the heart sits in the chest, if you sort of hold your fist where your sternum is um in Daisy Hill. And I imagine that's your heart. Um The overall wave of depolarization is going from the right bit of your wrist down to your knuckle of your index finger. Um So that's basically down towards the feet. So that's normal if we look at this example. So lead one. Is it positive or negative? All positive lead? Oops lead two by Facebook lead three, negative lead. Oh Sorry AVR negative aVL positive aVF. Yeah, it's predominantly negative. I know there is a we R wave there but it's still more negative than positive. OK. So our biphasic lead this time is lead two. So if we look at right angle to lead two, it's either gonna be aVL or minus 150 which we don't have a uh a lead at. So lead three is our closest approximation. So A VL and E three, one's gonna be positive, one's gonna be negative and VL is our positive one. So now we can see that the overall wave of depolarization has swung around and is heading up towards the left shoulder. Um So that's left axis deviation. Why is that important? Well, because it can give you a clue to some underlying conditions that might give you the left axis deviation. And depending on how the patient presents. If they present sort of acutely unwell, it might push you down a particular diagnosis or certainly give you an idea of what options you might want to organize. Yeah, you're gonna shout out uh and see that how, well see on the last slide. Yeah. Um When you're like lead three and 90 degrees to lead two. I was on until I got to this one. OK. So which is a bit that is, you know, to look at the lead three. So ideally you'd be looking at minus one or sorry, plus 150. Yeah, but we don't have a lead at plus 150. So we have to go with the closest one, the one that's nearest. So it is an approximation. It's not an exact science, but that's sort of where we get that lead that we look at. That makes sense. That's why it's always better just to shout out rather than go back to it. Um So left eye deviation you might be thinking about maybe if they're presented with acute chest pain. Have they had an inferior M I um have they got a history of aortic stenosis or hypertension for some reason that might have left bundle branch block cause left bumble branch block can give you lad as can LVH, I don't know why I got inferior down twice. I must remember to just to leave that bit. WPW. Um Hopefully you guys know what it stands for surgery or have you come across? Yeah. Yeah. OK. You maybe don't know an awful lot about it at the minute, but hopefully that will change when you're on cardiology for two weeks. Although it may not two weeks isn't very long. See, it may not see it on the word. Um OK. So if we do another example. So again, lead one positive or negative, negative lead two positive lead three positive r more negative than positive. But it's a really small uh uh complex. This one's definitely negative, this one's definitely positive. So I think this is going to be our closest approximation to the biophysically, it's not exactly biphasic but it's the smallest complex. So therefore, it's so it could be the closest approximation. So VR is our biphasic, we're taking it. So then we're looking at 90 degrees to AVR. So again, it should be minus 60 would be closer, but we don't have an electrode there. So minus 30 is our, our closest one and then lead three is our other one. So if you look at aVL and lead three, one's going to be positive and one's going to be negative and the positive one is lead three. So this time, it means the whole wave of depolarization has swung around to the, the right side of the heart, um such right axis deviation. And again, why it's that important because it can reflect the underlying condition. Now, it might be a chronic condition, it might not be ac condition and that goes for a left, left axis deviation as well. Um But certainly one of the classical ones would be the patient that presents with sudden onset pruritic chest, severe pruritic chest pain and shortness of breath comes in hypoxic maybe has had surgery recently. And um, when you see right axis, deviation on the ECG with that history, it's P and T profen otherwise. Yeah, I know this might be safe but it's going to be the most negative or the most positive the way that the uh to polarizing. So why can't you just look at these once a day? So you can, so that's the other way of doing it. So, um you can just sort of look at that bit and, and give an approximation that way, this way is probably slightly more accurate because it's taken in more of the leads. But a lot of people do just look at leads 12 and three. and I'll be honest, I always have to work it out from first principles because I, I tend to do it this way and then I can't remember without thinking about it what it should look like because I do it from first principles every time I know when right deviation, they tend to lead one, only three point towards each other. Well, that way, that way. And then, you know, which is, uh, you know, like it's most uh whatever, II don't actually know, know which one, but it would be that one or if it's going all right, you could just be that later and then you just, yes, you can, uh you can sort of work it out and that, but you still have to have an understanding of how it all work to kind of get that much, which is why I, I'd say I tend to do it this way just when I'm teaching because it gives you a bit of an overview. Um But I always say to people if it doesn't make sense, go and read it up in one of the ECG textbooks, like ECG made easy or something like that. Um And if the first principle's wife still doesn't make sense, you can just learn off where your needs need to be and just memorize it. Um I don't think I understood that cause nobody explained it to me as a student. And I think I was in sho before I really understood. And that was because back in the days when the drug reps gave you freebies, I got this um little ruler that was uh paper fastened together and it had that um graph. So it actually managed to learn where everything was and it had a narrow so picture by lead and got your arrow to line up and then it told you what need to look at and it was like bingo. This makes sense now. And then it made sense from that point on. I think just that they explained it well to me because act teaching was rubbish for her undergrad. Um Anyway, so hopefully that makes sense to say if it doesn't, don't panic, go and read it up in the textbook and if it still doesn't make sense, just learn off the rote learning bit. Right. Let's read through some EC GS, um, oh, bundle branch block. Are you happy about that? We'll talk about branch block. Hopefully another time whenever I've got you individual or come to me and I'll go through it another time. Um, that's probably relevant for Axis. Ok. Let's just work through. I'm not gonna go through first principles. That's what I didn't say at the start. Actually, when you're looking through ecgs a bit like doing x-rays, you should have a um format for going through so that you go through the same thing every time and don't miss things. I'm not doing that at the minute because I'm conscious. We don't have very much time left. Um So we are going to look for the glaring abnormality, which is not a good way to do it because sometimes you can miss a subtle things then. Um But thinking about ST segment changes, can anybody pick out the glaring abnormality in this E CG? Can we see any ST elevation? Yeah, chest leads V one to V four. Yeah. So ST elevation is measured from the isoelectric line. So where the pr interval is essentially and we wanna know how many millimeters it is above the isoelectric line. So the isoelectric line is there. My ECG is so crap. I can't tell you how many small squares it is, but it's quite a few. Um There's your isoelectric line there. I mean that's gonna be uh 789, 10 milli nine millimeters. Anyway. Um, this is even more because there's, is iso electric line down there and we've got our ST segment away up here. This is what we call. Tombstone. ECG. Tombstone changes. Um, I think sometimes when there's as much ST elevation as that, it nearly looks a bit bizarre and you're sort of going, where's the ST segment and all of that? It's just a bit weird looking. Um But this is the ST segment up here in here. So I got ST elevation V four V one through to V four. Is there ST elevation anywhere else on the ECG not trying to push you into any particular answer at all? Yeah. So again, there's your p interval there and if we continue it all up a little bit and do you know about um territories of, of uh what am I trying to say where the electrodes are sort of reflect different territories of the heart? So, um our chest leads, look at the anterior surface of the heart um through the septum through the lateral lateral anterior surface of the heart. Um One and aVL look at the high lateral side of the heart. So it is still lateral but it's not as low down as these leads. And then 23 and aVF if you think about where they sat on our graph for axis there, looking at the bottom surface, the inferior surface of the heart. So if you saw ST elevation in one, I'm sorry, in IVL, I would be looking at one automatically because it's the lead that kind of goes with that, looking at that high lateral part. So we do have ST elevation in the high lateral surface. We actually don't have an ST elevation in these lateral leads, but that's obviously just whichever bit of the coronary arteries affect. So it's not affecting the no lateral. What about ST depression? Do we have any? Can you read this way straight? Yeah. Anywhere else? Yeah. And what goes with sleep three and IVF two. And so there's a isoelectric line up there and then you've got a couple of millimeters of ST depression a bit more in need three and not really quite as much an IVF but still a few millimeters. So we've got an anterolateral M I with that, sorry, an anterolateral stemi ST elevation MRI. Um And then we've got inferior ischemia. So that's known as a reciprocal change. So you're probably aware of that. Well, I don't know if you guys are aware of that. Um So when you've got ST depression and elevation on the same ecg, it just reinforces the fact that this is an acute mi um you see the depression on the opposite side of the heart to where the infarct is and it's just reflecting ischemia and the rest of the heart. Um So it just makes you think, yes, this is likely to be a very recent occurrence and probably is still within the threshold of. Ok. Um, again, we're going for the glaring abnormalities. So we're looking at our ST changes again and can we see any ST elevation anywhere? Yeah, of course. Yeah. Yeah. Uh Inferior M I, so there's your isoelectric line down there. You can see her squares more easily this time. So it's probably almost 43 anyway. Um, sorry, excuse me, almost four and three and four F or sorry, nearly five there. So, an inferior stomach. Now, if we look at the chest leads, well, let's look at the rest of the limb leads, first of all. So we've got inferior stemi and we've got ST depression and one in VL. So that's a reciprocal change in the high lateral leads. When we then look at our chest leads. We've got a V four R or I would call it an R four, an R four V. No, what do I call it the right side of P four anyway, or V four. So inferior mis which coronary artery is most likely to be the culprit? Right. Right coronary artery. Yeah. And what else is the right coronary artery most likely? Um uh perfuse. Yeah, even sort of a bigger, bigger part of the heart. What would you sort of call? So it's the inferior part of the left ventricle and then the, the right ventricle is really what I'm trying to get out would be the other big thing that it, um, supplies. So, but also the node conduction system disease as well. But that's not what on, on this. But, um, so we don't, we can't look at our right ventricle very well with our standard ECG. It just doesn't look at the, you know, because it sort of sits in behind the left ventricle. Our leads don't look at that. But if we take our chest V four lead and put it on the opposite side of the chest onto the right side of the chest. So literally a mirror image, then that's an RV four lead or four our lead. Um And if you see ST elevation in the right sided V four lead in the early stages of an inf far. So it has to be in the early stages. You can't, you can't go back and look for it the next day or anything. Um That suggests that the right ventricle is involved as well as the inferior part of the left ventricle. Why is that important? Because some of the complications that you may get could be treated slightly differently if the right ventricle is involved. Um I will not go into the detail of that at the minute, but just be aware of that. So it's better to know about it. Um And then, as you mentioned, you mentioned, I can't remember now, um you often get conduction system problems with an inferior infarct as well. Um So you can quite often get heart blocks and things in the very early stages which then settle down as the heart is really perfused again. All right. So having a heart block in the early stages of an inferior MRI doesn't automatically need the pa a automatically need the pace patient on the permanent pacemaker. And, all right, OK. Complexes are present through the like regular or irregular, irregular. So if we took our page and marked it out, we can say it's irregularly irregular. Um Our CS rate is normal and our CS width is normal. Um What about atrial activity? Can we see any P waves, flutter waves or fibrillation waves? So, maybe flutter, any other fibrillation, maybe. So, we certainly can't see any P waves. Um And there are the odd bump that looks like, you know, could that be flutter, but it is only the odd bump and I would say if it was definite fluttering, you would be getting lots of consecutive ones. So I think it probably is just a bit of an artifact coming in rather than a flutter wave. I think it's probably more likely to be just fibrillation. Um Sometimes I think it can be difficult to see fibrillation waves. And if you put your hands over the C complexes, um I can't do it sort of on without having the paper really. And I can't do it for Daisy Hill. So I'm really sorry. But if we cover up the ces complexes with your hands, sort of above and below the isoelectric line, you're hiding the cures and you can see better what's happening in that isoelectric line. Um And it, it makes you realize that the fibrillation is completely chaotic, wobbly, there's no pattern to it. Um So this is atrial fibrillation and there is a clue up here because it says pre DCC. So this person's come in for a planned elective cardioversion for their af and this was what they had before they had the shock. Hopefully it was back in sinus afterwards. Um Leave that one. No, we put that. So again, complexes are present, they're irregular, they're narrow. The heart rate looks all right. Um What about the atrial activity in this one? So flutter is so, yeah, a bit more sort of convincing there. So nice consecutive bumps all look like they've been pushed over to that left hand side of the room. Um So that's the atrial flutter. Ok. Uh Cur complexes are present, they're regular. Uh The heart rate is fast. It's what about I wanna do big about 200 BPM, roughly something like that fast. Let's go fast. Um Save me counting out. I can actually see where our three seconds is on this ECG, but it should be marked and, and normally, oh, there's 11 there and yeah, I'm not sure where the other one is there. Maybe. So. It's a and the Curis complex is it narrow or broad? Is it less than three small squares or more than three small squares? It's really hard to see square, but it looks, does it look normal or not normal? Hard to say. So if that, if I tell you, it's pure, as complex measures two small squares? No. OK. So that's a narrow complex, a regular narrow, complex tachycardia at the minute, we don't know what the underlying rhythm is because we need to find out about our atrial activity. So, can we see any P waves, flutter waves or fibrillation waves in this? No, uh not all of the above. So we're not sure if there's atrial activity or not. Basically. Yeah, fair enough. Um Sometimes when I've shown that ecg to people, uh they have said, oh, but is this not AP wave? And what I would normally say to people is when the heart rate's fast like that, if you're only seeing one bump between two success of CS complex, it's probably at wave rather than pain. So if you can't be sure that there's ap wave as well as at, you can't really comment on the pee. That makes sense. OK. Um So it's a narrow complex tachycardia. We're not sure if there's atrial activity there or not. What could we do next? Check our patient, first of all, because if they are unconscious with a BP of 60 we're gonna cardiovert them. Um But if they're conscious and talking to us and they might have a bit of palpitation, but doing fairly well then, yes, we'll try our valsalva maneuver. If that doesn't work, we could try a fence massage. And if that doesn't work, we could try our dent providing it's not contraindicated. Um And that's actually an S PT. So that's one of our reentry tachycardias. Um So if we give adenosine to that, it would likely just switch over into the sinus rhythm again. All right. OK. Cures complexes are present. They're regular. The heart rate looks OK. Um The cures complex measures four small squares. So do we think it is narrower, broad, broad. So we know that either there's a bundle branch block there or else that complex is originated from within the ventricle. Um Can we see any atrial activity present? And if so, what is it? Yeah, little P wave can't say it well, in all the leads. But if we look in V two, probably V one and V three, we can see it. So there's ap wave there and the pr interval looks, um it's really hard to know how many small squares but probably about four. So on the face of it, it looks like the pr interval is OK. But the complex is wide. So normally I'd be thinking is that a bundle branch block fault. If we look very carefully at the start of the cures complex, there's a little line, just a vertical line, you can see it best in probably V two, V three and V four. Anybody know what that we line is or represents. Yeah, like a spike. So um somebody's got a pacemaker in pacemaker leads in the ventricle. It's causing the contraction of the ventricle. So it gives an impulse and then that impulse spreads through the ventricle in an abnormal fashion because it's come from an abnormal pa pa pa pacing lead rather than the node. Um So if that pacemaker was switched off, that patient may very well may well have either PW vys or complete heart block. Um because the A are working, the sinus node is working. OK. Um It's just something to do with the way it's getting through the A V node is the issue, which is why they've needed a pacemaker. OK. Complexes are present, they're regular, they're fast and the heart rate again is very fast. 200 ish. Um Our Q ri width is four or five small squares. So it's broad. So either it's a bundle branch block or it's originated from PTP T. Yeah. So you know that even without starting to look for atrial activity, but when we start to look for a atrial activity, can we see any, can we see any P waves, any flutter waves, any fibrillation waves, the office like might be a wee one in there. Um maybe there, but you're not seeing it obviously clearly. And that fits if it's ventricular tachycardia, the P wave is doing its own thing. The, the sinus node is usually working. Um so it generates the impulse you get the P wave. But because the VT is the predominant rhythm and the VT is so fast and so big, the P wave gets lost in it. Sometimes you can see um AP wave that manages to get through the AV node. Whenever the ventricle has been, it's just in the process of being repolarise and it's ready to accept an impulse. So in the middle of the VT, you might see a normally conducted impulse which then deteriorates back into VT again in the next one. So it's a captured beat. Uh or you may see um what looks like AP wave and then a funny looking complex that doesn't really look the same as the rest of the, the rest of the BT complexes and that's a fusion beat where it's like half being conducted down the normal pathway, but the VT is happening at the same time. So you get the amalgamation of, of both. Um So if you happen to see any of those fusion beats or captured beats, it just makes you sure that you got the diagnosis, right? But any broad complex tachycardia, you have to assume it's BT until proven otherwise. Unless you're absolutely sure it's sinus rhythm with bundle branch block or atrial flutter with bundle branch block. You don't want to miss ABT. So you're better assuming it's BT and treating it as such than missing it. And that's why I've got the person doing CPR down below because obviously BT may have no pulse. Um, ok. But equally it could be my mom in the pre op assessment clinic that had no symptoms at all, you know. Ok, I'm sure that must be about half past, um, as always nearly quarter to five, sorry for keeping so late.