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Thank you. Right. So high there everyone. Um My name is Hannah. Um Doctor Beth. Oh, I'm one of the medical registrars working at King's College Hospital in London. Um I actually graduated in 2018 from Oxford. So quite a while ago, I'm not a cardiologist. I'm a general medical registrar, but um I get to see quite a lot of E C G S during my shifts. Um, and I've had quite a lot of exams on E C G S. So we thought would be nice today to go through a systematic approach in how to read an E C G. I'm aware that there's a range of levels on the call. So please, at any point, if you want to ask me a question or interrupt me, um, please, please do. This is meant to be as interactive as possible. Um Hannah will be looking other, Hannah will be looking at the chat. So if you want to type something in there, but I will um if you just a mute yourself, then you can feel free to ask any questions as we go. Okay? Can everyone see the slides? I'm assuming you can. Okay. So, the aims of this talk. So we're going to touch briefly on how we record E C G s and the basic pathophysiology behind them. And then we're going to go through a 10 point system for how to read EKGs so that you don't miss anything exam in exams or more importantly, in clinical practice. And then we're going to go through some cases and during those cases, well, hopefully touch on some common scg abnormalities that do creep into exams, but also real life. So hopefully be relevant to exams for you and also clinical practice. Okay. So we're going to start by looking at the basics of an E C G and how it's recorded and the basic physiology. So a 12 lead ECG is quite misleading because as you know, there's 10 electrodes put on the body. So six electrodes are on the chest and four are on the limbs. Um and you can see the V one to V six across the chest and the fore limb leads up, make up the other six readings we see on our 12 lead E C G. So when electrical activity or deep polarization travels towards a lead, it creates a positive deflection. So as you can see if the things are moving down the heart, you can see that the positive deflection you'll see in vi too is because there's deep polarization traveling from the atria to the ventricles where as as it's traveling in the opposite way to VR you'll see a negative deflection there. Okay. So this is really important and when you see it traveling at 90 degrees to the access of the electrical activity, it will appear almost isometric. And this is particularly noticeable. I think in V four where you can see the upstrokes of the positive deflection and the negative deflection are almost almost equal in size. And the reason this is important is because due to the relative predictable nature of the coronary artery anatomy, which vessel is affected by a ski me A can be commonly predicted. So here we have a 12 lead ecg in front of us and we can divide intersections depending on which territory of the heart is affected. Everyone has a different system, but I'll tell you mine. So I think of leads two and three and A V S F as inferior. And that's because they're at the bottom. There are the inferior aspect of this E C G. The left bottom corner, I think of lateral leads as the peripheral leads. So lied one is to the left aspect and V five and V six to the other aspects. Okay. And then the septal and anterior leads you can see are just completely within the middle of the E C G, which is helpful. Sorry, I've got a Microsoft teams MDM going at the same time. So I need to mute them. Thank you. Okay. Sorry about that. And then as I said this is really important because when we think about the coronary artery anatomy, we can then think about which leads are affected, meaning which territory and then working out which vessel might be blocked, say in a stemi or an end stemi. So in most people, um if you're looking at the lateral aspects of the heart, so leads one and then these A V L L for lateral, I remember and V five and V six, it's the left circumflex. And in some people, it's the diagonal branch of the L A D. But in a lot of people, it's the left circumflex. The anterior septal is easy because it is the completely the left anterior descending. But then the inferior again, has some slight anatomical variation between people. So in 70% of people, the heart is right dominant. And so you see the right circumflex supplying these this inferior territory of the heart. But in 10% of people there left dominant and it's the left circumflex for 20% of other people. It's a combination of the two. Okay. I hope that makes sense. I'm sure you're probably all aware of it already. So then to look at the E C G, as I said, the E C G is just a way of seeing electrical activity and deep polarization in the heart. So if we break it down, we assume most E C G s are running at 25 millimeters per second and this is really helpful because you can think one large square is not 10.2 seconds and a small square is not point not four seconds. So if we're looking at the way form and what it represents at each point in the heart, and then I've got a nice little video to show you because it's better to see this kind of in an animation really. So the P wave is deep polarization of the atria and therefore atrial contraction. And then the PR interval is the time taken for that electrical activity to get to the signer H your node, then the Q R F and down the bundle of hiss. And then the QRS is where you see ventricle contraction and deep polarization. And then the T wave is where you see re polarization of the ventricles. So the ventricles in um Estili, it's important to think that somewhere within the QRS, you probably will get the P the, the atria re polarization. But because it's quite small, it gets lost in the, in the QRS complex of the ventricle because the ventricles are much bigger than the atria. Now, hopefully, I'm going to be able to show you this youtube video which just shows you kind of in a nice animation, the movement of electrical activity. It's quite hard to explain. So I thought a video might need to move on and now you're going to get a nice and uh someone else I'd like the extra cash. Yeah, this is a cardiac rhythm strip. It represents electricity, traveling through the heart and repetitive cardiac cycles. You can't see it, you can't see it. This is one cardiac cycle. Uh Okay. Thank you. I'm sorry, I could see it but I think maybe my only my sec my slides are share ing not my full screen. Thank you. Um That's fine. I'll um send I'll put the link in the chat so that you can watch it another time. But thank you for that. Ok, we'll move on. Um So this is the 10 step approach to reading the E C G. Has, is everyone familiar with this? Has everyone seen this before? Anyone just meet someone? Pardon? Yes, I have seen this before. Thank you. Brilliant. Okay. Um Is there is everyone if, if anyone's not seen this, can you say just trying to get a scheme of? No, I haven't seen. Okay. Fine. Um So I know that there's a variety of different levels on the court. So we'll just go through and it's really helpful. Um No matter what stage you are, I use this um to make sure I'm not missing anything. So it's 1 to 10 steps to make sure you're not missing anything on your E C G. Okay. So firstly, the patient details. So this is quite important when you're thinking of where is the patient? So are they in the emergency department or in an acute medical setting? Um or are they in their G P practice? Because it can sometimes to tell you how sick the patient is and particularly if they're in a particular area of your hospital and you get shown an E C G, it might be that you need to move them to somewhere with more high dependency. And it's really important that we have that documentation of that E C G belongs to that patient. So knowing the patient details is the first point. Okay, then the next time the next step is situation details. And to me, this really goes down to two things in terms of time and then clinical status of the patient. So when is the E C G done? It's really important to look at timings of E C G S. Can anyone think of a reason why timing of an E C G is important just to meet us up if there is any uh identify? Yeah, exactly. So how long has it been going for? And particularly in patient's with chest pain or you're considering if there's dynamic changes, often what we'll ask for is dynamic changes. So cereal ccgs and these can be E C G S taken over several. Um Typically we will do them every 10 minutes, but you could do them over longer, longer periods with the troponin say and see if there is a dynamic change. So it's really important to see if when that change has happened and that's why the timing is very important. The clinical status of the patient is very important. So how they look what their observations are doing. If you've got someone in a S V T sinus ventricular tacky, it's probably likely that observations are very deranged. And it's important when you're correlating that with your E C G. And also thinking, are they having any chest pain at the time? Other things that you can sometimes think about is their medical records and thinking about looking at their potassium levels, it might be helpful to see what their potassium levels are doing. If you're thinking of looking at the E C G for hyperkalemia, which will go into later. But the and also what drugs they're on because that obviously, we know that drugs can affect the electrical activity of the heart. So it's really important knowing the situation and that boils down to the timing and then the patient and then we look at the rate. Um So there are different ways of doing this. I've suggested two ways here which I use. Um counting the number of QRS is on one line. Um So I always use the bottom road, the lead to and you know that that bottom lead of the E C G is over a 12th period. So if you multiply the number of Q R S S you see in that period by six, you will get the rate, the number of BPM this is quite useful, especially when there's an irregular rhythm seen. Because obviously, if you're looking between the QRS complex is, it depends which bit you use of the E C G will determine which rate you get. So the second way is if you look between the QRS complex is so counting the number of large squares between our waves and divide 300 by that number and you'll get the rate. But again, I caution you about that. If there's an irregular rhythm this way won't be very accurate because it depends which, which QRS complex is you're using. So I think the best one is the top one for me. And then assessing is it regular or irregular? And if it's irregular, is it irregularly irregular? Um and this can be sometimes quite challenging, especially when you've got someone's heart rate going very fast or slow. And so I use the paper test. Does anyone used this before in practice? Yeah. So, so this is, so here's my fruit animation. So you get a piece of paper mark on where each QRS complex is and then you can move the piece of paper along your E C G, making sure that it's always lining up. And that's a really crude way, but quite useful. Actually, when you're not sure to make sure that the QRS is are all the same distance apart, okay. And then assessing the axis. So we have to think of the access with some of the electrical activity of the heart, as you know, the um, electrical activity and contraction will go from the a tree it to the ventricles. And because the left ventricle is more muscular than the right ventricle is often normal to have a slight left axis. Um uh the normal axis of the heart will lie to the left. But then we talk about left axis deviation, which means it's even more to the left and right access deviation. And the leads were looking at really are leads one. So you can see what is my uh sorry, leads one. And aVF um So although I've said aVF, typically you can use. So my schematic, I'll just try and go back, sorry. So you can see on here, you typically, so aVF and lead one are the ones we're looking at for. But you can use lead to as quite a crude marker of aVF because you can see they're quite similar to each other. And what you're looking at is this is what I use. So if you're looking at your E C G and lead one and lead to are both positive deflections. So the majority of the QRS is positive, you can say this is a normal axis deviation. If you see leave one and lead to separating, then you can say they are leaving. So leaving L for left. So that's how I remember that. And one and two, if they are, if one is very, very negative and two is very, very positive. You can see the arrows are returning or coming together. And that is how you remember right axis deviation. So that's what I would look for if I'm looking for access deviation leads one and two. Okay. And there's lots of different causes for left and right access deviation. Sometimes it can be completely normal. Um So when the abdomen is distended, um it says ascites or pregnancy there, but particularly cause the diaphragm, pressure's up and rotates the heart. Um in left ventricular hypertrophy where you have thickening of the heart muscle and in other conditions like hypokalemia, you can actually see an access deviation on the left, right axis deviation. It's very important. So when you see those two sides returning, that can sometimes be a normal variant in young Children or young adults who are very thin. Again, you can see it when the right side of the heart is thick and so right ventricular hypertrophy or if there's right strain on the heart and things that cause right strain on the heart of problems with the lungs that causing pressure. So particularly things like P E S. So pulmonary embolism. Okay. Am I talking too fast? Is everyone okay? Feel free to stop me at any point? It's fine. Thank you. Ok, great. Um So now we're looking at P waves. So the first question is, can you see them if you can't see them? It's suggested that this could be h your fibrillation or atrial flutter or even a reentrant junctional tachycardia. So it's really important. Can you see them the first question? Then are they associated with QRS? If your P waves are not linked with your QRS, then it means your atria and your ventricles aren't contracting in sync. And this is what we call complete heart block. And then you look at the P wave morphology. Um So typically P wave is 2.5 millimeters high in the limb leads. So that's the leads on the left side of the E C G and 1.5 millimeters high in leeds V one to V six. Any deviation of this means it's slightly abnormal. So looking to the diagram on the left, this is a bifida P wave and this is called by left atria hypertrophy. So we've talked a bit about hyper left and right ventricle hypertrophy, but the P wave is really good to look for atrial hypertrophy. And if you imagine the squares are the deep polarization, electrical activity. When the left atria is bigger, the deep polarization lasts for longer. And what you get is a slightly longer broader P wave with a little bump in it. And this is called a bifida P wave. And it's a sign that your left atria is more hypertrophied and things that cause that can be things that cause difficulty for the left atria to pump blood out. So things um like a mitral stenosis um could cause this. And then similarly, this is an abnormal P wave that peaked. So it's much higher than we would normally see. And this is in right Atria hypertrophy. And again, if you take that the red triangle was the atria um deep polarization that becomes broader and therefore, it overlaps the left atria. So you get this cumulative effect of atria and right and left atria depolarizing the same time effectively, they're making it a bigger P wave. And this is seen in right atria hypertrophy. And this again caused by things like tricuspid stenosis. So the um right Atria is trying to go against that or things that cause right um pressure on the right heart. So problems with the lungs again. So things like hormonally hypertension and then finally, you look at the pr interval. So normally this is 3 to 5 small squares any longer than this. And we start to think that there might be heart block and this is problems with the conduction system. Okay. So when I'm thinking of heart block, I like to think is it a constant interval or is it a variable interval? So if we go down the left side of the algorithm, so if it's a constant pr interval and it's always that you always get a Q R S after it, you know, this is first degree heart block. Does anyone know any common causes of first degree heart block? So sometimes um there can be any kind of electrical activity or, but ischemia can definitely cause heart blocks. So I would always think any heart block. I'm worried that there's been some kind of a ski mia affecting conduction systems, then the second degree heart block. So again, the pr interval is constant. But the difference in this one is that after every P wave, you don't always see a Q R S. So you see there's a P wave know Q R S P wave Q R S P wave, no cure S P wave QRS. But this is regular and this is a second degree heart block type two. And this is a bit different to a second degree heart block type one where the pr interval is um irregular. So with each P wave, there's a bit of a longer gap before the next QR and it gets longer and longer until eventually you see it doesn't conduct. So it gets longer, longer, longer. And then there's no QRS. After that P wave and third degree heart block again, there's a variable pr interval because as we said before, there's absolutely no communication between the atria and ventricles, they're doing completely their own thing. So the eight you can see here, the atria is firing here here. But also this is a bit of a atrial um P wave in the middle of the QRS complex. And third degree heart block is an emergency and needs pacing, either a permanent pacemaker maker or temporary pacing um by pacing wire. So it's important to be able to recognize. So seven, we're looking at the Q wave is normal when you see it in V five B 61 and aVL, but it's only normal if it's once more square long and two millimeters deep any bigger than this is an abnormal Q wave. And a Q wave basically suggests that there's been previous myocardial infarction. So always remember to look for pathological Q waves because that might be someone who's had a previous M I and then looking at the QRS complex. So if it's greater than three small squares, it's broad and it's, that's really important to know. And that suggests that there's a problem with conduction down your bundle branch. And that's why we get left and right bundle branch block when you see a wide QRS and we'll go into that in a second and then looking at the shape and the height of it. Um So, is it particularly um tall? And this is particularly important when you're thinking about left ventricular hypertrophy? So, in left ventricular hypertrophy, you will see a really tall are wave in V six and a very deep S wave in V one. And if you add up big squares of this one in V one and V six and then more than six, and then you can say this person has left ventricular hypertrophy, it's greater than 35 millimeters. But I think it's easier to work in squares when you're seeing these in front of you. Um Has anyone heard of William Marrow? This is something we get taught in English medical school. I'm just wondering and read the um the breathing. Pardon? Sorry, w sending information on the Yeah. So it's helpful to look at William. Uh Sorry, your microphone I can't hear is uh left bundle, bro, bundle branch block and right bundle are, are, is that right? So they, you've been taught this? Uh No, not, not here. I had a friend who was studying in India. Yeah, he don't. Brilliant. I just think it's an easy way for people when looking at SCG to see if it's left or right bundle. So you've got to think is it a broad QRS? So is it more than three small squares? And if it is, does it show characteristics of left or right bundle? And we'll get talked about this person's name, William Marrow. Don't think it's ever actually someone's name, but it's an important pneumonic to remember what to look for in the leads. So this is a left bundle branch block. So you remember it as William and William has two L's in the middle and you look at V one and V six as leads to compare. Okay. And in V one, can I convince you that that looks like a W and what you're seeing is a very negative? Are wave okay with an S wave following this. So it looks like a basically dominant S wave. So it's negatively down. So it looks like William. And then in V six, you're seeing this broad notched are wave okay. And that looks like an M. So it's a positive deflection and it's notched upwards. And that's how when you're looking at it, does it look like a W, does it look like an M, the things you're really looking for are a big negative S wave in V one and a broad notched are Wavin V six. Um And does anyone know why it's particularly important to look for left bundle branch block, contraction of the left ventricle? Yeah. So it's really important thinking about if there is, if there's too much, if there's a scheme ear affecting the left bundle, because you think your left ventricle is more dominant, then it might suggest that actually this person has had a myocardial infarction. And when you see a left bundle branch block, you can't necessarily interpret the ST segment. And the ST segment is what will come onto is really important in diagnosing a stemi. But if someone doesn't have, if someone has a new left bundle, you can't interpret that ST area. So you, you see they've got a new left, the new and as an M I. Exactly. Exactly that. Yeah. Thank you, Jasmine. So a new left bundle, you treat as an MRI and you get on the phone to cardiology. Exactly. That's why it's particularly important to be aware of these. Um There are other causes of, of left bundle branch other than other than M I, things like aortic stenosis and hypokalemia can, as I said, make your QRS broader and look a bit like this. But that's the most important thing to think about. And then you can see this bottom schematic is the marrow. So right bundle branch block and what you're looking for is this our s our pattern inlayed V one. So it looks like an M. So you see, you get an R wave goes down and then you get another are wave and it's a positive deflection and it looks a bit like an M, I'm sure you guys will be sent these slides, but this is where I got, I'll put the reference is at the end. But life in the Fast Lane has really nice examples. Um V six, you're looking for a broad S wave and I know this doesn't look exactly like a W but you have to take my word for it that this is a broader S wave and it's a bit notched and it looks a bit like a W. And if you're seeing a, the main thing to think about is, is there a broad QRS? And what does it look like? Does it look a bit more like this or does it look a bit like this? And this will help you differentiate between your right and your left one's a French block. Is that, does that make sense to everyone? Yep. Thank you. That's all right. Um So again, you can see this in right ventricular high, you can see this in right ventricular hypertrophy, you can see anything that's causing strain on the right side of the heart. So the things I mentioned before like a pe pulmonary embolus, but you can also see it in things like a scheme of heart disease as well because the scheme of heart disease can affect the conduction, but it's the left bundle. I want you to be particularly worried about when you see it on an E C G. Okay. And then we go into the ST segment, which is classically what people think about when they think about an M I. So S your ST segment can be normal, elevated or depressed and to be significantly elevated or depressed, it's got to be more than one millimeter in your chest, in your chest leads and um sorry, in your limb leads and two millimeters um in your chest leads. So those are the distances you're looking at. And if you're seeing it in a particular territory that we saw on that first TCG, then you can be thinking, oh, look, this person is having an inferior stemi pericarditis. Does anyone know what the pericarditis E C G might look like the, the ST depression? Um No, so you actually get, you can get some reciprocal ST depression but typically pericarditis different, differs from a stemi. You said they feel ST elevation. Yes. Exactly. Thank you. So, across the E C G you'll get this way, widespread ST elevation that doesn't fit a particular territory. And that's what makes it different to a stemi. And sometimes it looks a bit more like a saddle so it goes down and up and that's why we say it's a saddle shaped. Also, you've got to think about the clinical history. This is typically seen in young people who've come in with chest pain, who have had some sort of preceding viral illness. Um That's a, that's a typical ST elevation. Um And you can sometimes see reciprocal changes where you get depression in the reciprocal leads and this is a pericarditis E C G. So if I can convince you, you can see widespread, you can see ST this kind of saddle, this looping down in the inferior leads, but and it's also present in the anterior lateral and the septal, it's everywhere basically. So when you see this everywhere, you think of pericarditis and then ST depression, as I said, could be a reciprocal change seen in an M I. So if you see ST elevation somewhere, always look for other places, there might be some ST depression. Um and then also in digoxin toxicity. So people who've had too much digoxin, they can get this reverse tick sign. So it goes down and then up and this is a classical SCG sign that one on the right that we see in people who've had too much digoxin. Um OK. Brilliant. So the Q T interval is the time between the start of the Q wave and the end of the T wave. Um So this is uh important sometimes to think about the rate of the heart. And that's why we look at A Q T C and A Q T C basically means the QT interval corrected for how quick the heart rate's going. And I always just use MD Calx on my phone. It's a nice app. You can put in the rate of the heart and the length of the Q T. Um And then you can kind of roughly work out from their Q T is a bit different in men and women. Um Typically, it's 350 to 450 in men and 360 to 460 milliseconds in women. Um This, to be honest, in, in reality, looks a bit like 10 small squares. But if you're looking at the E C G and you see that the T wave is almost halfway between the QRS and the next P wave, it gives you a good idea that this might be a long Q T C. And, and it's really important in people who've had a sudden episode of syncope or um collapse because it might be that they have some congenital cause that's contributing to a long queue tea. And there's a long list of things that cause long Q T typically, drugs causing it. So you can think about certain antibiotics, Erythromycin, Clarithromycin, and then some antidepressants that particularly tricyclics. There are some metabolic disturbances that can change things so low, low potassium, low calcium and also hypothyroidism. And then these are the things I was talking about that you want to, you don't want to miss out that if it's a young person coming with a collapse, they might have a family history of this. So a family history of sudden cardiac death and this is long Q T brick Garda um syndrome is another one. And then ischemic heart disease is always there because it's always going to be something that affects the conduction and the electrical activity in the heart. And finally, we're onto our last step. So looking at the T waves, so flattened T waves, so the T waves can either be bigger than normal or smaller than normal if they're smaller than normal and they're flattened. This can be normal. So particularly in a V R V, one V T V, three people of Afro Caribbean descent. This can be a completely normal variant. Um but it can also indicate that there's other problems going on. Like a ski me, a digoxin toxicity left bundle branch block and low potassium. A peaked T wave is a classic E C G that we always see in people with hypokalemia. And normally this is people with a potassium of over about 5.5. You get some other associated changes in it. You get flattened P waves and broad QRS waves. Um But the main thing you'll see, most blindingly obvious is a big T wave and I think I've got yet. So here we go, we can see huge T waves almost as big as the QRS. And this is in someone who's hypokalemic. Um ok. Brilliant. So that's the end of me talking. Um Does anyone have any questions at this point? About those 10 steps? Um Yes, doctor is the way to differentiate between a CV elevation of em I and pericarditis is with it, the Codec enzymes, I mean, as a troponin and stuff like that. Yeah, that's a really good point. And as you know, troponin can be elevated in anything that causes stress on the heart. So with pericarditis, you can still get an elevated troponin. So troponin isn't specific just for an M I troponin can be caused by anything that's causing heart strain. So you can see a raised troponin, things like pulmonary embolus or if the heart's beating particularly quickly in something like fast atrial fibrillation. So, a person with pericarditis who's got an inflamed pericardium might also have a hydrophone, probably not quite as high as a stemi. But the main thing I would say is that the stemi it often follows a territory because a stemi is cause as you know, is caused by a blood clot in a coronary artery and it's a particular territory will be affected. Whereas pericarditis it's broad and it covers all the leads basically. Um And the patient will give you quite a good story of having had a virus before. But that's a really good question. Thank you. Thank you doctor. Um So I thought we could go through these cases. Um I don't know if you've taken notes of the 10 steps, but it might be if we show you each, if I show you each case and then from that, you look at the E C G and try and apply the 10 steps. I have to say some of the image quality isn't as good as I would have liked. But I think we'll work with that and see if you can um see what's going on in each, each E C G and it might be helpful if we take it in turns to present what we found. Um If that's ok. So the first cases a fit and young. Well man, um he presents for a routine insurance medical. This is his E C G, present your findings and give the diagnosis. We'll miss out step one. I'm going to say, you know, all the patient's names. So just go to step two and then work down the system and see. And if someone could present it at the end. That'd be brilliant. Okay. I miss you. Yep. Okay. Does anyone want to have a go presenting the C C G? Don't worry, I'm probably trying to speed you up too much. I'm just aware we've only got 20 minutes left. But does this look like a normal or an abnormal E C G? Two U looks normal. Completely normal. Exactly. Sorry. The first one I shouldn't have spent so long on because it's a trick. Just this is a completely normal routine. E C G. We can see it's got normal axis deviation. You should have been able to cpr intervals, normal, normal QRS. Um, normal Q T C T waves aren't abnormal and it's just a good one too. It's just important that you recognize what normal looks like because now we're going to go on to some abnormally cgs. So this is a 35 year old man who's presenting with palpitations. He's been drinking heavily with his friends over the weekend. This is his E C G. So in the interest of time, don't worry about going through the system. You can try and go through it, but after maybe I'll give you 30 seconds and then we'll talk about what you think is going on. Yeah. How's that? If there's a regular irregular uh via, is uh this space in the, again for filling this uh, skin beat in between? Sorry, I think you cut out just at the end there Yes. Uh Like if you check anyone would see anyone who do you see there's uh two or three through and then this space again, this techie card here. Yeah. Brilliant. Yes. And it's tachycardic, irregularly irregular. You're right. Can you see any obvious P waves? Can anyone C P waves? Nope. Completely. Yeah. So this is a rhetorical question. There's no P waves. So if you know someone's got an irregularly irregular pulse and no P waves, what do you think the diagnosis might be? Is the atrial fibrillation? Great Lola Yeah, atrial fibrillation. Um So it's an important diagnosis because people come in sick with it. Um And the treatment is rate control, rhythm, control and anti coagulation. The reason we give anti coagulation is these patient's have a much higher increased risk of stroke and I'm sure you might have had other teaching on doing assessment. Uh um So the Chad Vask score is particularly good at looking at people's risk for stroke and deciding if they need to be started on anti coagulation. But exactly right. This is irregularly irregular tachycardic, no P waves. This is fast atrial fibrillation. Brilliant. Um So the next case is a 45 year old businessman who presents feeling his heart is racing. He has some shortness of breath and here is his E C G. Sorry. The quality is not fantastic on this one. I'll give you 30 seconds again just to have a look at it. And then we'll discuss. Is this normal tacky tacky? Yeah, brilliant. You came in before 30 seconds as a thank you. Um, so this is a tacky cardia, correct? Um, so the rate on this, um, if anyone's going to try and use my method to calculate. So 123456789, 10 11 12 13 14 15 16 17 18 1920 21. 22. 23. What's 23 times six? Let me get my calculator. Yeah, heart rate of 100 28. So tachycardic. Exactly right. What I want to show you on this E C G is again, you can see this kind of irregular rhythm between each QRS is what we call a fluttering baseline. So it's not obviously a T wave, it's not obviously a P wave, but it's a seesaw. Is this seesaw up and down. Does anyone have any idea what this SCG is showing us when we see that? See soaring baseline. Yeah, this is flutter. So this is atrial flutter and atrial flutter can be divided into different types of block. So it can be 4 to 1 block, 3 to 1 block or 2 to 1 block. I think this is 2 to 1 block. You can see the to see sores and also particularly the rate I calculated as 100 and 40. We would say it's about 100 and 50. So when you have an egg that's 100 and five 50 you can know that it's 2 to 1 block when the rate goes down to 100 you know, it's 3 to 1 block and when it's 75 you know, it's 4 to 1 block because you know that it's taking four cycles to get through. And this is all because the Atria is going at 300 BPM. And so 2 to 1 block, you have it 3 to 1, you third at 4 to 1, your quarter it and that's how you can see that um flatter you actually treat pretty much in the same way as atrial fibrillation. Um So it's important to get rate control. Um typically with something like bisoprolol, a beta blocker or you could use another agent like digoxin for rhythm control. And then thinking about these patient's still need anti coagulation because they still have an increased stroke risk. Brilliant, good question. Sorry doctor. Good question. Uh um So in regards to rate calculation, so you, you calculated the QRS total Krs and yeah, times you buy six. Yes. If, if it's a regular um E C G, right? That's when you use six, you can. So the reason I like this way is you can use it for regular or irregular. So I'll take you back to the E C G of A F. So if you were to use the other method which is counting the squares between and dividing 300 by that number, I hope you can appreciate that because this is a regular, if you were to say, use the difference between these two Q R s and then use it between these two Q R s. I'm hoping you can see my cursor, you'll get a regular, you'll get a very different rate. Whereas if you're using the whole strip, so this E C G doesn't have the whole rhythm strip. But if you use the whole lead to, it doesn't matter if it's regular or irregular, you're getting a good, a good approximation for the rate. So I think that's the better one. I always use it because it's good for irregular and regular and you always uh the use W T. Yeah. OK. Sorry. But where does the six come from? Oh yeah, that's fine because we're assuming the rate that the E C G is the rate of the paper going through the machine. Um And so that is 25 millimeters per second. So that therefore we're assuming that this baseline is 10 seconds to the E C G is the 10 seconds. Does that make sense? Okay. Yeah. Okay. Um So case four. So this is a 65 year old man who's found unresponsive. He has no central pulse and is making no respiratory effort. Um Someone's done an E C G. What would you do? And this is the E C G looks like a block spready cardia. Yeah, it's Braddy card. It gets slow and can you appreciate as well? It's very slow, slow, small height. So it's really reduced amplitude of electrical activity. And this is an important one to think back to one of the first steps I told you about which is looking at the patient, what did I tell you about the patient? He's unconscious, he's unconscious. Serious. And you can't feel a pulse. So, what do you think if you see this E C G? But you can't get a, this is a cardiac arrest. Exactly. So this is pulseless electrical activity. So if they've not got a pulse that unresponsive, even if you're recording electrical activity, this is a cardiac arrest and we need to start CPR. Um It's important to know your different rhythms um for cardiac arrest because there are some rhythms that you're shock and some rhythms you won't shock. So, pulseless electrical activity and a sisterly, which is just a flat line. You don't give electrical shocks to whereas the other two you do VF and VT. But yeah, exactly. Right. This is a bradycardic rhythm, low amplitude, but it doesn't matter because your patient is pulseless and unconscious. So the most important thing is you start CPR okay. Brilliant. So a 60 year old man presents with tight central chest pain radiating to his left shoulder. This is his initial E C G. What's your findings? And what's your diagnosis? It looks like stemi microbial infection, but it's an ST elevation. Yes. Which which areas of the heart? Are you seeing the ST elevation in on the lateral um side? Lateral? Yeah, brilliant. So I would agree with both of you. So you can see it in lateral, you can also see it in. Um so this is a lateral lead as well and you can also see it in um in, in the anterior anterior leads as well. You can see there is reciprocal ST depression in the inferior leads. And this is back to how do you know this isn't pericarditis because pericarditis doesn't look like this. You would get ST elevation everywhere, not some reciprocal changes. Brilliant. Um So this person is having exactly a stemi affecting the anterior and the lateral leads. Okay. Um This is sometimes called tomb stoning because of it looks like a tombstone and because it's got very high associated mortality if you don't get your person to a cardiologist and a Cath lab urgently. Um I suppose particularly thinking about the distribution of, of, of where the leads are affected. Does anyone remember which blood vessel might be the one that's causing the problem? Don't worry. So it's the left anterior descending is typically the one that is involved particularly with the anti receptor, but can also involve these lateral leads. So this person has got an L A D lateral ascending um uh dissection or clot or something and they need to go for a cardiology Cath lab urgently brilliant. So another chest pain. This is a 65 year old woman who presents with chest pain, radiating to her jaw and down her left arm. It feels like normal angina and she's had her G T N spray. But this is what her egg looks like. I think it's still by cardio infection. Is that in? No, no, non ST elevation. Yeah. So I would agree in that. Most of the leads are showing ST depression. So this would be in keeping with an N stemi, but I want to draw your attention to a VR. So this top lead up here. Can I uh like experience? Yes, we saw a large appearance. Yes. Yeah. So there's some ST elevation in a VR um which is really important that because this looks exactly, I agree. It looks like an N stemi. But if you look at a VR, you can see um you like, it looks like an inferior lateral end stemi. But then you look at a V R and you can see some elevation here and this might suggest to you that this person has a left artery occlusion and needs to go to the Cath lab quite urgently. So I think, yeah, I agree. This is an end stemi, but there's something odd going on here. And that's the important thing you get drawn to these leads. But remember to look all through all your leads to make sure you're not missing anything and pick up the phone to the cardiologist and as someone said earlier about proponents, I mean, troponin is, are really essential in our diagnosis of em stem ease. If I was seeing this E C G, I'd be very worried about this patient. Okay. We're almost there because we're almost out of time. So, can I have a quick silly question? I always wondered this if you just go back to the E C G, please? Of course, it might sound silly. But why is it that on E C G you always get to, um to lead to and, and the last one is the one that you 10 people tend to look at for diagnosing. Know. That's a really good question. Yeah, you're right. So two is always the one that's the bottom of, of the tracing. It's just because that's the one that gets the best imaging of the heart. I don't know the exact reason why we use it is typically on all E C G s. I've never really asked anyone or thought about that in terms of, but it always just is there. I think it's because we get the best, um we get the best rhythm strip, the best view of the heart through lead lead to when you're thinking about and I say lead to, it's a bit confusing, isn't it? Because there isn't actually a lead to there's six on the chest and then one on each limb. So by lead to, I mean, that view of the heart that they're combining together is the best for you. And that's the one the people who came up with this have decided is best to use. Good question. Okay. Thank you. Um K seven. So 29 year old presents with central chest pain. She has a history of recent flu like illness, but no significant past medical history. Here is her E C G. And what's the diagnosis? It looks like thirst degree block? Yep. So there's definitely a long P R agree and it's regular. Yeah. What about the ST segment particularly? Is it normal? Never know. No. And does it fit a particular distribution is what I would always think is this uh you know, I don't know whether is this WPW. So this is pericarditis. Yeah. So you can see, hopefully I can convince you that there are lots of leads in different territories affected. So lead, one is a lateral lead. This has got ST elevation lead to is an inferior lead and this has got ST elevation and then all lots of the anteroseptal leads do have ST elevation and so did these lateral leads and particularly this in V five and V six. This is the saddle shape I was telling you about earlier. Also the clinical history. This is a young woman normally fit well, no cardiovascular history but has had the viral illness and is coming in with chest pain. Um So this is what I would think of as pericarditis. And although the tro troponin could be elevated, it probably won't be as elevated as if this is an M I. Okay. So a 45 year old woman has stepped off a flight from Japan when she developed severe pleuritic chest pain and shortness of breath. So, from that vignette, you probably know the diagnosis on. Exactly. Yeah, her examination is of her chest is clear, present your findings. So the whole point of this is, you know, it's a P but does anyone know what the textbooks say we should see on an E C G with someone with a P uh so Teligent ST interest? Yeah. So you can see some ST elevation. What you typically this, this is what you'll learn in the text books. And for exams in reality, someone with a pulmonary embolus would generally present with sinus tachycardia. So that's normally what you'll see. But what, what you're reading the text books and what you might be examined on is this phenomenon called S one Q T um T three. Yes. Have you heard of that? Yeah. So in lead one, you can see there's a big s wave inlayed three you can see here if I can just about convince you that's more than two millimeters, that's a pathological Q wave. And then if you go to V three U C A depressed T wave and they're the 33 findings that they say are typically associated with a pulmonary embolus. I've never seen it and I don't really know anyone that has. I think this is something we get examined on, but it's something to be aware of. Typically. Like I say, it would be more likely to be sinus tachycardia. And also a, a point for that E C G is this is an in valid E C G because there's no trace in view one. So if you a nurse gives you an E C G that looks like this, always ask for them to reconnect the leads and do another E C G because you have no idea what's going on in that. Sorry. Yeah. So um the diagnosis of P isn't on S E G L0. Generally, it's by doing a CT P A and the treatment you're right can either be anti tabulation dough ax or sometimes it can be with, if they're very sick, they might need thrombolysis. And there's criteria for that. But thrombolysis is basically giving clot, busting drugs through a drip. But most people who are stable would just be put on anti coagulation and typically a doe act like River Oaks album. Brilliant. I'm aware I'm running over, so I'm just going to hurry up. So case nine is a 50 year old man who presents with collapse. He's been unwell recently with chest pain for which has been prescribed Clarithromycin from his GP. He also takes medication for hay fever at this time of the year what is concerning here now in the history I've mentioned he's taken Clarithromycin and another medication and medications could do strange things to EKGs. But what this E C G is meant to show you is there's long Q T C. Um, so if you get a vignette thinking about people on lots of medications, start thinking about measuring the Q T C, I remember it's a start of the QRS to the end of the tea. And if that's longer than 10 small squares before you even calculated the Q T C, you can be pretty sure this person's got long cute. It's really important to diagnose because it can be something that goes on to cause quite serious arrhythmias. So something called torsade the point, which is basically a strange version of ventricular fibrillation so they can die from this. Um So it's important to look at the Q T and my final case, sorry, I'm rushing is a 29 year old presenting with a syncopal episode. He has a family history of sudden cardiac death. And this is really important thinking about what their family history is because thinking about long Q T, it might be familial or I mentioned earlier, a syndrome called Brick Garda. Has anyone heard of Brig Arda syndrome? No, don't worry. It's something that can sometimes come up in exams and is in these young fit people who come in with collapse and it's a problem with the sodium channel gene in the heart and it can basically cause a sudden V F or V T arrest. So it's very important to pick up and what you can see on this E C G. The findings that are significant for brick Garda or they get ST elevation in Leeds, V one to V three and then T wave inversion following that. And that's, this is a very typical brig, Arda E C G. It's important to see because if this person has this, they should probably have an eye C D, so an implantable cardiac device so that if something happens that they go into VFL VT, they will be shocked out of it. So it's really important in young people who come in with collapse to make sure you don't see this presentation. Okay. Sorry to rush through the last two. Um I know you've got another talk. So, um so we've briefly gone through how stds have recorded and the path of physiology and then we've gone through that 10 system step, which some of you were familiar with you might all have been and hopefully it was a refresher for you. But if you've not heard of it before, hopefully it will be something that will help you in your practice. And we've talked about common scg abnormalities and we've applied those systems and looking at some SGS that we might see in patient's and in exams. Um ok. Brilliant. Does anyone have any questions from all of that. I'm really sorry. I'm really sorry, doctor, but we have gone over a few minutes already. All right, that's fine. Yeah, I'll go. I just thought this final slide just for looking at E C G S. Life in the fast lane is a brilliant resource. So is geeky medics and so is Oxford medical education. So, life in the fast lane is the main one to look for. Nice library of E C G S if you need it. But thank you so much and good luck, everyone and sorry to run over. Thanks a lot doctor. I really did help. I hope so. Thank you so much. It's a privilege to talk to you all. Thank you. Thank you very much. Thanks. Bye.