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Thank you. I think we can start. They should join right now. However, join. Okay, cool. Um, so hi everyone. My name is Hannah. I'm a medical registrar working in Southeast London at the moment. And it's an absolute pleasure to talk to you all today. I'm aware you've had a very long day of lectures and I'm the last spot. So hopefully we'll try and make it quite quick. I know. Um, there, there's a lot of you on this call previously, I've done this um, session and made it quite interactive. My experience with large zoom calls is that, um, when there's lots of you, it can be quite hard to make that interactive. Um So I'll just be going through it. But if there's any points you want to stop me or ask questions, just raise your hand and hopefully we'll be able to answer them as we go and hopefully you'll be looking, someone else will be looking at the chat for me. So if anything pops up in there, we can answer those questions as well. Um So I'm going to start now. We are gonna be going through basically the basics of ecgs. I'm sure you'll be at various stages in your training and have had different exposure to ecgs. Um And lots of you will be aware of some of these basic steps and it would just be a revision exercise. But that's really helpful if you're coming up to exams or particular, I was told to focus on things that are common in the Plavix Sam. And I've spoken to quite a lot of colleagues I work with about Kameni CGs that come up in, in plaid. So hopefully this will be useful for that. I'm going to go through a system for going through your SGS and making sure you're not missing anything. Um And then those common ECG things we see clinically, but also that come up more commonly in exams. Um and then we'll go through some cases. So, like I said, previously, I've made it quite interactive, but it might be best you have a piece of paper and go through your system and we give you a minute on each one and then we'll go through the findings of the ecgs together. So that's our aims at the end of today. So to start with just looking at the basics of an ECG. So quite misleadingly, we call it a 12 lead ECG or there are, there are only 10 points were actually sensing electrical activity on the patient. Um So there are six chest leads and four limb leads. And basically, these are uh more we should think of as electrodes. So 10 electrodes that give the impression of six different directions of electric, 12 sorry electrical activity of the heart. And we can just think of it as taking a picture of the electrical activity of our heart. So here we are looking at all of those different leads. So when electrical activity or deep polarization is traveling in the direction of an electrode, it will create a positive upstroke. So this is important when thinking about the electrical activity activity traveling from our atria to our ventricles and representing deep polarization and therefore contraction. So you can see when our lead to is because it's placed, it's picture is placed down here, it will see positive deflections because the electrical activity is moving down from the Petricka to the ventricles or as if we're looking at leads that are higher up. So such as VR, you'll see this is a negative deflection because the electrical activity is moving away from it. However, when you're looking at leeds, where things are a bit more isoelectric, so they're moving in the same direction. Um as in VL, you can see it's a bit less clear whether it's up or down perfect. Um And so then we're looking at our 12 leads and it's really important when we're looking at them because we can think about the anatomical anatomical structure of our heart and we can think about which leads a corresponding to which areas and this is really important when you are thinking about people and particularly their coronary system. And therefore you can work out if there's a problem with an area, what's going on and what, what, what place we might need to go and do an intervention too. So here you have your 12 lead ECG. So as you can see, it's divided quite simply. Um So I always remember my inferior leads are at the bottom, this bottom L shape. So they're made up of leads to Leeds, three and aVF. And this is important because with most people, this will be a result of the right side of the heart. Um And that's to be said, in about 70% of people um obviously, in about 10% of people who are left sided dominant, it will be um from the left vasculature and about 20% it'll be a combination of both then looking at the lateral leads. So looking at Leeds, one aVL and V five and V six. Now, I remember these because I think about actually, shall I minimize that? So you can see properly. Thank you. Um So I always think of the lateral so to the sides. So one V five and B six R on the outer aspect of your ECG and A VL has an L in it. So it's also thinking of lateral and that's just a way I think of remembering it. Um And these are most commonly the left circumflex artery in the heart. Um Although for some people, they can be a diagonal branch of the lad so that left uh artery. Um But most people would be the left circumplex. So that's easy. The lateral leads and aVL are those ones, then we think about anti receptible. So these are easy V one through two V four. And these are commonly supplied by the lad. So when looking at this, you can have a good idea that if you're seeing ECG changes in a particular distribution, you want to have a good idea about which part of the heart has been affected. And this is just to reiterate this really. So as you can see clearly, um you've got your lad and, and this is kind of a showing the anatomy of the heart. So what does each wave in the ECG show us? So it's all showing us thinking about deep polarization. And as I said, electrical activity going into each direction, you've got to think that most ECGS are set up to be going um at a rate of 25 millimeters per second, which is important to think that one large square will be naught 0.2 seconds and then one small square will be not point not four seconds. And from that, you can start thinking about the timings of when these all these electrical activity happening. Now, I'm hoping this is going to take us to a youtube video um that would just quickly go through the cardiac cycle. You need some help clearing out your wardrobe, your clothes on vintage and you can make a doctor. We don't quite see the video. Ah, that's a shame. Okay. This is a cardio. You don't see it. No, you only see the presentation. Okay. Never mind. Hopefully, if I could, I'll try and send that link through the chat at the end of the call. It's just a nice schematic showing is the electrical activity goes through how each wave, but I'll just, I'll just talk through it. So obviously, your P wave is your atria contracting an electrical activity traveling down. Then your pr interval is the time it's taking that electrical activity to get from the sinoatrial node down the Kinji find buzz down the bundle of hiss and for the ventricles to start contracting within this QRS complex, you would expect to see the, see the atria deep polarization. But because the ventricles are so much bigger muscle mass, it's completely lost within this complex. And then your T wave is when you're seeing your ventricles re polarizing. So therefore relaxing and that's your cardiac cycle. There's a really nice little video. So I hope I can send that through to you later. Sorry about that. Okay. So now I'm going to go through the 10 steps of reading an ECG just breaking it down really, really simply. And hopefully this will give you a good system to make, make sure we never miss anything, both in exams and in clinical practice. So the first thing is the patient details. So in any exam situation, it's really important to have that, to know who the patient is, what their date of birth is. Um And where in the hospital you are, that's also quite critical because you're thinking about if you are seeing a patient in a and E um this is an acute setting or if you're seeing someone on the wards, if they've been in for a longer time, are their previous CCGS? Are there other things I need to be considering? And then thinking about again, the situation which is partly where participation, but also what's the time on your ECG? So when was it done? And when was it done in relation to the chest pain, the patient might be having. Also, it's important thing about when the ECG was done because we often do something called serially CGs, which is if we're looking for a change and then we see if it's still there after a couple of hours. This can be really helpful in looking at patient's with chest pain. So when was it done? Is there more than one ECG? And did they have pain when they, when the CDC was being done? So this is looking at the situation and the clinical patient then the first thing to look at is the rate. Now there are different numbers of ways I think there is one easier way than the other, but I'll tell you both of them. Um So the first one is to count the number of QRS complex is, um, and you know that the, the time of an ECG because if it's going at 25 millimeters per second, you know that, that ECG strip, that when you're given two is 10 seconds long. So you can simply count the number of QRS is, you see along the bottom rhythm strip and times that number by six. And then you have the rate. This is also really good if the patient's in a regular rhythm. So if they're in atrial fibrillation, because you're capturing all of those QRS complex is whereas the next method, which is some people like as well, which is, you count the number of large squares between the R waves and divide 300 by that number, I think that's quite good. But again, if they're in an irregular rhythm and you pick a particular QRS complex with another one, they might be very closer and then the irregularity might mean further along they're much further apart. So you're not truly capturing the rate. So I always put a preference for the first one. The maths is easier and it's, it removes variables. So that's quite good then looking at the rhythm. So you're mainly trying to work out is this regular or irregular? Because the regular means that they could be an atrial flutter atrial fibrillation or they could have a heart block. Um Sometimes it can be quite hard, particularly when you're seeing a wandering baseline. So I always use a piece of paper to just check. So I'll get a piece of paper, I'll make two little marks between the QRS complex and then I'll move it along the ECG and I'll double check, making sure that each complex is the same align apart apart. Then looking at the axis of the heart. Now, looking at this, you can see sort of the direction. It's important to think that most hearts and normal access will have, will be to the left. And that's because the left ventricle has a bigger muscle mass than the right. So therefore, it's normal to have a slightly left um, left axis beyond this, we can call it deviated. And this might mean it's deviated to the left or it's deviated to the right. And if it's deviated, either way, it might give you a bit of a picture that one side of the heart is bigger than normal. So to look at this, this is a really simple way of doing it to look at the access, you look at leeds one and needs to and you try and look at the QRS complex. Now, the first picture you can see is what we would call normal. And you have an upward QRS stroke in both leads one and leads to then in left axis, deviation so lied, one, the ups the QRS is going upwards and then in lied to, you can see, um, that there's a big s wave going down and this is negative. So we think of these arrows. So in English L left equals leaving. And then, um, if it's a right access deviation, you're looking at returning so that these, these, um, it's positive in one and uh sorry, negative in one and positive and two and the two arrows are almost effectively returning to each other. So they're going towards each other. And that's just a really helpful way of looking at it, just looking at it, eyeballing it, you can work out whether there's a deviation. Like I said, left axis deviation is more suggestive of things like left ventricular hypertrophy and could be could be due to sort of obstruction and also right axis deviation is right ventricular hypertrophy and this is when the right side of the heart's working really hard and patient's often have this, you have like chronic lung problems because their heart is pumping really, the right side of the heart is trying to pump really hard against, against the increased pulmonary hypertension in the lungs. So there is just a short table um looking at the different types of of access deviation. It's important to comment actually that they can be normal for certain people, but like I said, left axis deviation most commonly is left ventricular hypertrophy um but can be caused by other things such as an infarction and right axis deviation is right. Ventricular hypertrophy often caused by respiratory problems or other things that might increase pressure on the heart from the lungs such as a pulmonary embolus. So now we start looking at our waves. So can you see P waves is the really important question here? Because if there are no P waves, then it's suggestive that your hr aren't contracting and you might have what we, your hr aren't contracting in a conformed way. That means it's picked up on an ECG which is highly suggestive of atrial fibrillation. Or if you're seeing a sea soaring of the P waves, they're not coordinating well and they might be an atrial flutter. Then you're looking at your P waves, are they related to the QRS? And we'll come on to think about that later in our pr interval but does A P wave always correspond? A QRS? And then you can look at the shape of them. So you can see on the left side of the slide, a P wave that does a little bump, this is called P ME trolley. Um And this, this can be a sign that the left side, the left atria is basically bigger than the right. And that's so the deep polarization of this becomes longer and effectively, that makes a little bump in your. So it looks like a little M and I always remember may trolley because it looks like an M may trolley starts with M and that's a sign that the right atrium might be a bit bigger. Then Pete Pull Manali when the P wave goes higher than normal, um is suggestive that there is a right side of the heart that might be bigger. And therefore the right side to polarization catch that the left and you get this superimposed right and left deep polarization, you get a big P wave and that's a sign that the right side of the heart of the Atria is bigger. And then you look at your pr interval. And so you're looking to see how many I was just working squares. So there are 3 to 5 small squares and you can see um um sorry, I'm doing a session, I'm doing a meeting. Sorry, thank you. Sorry about that. Um So then to look at the pr interval, um you're doing a uh you're looking at pr interval for heart blocks. And I was because I'm simple divide this simply into, is it constantly there or is it variable in how, how it changes? So I've just said that a normal pr interval is 3 to 5 squares if it's longer than that, but it's constantly longer, then you're probably looking at something called first degree heart block. And this can be caused. Typically, we can see it with drugs like beta blockers um and other medications that can prolong this and then the second degree heart block is where you, it's again constant but instead of always getting QRS after the P wave every now and then you just drop the QRS. Um So this is important to, this is a type two, second degree, type two, then if it's variable. So if the pr is changing, you think about the second degree? Hello? Does someone need to ask something? No apologies. I think someone just wrongfully unneeded themselves, but no problem, we can continue doctor. All right. So the second degree is where, where it increases. So the first bit is short, then it gets longer, then it gets longer and you lose a QRS complex. And finally, third degree heart block is when they're not talking to each other at all. So the P waves and the QRS waves completely unrelated. So they're just really, really not talking to each other and you're seeing P waves completely at different points of the QRS. Um And it's really important to know these because the third degree heart block and the second degree heart block type two are the ones that are really dangerous and often do need pacing. So they need a pacemaker putting in. Um and then the QRS complex. So this is important looking at your, basically, like I said, how your ventricles are working. So um Q waves can be normal and you can see them in the lateral leads. So if you remember recg there, the V five V six the one in one and the aVL and they can be normal, but only if there are certain size. So only if there's one small square long and two millimeters deep. Anywhere else a Q wave is seen and bigger than this is suggestive that there's been an infarction of previous myocardial myocardial event. So always look for big Q waves, particularly outside of these lateral leads, then looking at the QRS complex. So again, thinking in your small squares, it should be less than 0.12 seconds, which is equivalent to three small squares. So if you count from the start of your cu wave to the end of the S wave and it's longer than three, you know, you've got a big QRS complex. There are lots of things that can cause this um some things like hyperkalemia can cause it. But the thing they're really hot on in exams and the things we really need to look at for a bundle branch blocks. And this is when there's a problem that's probably caused by sort of an ischemic change to the bundle of hiss fibers. So the conduction isn't working particularly well between the sinoatrial node and the rest of our ventricles. And that basically makes it slower. And that's why the QRS complex takes longer and it equivalents to more than the three small squares. So just always looking to count three small squares. And then finally thinking about the shape and the height So this, I think the main one to think about not to get bogged down and it is just left ventricular hypertrophy because this is a really easy one to spot. So I've got an example here. So you look between V one and V six and if you see a big, like a very tall, often, I think of it as more than 33 big squares um are complex in, in your V six and a big deep s wave in your V one, then you know, you've got a left ventricular hypertrophy. And if you add up how many big squares the S wave is here and there are wave is here and it's greater than six. You can think this is left ventricular hypertrophy. A left ventricular hypertrophy is really common and it's seen when the heart's working hard. And often that's when there's a big after load on the heart. And this can be caused by things like hypertension, cardiovascular vascular disease, peripheral vascular disease. That's the main one to think about when you think about the shape of your QRS. Um This is just a little aid memoir. I don't know if anyone's heard of it before William Marrow to help looking at your bundle branch blocks. So the top, we're looking at a left bundle branch block and you're basically looking in your V one and your V six and trying to see if you can see these configurations. So in lead V one, you would, if it was a left bundle, you would see that there is a big, big, deep, um uh sort of a notched S wave um coming down and in the V six wave, you're seeing what looks like an RS are sort of formation that equivalently looks like an M. Um And you remember this as William and that's a left bundle and left bundle is really important to pick up because often if we see a left bundle, we can't interpret the ST segment after that. So it's really important to see and then a right bundle. So again, you found it's more than three small squares. And this time, you're looking for a marrow fat formation. So in V one, it's RSR and then V six, you're seeing this QR and then a deep S wave at the end and it looks more like a w where you see this negativity. Sometimes you need the eye of faith to use that. Okay. Fine. So now we're going on to, we're getting close to the end of our looking and then we'll look at some ecgs. Um and hopefully some of you guys will be able to say some comments on them. So the ST segment is really important. This is when we're looking for stem ease. So we're looking for any evidence of infarction. And again, you can look at the particular territories that these are looking at. So particular areas of the heart that are affected when you refer back to that side at the very start where you think about which artery affects which, which bit of the ECG and then pericarditis. So this is a patient who often has a preceding viral illness comes in with chest pain, unlike in a stemi where you see particular distribution, where a particular coronary artery is affected, you'll see these widespread ST elevation throughout the ECG. Um So this is a sort of an ST elevation example. And you can often see reciprocal changes. Whereas this is a pericarditis where you see there's more sort of scooped out ST segment. But in a pattern that doesn't, doesn't represent any particular artery area. So you can see throughout like all through the antri leads into the lateral leads, inferior leads, affected, it's everywhere, basically ST depression. So again, this can be a reciprocal change when you've had a scheme ick damage, but it can also be assigned, sometimes they pick up on exams of digoxin toxicity and you get this reverse tick. So instead of a tick going like that, it's a reverse tick and it's a downward sloping ST segment and finally, the QT interval. So this is from the start of the Q wave to the end of the T wave. It's really important to calculate it using um correction for the heart rate because you've got a particularly slow heart rate, it could be falsely, falsely slow or if it, it could be falsely quick if your heart rate's too quick. So I always use MD CAL, which is just an app on my phone to work it out and you just count the number of small squares. I always have to look it up, but in a uh sort of around for under 450 would be an acceptable heart QTC in a man. And you just have to calculate it based on the MD CAL calculation. And it's really important looking at Long QTC because it can be something that can cause real problems, particularly in patients who have a history of sudden cardiac events. So a history of sudden cardiac death in their family or loss of consciousness because this could be a sign that they've got some serious congenital abnormality that's causing Long Qt Syndrome and there's a whole list of different causes. So, drugs are really common causes particularly particular antibiotics like Erythromycin Clarithromycin metabolic causes. So looking at your particularly potassium and calcium and then I was talking just now about wanting to not miss these familial causes. So long QT syndrome and these are young patient's who have a history of sudden cardiac death. And they're really important that we don't miss finally the last step. So you've got to your T waves. Um So you're just trying to see if the T waves are normal height and when they're slightly flattened, this can be completely normal. And people of Africa Caribbean heritage particularly in V two and V three. But in anyone, they can be present in a VR and B one, just a flat and T wave. And this is normal or an inverted T wave. Beyond this, they can be a sign that there's a ski mia and that's when it's important to do serial SGS. They can be digoxin toxicity as I showed you earlier that reverse tick and they can be a sign of there's a left bundle branch preceding this. And they can also be a sign that your potassium is really low. Peak T waves are, ones are really hot on an exams because a peek T wave is suggestive of hyperkalemia. But there are a few other causes of what's going on in hyperkalemia. So you look for a flattened P wave abroad QRS and a peak T wave. But the T waves are the ones that really come out at you. And here's just an example of these massive T waves. They're almost as big as the QRS complex actually. Ok. Brilliant. Well done everyone because I know this is your last lecture of the day. So thank you for sticking with it. Um We're now just going to go through some cases so that you can practice using that sort of 10 step technique, thinking about how to go through different CCGS. Um So the first cases, a fit, well, 31 year old who's coming for an insurance medical and this is his ECG, I'm just going to give you a minute to look at the ECG and if someone wants to come on speaker at the end and just explain their findings, that'd be brilliant. I know there's lots of you. So if you don't want to, that's fine. But I'll just show you the and give you a moment. Okay. Does anyone want to go and speaker and explain what they can see or you can write in the chat? That's fine as well. Um We've got someone saying ST elevation, okay. Um So this example probably a bit of a trick. Um So this one is basically meant to be a normal ECG. Um So one of the most important things when you're looking at ECGS lots is you need to recognize what normal looks like. So sometimes people comment on this T wave inversion in a VR but that's normal as I explained. Um And I mean, I can't really see any ST I mean, this, I think is an artifact of the ECG. I'm sorry, they're not brilliant, but there's no cause you're always looking is the ST segment a bit higher than the pr interval before. Sometimes you can get something called high take off where it looks like it's going into ST elevation. But actually you see that this starts at the same area as the, as the one before. So it's reassuringly normal ECG. Um So this is the second case. It's a 35 year old with palpitations. He's been drinking heavily with his friends over the weekend and this is his ECG. So I'll give you a moment just looking at that. Um, I apologize because some of these ecgs don't sort of show it in the normal nice 12 lead format that we're used to for looking at the territory's. But it's more, I, I would, my advice to you on this one would just be to pick a lead. So maybe it lead to and just have a look at it and just using the system, just have a look what you can see. Yes, the cardia, but there is a chainsaw appearance. Brilliant. Yeah. So, um, yeah, definitely tachycardia. I think the rate it depends which method you're using. I would definitely advocate for when you see this kind of ECG and it's a regular, you can see that actually, if you were to measure using the second one I showed you with, which is if you divide between 300 between QRS, if you pick these two QRS, it will come up with a heart rate that's completely different to a QRS further along. So I think if you were two times these by uh six, you'd get a heart rate of somewhere between 100 and 100 and 50. So, certainly a tacky cardia brilliant. And also, yes, there's, um, there's kind of slight see soaring baseline which is sometimes indicative of atrial flutter. I certainly would say looking at this ECG you can't see P waves. Um And so you would say that this is a fibrillating baseline. It doesn't necessarily show the obvious sort of definite seesaw, but I can, I, I agree with you, there's definite aspects of it um that show some areas of sea salt which might be suggestive of flutter. Um but there's absence of P waves. So you would definitely be treating this as fibrillation or flutter. So this is meant to be an easy G looking yeah, H or fibrillation. Brilliant. Um So the next case is a 45 year old businessman who comes in present presenting with his heart racing. He is also having some shortness of breath and this is his ECG and if you can have a look at it, see anything obvious and if it could give you in any way a diagnosis. Um Well, a tachycardia, I'm sorry, what was that? Vitech ventricular tachycardia or? Yeah, so they're really good. So definitely it looks like the ventricles are working really quickly. And so this is definitely a tacky cardia. One thing I would say is, you know, your colleague mentioned earlier, the see soaring, I think this is a bit more classical of a see soaring baseline. So you see this up and down stroke, up and down, stroke, up and down stroke. And the reason I suppose it does look like a ventricular tachycardia is because it's regular. Um but in atrial flutter, it does come out as regular because if you imagine, um, the h your contract normally without the signature or no slowing things down, they contract really quickly. And so when you have a block, you can basically, you'll always, uh atrial flutter will always come out as 100 and 50 or 75 or 300 depending on how, what the block is, whether it's a 32 to one block or 2 to 1 block. But this is an atrial flutter with a c soaring baseline and a 2 to 1 block. But I certainly agree that there's because of how quick the ventricles are going, it looks like a, it could be a VT but I think because just because of the nature of, of that, um see soaring, it's more like atrial flutter and you manage atrial flutter in the same way as you meant, manage atrial fibrillation. It's important to get rate and rhythm control so often trying to work out what's the cause of what's causing this person to be in atrial flutter or fibrillation. So in our past case, it was someone who had had a lot of alcohol, alcohol because and also dehydration. Um could the patient, could they have taken any drugs? Could they be septic? Could they be in pain and trying to treat that cause? And beyond that, then you start thinking of rate control and that's when you reach for your digoxin and Bisoprolol. Uh okay. So next case. Um so 65 year old man is found unresponsive. He has no central pulse and is making no respiratory effort. Surprisingly, someone has done an XG. What would you do? So this is just a quick one to look at the ECG. And then what do you think would be the next thing you you would be doing in this patient defibrillation spot on? Yeah. So this is a uh perfect. Exactly. So this person is pulseless. So what you're seeing here is pulseless electrical activity, pee a so this is a cardiac arrest. Um So if someone shows you an ECG and says there's no pulse, you go and feel the pulse and see if there is no pulse and if there's no pulse, you put out a cardiac arrest call and start doing chest compressions um and start managing it as a less. Um So yeah, this is a bit of a weird one but I suppose it goes back to always think about what is the patient doing when you're presented with a piece of paper for an ECG brilliant well done. So case five is a 60 year old man who presents with tight chest pain radiating to his left shoulder. This is his initial egg, present your findings and give a diagnosis. So this is a man with chest pain. So just have a look and let me know what you think. ST elevation. Yeah. Spot on. And can you tell me a bit more sort, sort of, which area do you think of the hearts affected the left, the right ventricle? Many? Yeah. Really good. So you can see the left affected so V five and B six. But to be honest, also, you can see that the anteroseptal leaves are affected pretty badly as well in V three and the four. So this is kind of a really serious stemi. So this is an anterolateral stemi where they're getting lateral involvement, you can see inferior early, they're getting reciprocal changes. So they're getting ST depression. Um So this typical ST changes is called tomb stoning. And I think it's kind of got, got its name because partly the ST segments become, they start looking like a tombstone and also because of often the poor prognosis you can get when you see this widespread tomb stoning. So unlike pericarditis where, you know, I said it can affect everywhere you can see here. Although it's pretty widespread, it's, it's the anteroseptal and the lateral leads, whereas it's not in the inferior leads. These are reciprocal ST depression changes. So, exactly right. This is a stemi and this patient needs to go to the Cath lab urgently. So case six. So there's only 10 cases. So you're almost done well done. So 65 year old woman presents with chest pain, radiating to her jaw and down her left arm, it feels like her normal angina. But on this occasion, it's not eased with her GTN spray. This is her ECG. So present your findings. This is so 65 year old lady who's known Angina but presenting with some chest pain. Yeah, lovely. So you can see that there's some sort of ST depression in V five and V six. So you couldn't call this a STEMI, but there's definitely CG changes going on. So initially, this does look like an N STEMI. The only thing I would point your attention to is an AVR. And this is why it's important to take the time to look through. All the leads is an AVR. There is a bit of ST elevation creeping in. Um So this could be a sign that this person, although it's a stemi, they could be having impending um left, left vessel occlusion. Basically when you see this in a VR. So this is definitely an end stemi but could be more serious and needs to be discussed with cardiology because might need to go to the Cath lab more urgently than a normal, normal end stemi. But brilliant. So case 7, 29 year old presenting with central chest pain history of recent flu, like illness. No significant past medical history. This is her ecg what is the diagnosis? Get up door. Pardon? Let's go. Sorry, you have to repeat that. A I said, is there a block or not? Um Yeah, so there's definitely, I suppose the pr interval is maybe a bit longer than not 0.2 seconds, which should be four small squares, but only just what this is looking at really is this ST changes you can see in V five V six particularly, but you can also see it on inferior leads as well. Um And up here, so this is this kind of doesn't follow any particular anatomy, doesn't follow any particular, the left, um, left, the anterior septal inferior. It doesn't follow that. It's kind of seen in random bits and it's this more sort of scooped out than what you see in a stemi which is tombstone, but there's definitely elevated. So this is pericarditis and it's a scene particularly in young people who have had a recent viral illness and are coming in with chest pain. Um So yeah, just looking for that scooped out ST segment in lots of leads that doesn't necessarily follow any particular coronary artery territory. Um Case eight. So this is a 45 year old lady who's just come off a flight, long haul flight from Japan when she develops severe pleuritic chest pain and shortness of breath on examination. Her chest is clear, present your findings and what is the most likely diagnosis? So, this is quite a hard one, but I just ask you to cast your eyes over it just for a moment. Pulmonary embolism. Yeah, it's a P but how did you know that apart from the history of the give a? Well, yeah, the history is one of the giveaway because of the long flights. And the other thing is SQ 33, like, uh, the 12 and three, there is an SQQ two Q three. I can't remember the proper needs but they are the, yeah, brilliant. Yeah. So this is something that I actually, I, I think is very rarely seen clinically, most commonly the ECG that you see in someone with pe is sinus tacky. But this is one that you read about in the text books and it certainly comes up in exams and it's exactly what you just said. So it's s one. So they have an S wave in the, in the, in their lead uh of, of one. So you can see that, that S wave. So the QRS complex is just a bit bigger than normal and then they have so, so that's S one and then Q three. So if you look at the Q waves in three, so you can see here this Q wave is wider and you wouldn't expect a Q wave in V three. So it's a pathological um key wave. And then you're thinking is I, I have, I think I really have to convince you that that's, that, that is there. Um And then finally T three, so in V three lead, they have a T wave inversion, so their T wave is inverted. So again, this is something that's quite rare clinically um but does come up. So it's S one Q three T three. So it's s weight big S wave in V one, a pathological Q wave in leave three and an inverted T wave in three V three. But in reality, it's the history that gives it away to you and a pe you often just see Sinus tacky, but it's something to look at when you're given that vignette think S one Q three T three and just look for those three findings. Brilliant, well done. Oh sorry. Um So penultimate case, a 50 year old man presents with collapse. He has been unwell recently with chest infection for which he's received Clarithromycin from his GP. He also takes medication for hay fever at this time of year. What's most concerning on this? Ecg we've got some people saying Long Qt. Yeah, perfect, brilliant. And the vignette gives it away that this person is on medication that puts them at risk of this. I mentioned earlier before those types of antibiotics, Clarithromycin, Erythromycin, a real culprits of this. Um but he's presented with a collapse and there's a risk that long QT can become something serious, which is called to Assad's D points, which is basically a type of ventricular tachycardia. And so this is a really worrying ecg it's important to stop those antibiotics and make sure that patient is on a cardiac monitor, but really good spot well done. And the final cases, a 29 year old presenting with a syncopal episode has a family history of sudden cardiac death. Um So this is the ECG. So if you're looking at your system, can you see anything particularly unusual about the ST segments here? We need to, yeah, you can see in V one and V two. So you can see leads V one V two, there's ST elevation and also following this ST elevation, there's T wave inversion and this is a significant ECG because this patient has something called regard a syndrome, which is a congenital problem that basically puts them at risk of sudden cardiac events and death. And so if a family, if they, it's a problem with a sodium channel gene in the heart, but particularly in people who have a history of having had collapses syncopal episodes themselves or any family history of sudden cardiac death. And you see this ECG they need to be seen by a cardiologist because they probably need um an eye CD inserted. So an implantable cardiac device because there's a risk that this just like the long QT could, could go into a serious ventricular tachycardia. And unlike the last one, which was long QT and it was caused by something it was iatrogenic by the Clarithromycin. This one's really serious because this is a congenital thing. Um So brilliant. Um So we've got to the end and you got to the uh please, I have a question, can I please? Yeah, I'm concerning the last ECG um If we, maybe I'm not getting the right. I feel that the, the s, um, let's weigh this kind of too deep or is it normal the S wave on VVMV one and V two and V three? Yeah. So you're definitely, so you're definitely right. There's a really big S wave here and it's, it's more like, um, the Q wave is actually like, there's tiny, like there's no Q wave, there's this tiny are wave and then a big S wave. And this is, yeah, that's exactly, you've, you've spotted that, right. Um What is probably more concerning here is the ST elevation after this S wave. Um But yeah, they've got big deep S waves and this is just, it's all to do with the sodium channel that's involved in the conduction. And if you imagine anything that's causing any abnormalities in conduction will really manifest itself with problems with the QRS complex because that's the QRS complex is basically showing your movement of your electrical activity through your ventricles. And if it's not conducting properly, it will either be broadened or abnormal, but you're completely right. But the thing we spot Foreign Burgard A is this ST elevation after that and the T wave, but it's a horrible SCG, hopefully you never see it, but it's one to, to be aware of. Um, and I have heard of someone have it in exam. So I thought I'd put it in there. Um Thank you. All right. No, Thank you for asking. Um So basically we've gone through a sort of a whistle stop tour of how we record the ECGS with the 10 electrodes and the basic pathophysiology of the electrical activity of the heart. Um Then we've gone through a system to a 10 point system. So looking at the way we look at NECG and it's just basically, so you don't miss anything, you go through each section. I know we've gone through those cases quite rushed in the interest of time. Um But really when you're sat down with an ECG, just try each time to go through, you know, looking at, looking at the rate, looking at the rhythm, looking at the access, then going from P wave to PR complex, then to QRS complex, then the ST then the T wave and then you can be reassured that you have not missed anything even when you see something really glaringly obvious to start with, which is like big ST changes. We've gone through some common ECG abnormalities in clinical practice and in exams and we've applied some of these systems with you going through those ecgs, I've shown you. So I hope that was of some help. And I'm really sorry, it's quite noisy here and I'm at work, but I really appreciate you staying on for the, for the end of the day. So hopefully today has been useful for you and please let me know if you've got any other questions? Stunned silence. Lovely. Thank you very much for such an amazing lecture today. Professor. I don't if anyone has any questions for the professor, I think called doctor. I think the we can go ahead. Um If not, I thank you very much for this amazing lecture yet again and I thank everyone else for participating and hope to see you next week. Thank you. Thank you so much for coordinating. I appreciate it. Thank you. Lovely. No problem if I can just have, but I can just have everyone to fill out the feedback form that would be very crucial for us to continue. And I hope everyone has a lovely evening. Thanks guys. Nice to see you all by, by et bye bye.