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Hello, everyone. Can you hear me? OK, just pop up in the chat. So my name is Sara. I'm one of the junior doctors in pediatrics at the moment and I've just rotated out from car cardiology about two months ago. Um So I'm doing the session by myself today. So if we could write down the questions you have during the sessions and ask at the end, I can do AQ and a session with you as well. So firstly, thank you for giving up your Monday evening to go over EC GS. Um I'm sure it would be helpful come ki time later on. Yes. All right. I will start sharing screen now. OK. So today's session is basically just ecg interpretation. We'll go through the basics in terms of what makes up the electrical pathway um of the heart that causes depolarization, contraction and the whole cardiac cycle. We'll go through the basic um algorithm through which we interpret an ECG. So that's going to be a rate rhythm and axis first and then you go through your waves, intervals and segments next and then to end it all, we'll do some cases as well. OK. So firstly to go through the electrical pathway, we've got the essay node in your right atrium right at the top in the corner. And that causes depolarization to go across both of your atria to eventually reach your A V node, which is also placed in and around your right atrium. Your A V node access a sort of break and then propagates that signal down your ventricles through your bundle of his, your right and left bundle branches, your left bundle branch then splits into your anterior fascicle which goes at the front and your posterior fascicle which goes down the septum and up your left ventricle, your right bundle branch just goes down septum and goes up your right ventricle and the fibers that go up your ventricle are called the purkinje fibers. Now, in terms of what this relates to in an ECG, we've got the P wave which is represented by your atrial depolarization. So that's going to be your essay node. Anything that goes down your Bachmann's bundle to your left atrium and any of the depolarization within both of those atria there. And then you've got your ventricular deter, which is represented by your QRS complex. And then you've got the time for your ventricle to actually pump and then you've got your repolarization of your ventricles represented by your T wave. So basics of the ECG as with any data interpretation, always check the name date of birth and your hospital number or address. So three things that identify that patient and check it with your patient in the exam as well. Don't just look at your, your E CG and say you've checked it, mention the type of investigation you have at hand. So that's going to be your E CG mention the date and time of investigations of when it was taken and always say you would compare it to a previous ECG. Now this comes in handy when you're doing something like a stemi where you can see changes within 10 minutes of each other. And you can say there is an evolving change in this ecg denoting acute pathology. The next thing you want to do in an ECG is to check the speed. Always check it's 25 millimeters per second with one millivolt. So all that means is it's going to be this dimension. So the horizontal axis is the time. So one big box is going to be 0.2 seconds or 200 milliseconds. And one small box is going to be 0.04 seconds or 40 milliseconds. And now looking at the amplitude, which is your vertical axis, one small box is 0.1 millivolts and one big box is very annoyingly 0.5 millivolts as opposed to one millivolt. So the first thing you want to do in an E CG is calculate the rate and that you would be doing using the horizontal axis cos it denotes time. The best way to do it is to first know whether your rhythm is regular or irregular. If it looks vaguely regular, just look at the number of big boxes you have between two R waves and 300 divided by the number of big boxes between two R waves gives you the rate. So five large boxes would be 64 would be 75. 3 would be 102 would be 151 box would be 300 BPM or you can do 1500 divided by small boxes. I'm not very good at mathematics. So II never can actually calculate that in my head. So I tend to go either for the 300 method or the easier irregular method where you basically count the number of R waves within the entirety of your rhythm strip at the bottom and times it by six. In that way, the only thing you actually need to remember is you're six times stable and you're winning. So the next thing you wanna do after calculating the rate is look at the rhythm. Some people tend to do rhythm first and then go on to rate. It really doesn't matter because you tend to sort of describe them together. So the first thing is whether your rhythm is in sinus rhythm, the way you can see that is always look for your P waves. And if each P wave is followed up by a QR S complex without any dropped beats. And if the distance between two hour waves is consistently the same across, if all of those factors meet, you're in sinus rhythm, the best way I tend to do it is to fold up a piece of paper max three uh waves on there and just move it along to the next and the next and the next wave. And if it's consistently falling on those dots, more or less, then it is a regular rhythm. So can anyone in the chat sort of put on there? What you think this particular rhythm strip is showing? And someone's put sinus tachy. Yeah. So it's basically sinus tachycardia. As you correctly pointed out, you can see the P waves very clearly. But what's happened is it's just been buried underneath the QR S complex. The only difference is you tend to say sinus tachy when your heart rate is a little bit on the lower side of tachycardia. So if it's around 100 to 100 and 40 100 and 50 then you would say sinus tachycardia. So here you can see there are only two big boxes between which means it's around 100 and 50 BPM. So at that point, you're sort of entering the regions of saying it's either atrial tachycardia or supraventricular tachycardia. So SVT S but you won't be wrong in pointing out that this is sinus tachycardia and same thing anyone in the chart. Tell me what this is summons for done A S PT S VT. OK. So if we look at the QR S complex here, is it? Yes. So people have put down BT now. So if the QR S complex is broad and they're going tachycardic, the first thing on your mind should be ventricular tachycardia. So VT so broad, regular QR S complex with the tachycardia will always be VT until proven. Otherwise, this could very well be SVT with a bundle branch block or something like that. But that will come very, very later on if you see this rhythm strip, the first thing that should be on your mind should be VT, but we'll cover curs complexes in a sec. So rhythm we've covered regular. Now, looking at the irregular rhythms, there are two types. So first you've got the regularly irregular where the RR intervals. So the distance between two R waves is different each time, but there is a pattern to that irregularity. So it keeps going longer and longer and longer drops, longer and longer and longer drops. So that would be your regularity within your irregular rhythm. So some examples would be anyone want to point this one's a bit more tricky. I give about 10 seconds for anyone to pick up on what this is, right? This one is a little bit mean. So I'll, I'll go through it. So you've got the PR interval here, which is tiny and then you can see it getting longer and longer and longer. And then you've got the P wave, but there's no QRS complex that comes after it. And then another P wave with a short pr interval and then a QRS complex and he gets longer, longer, longer, longer drop, longer, longer, longer and drops. So this is basically your second degree heart block, your wen back, heart block where your pr interval slowly prolongs, prolongs, prolongs until a QR S complex is dropped. Any idea what this might be? Yeah, you're right. There is a little bit of ST depression in some of those waves. I think I've been a bit mean here as well. This is something called bigeminy. So when you see normal narrow QRS complexes and then some random beats that look a bit too broad and weird in those T wave inversions, it means that there is a part of your ventricle that's just firing randomly. So this pattern where you've got a normal one and an abnormal one, normal, abnormal, normal, abnormal, it's called bigeminy. And these are ventricular ectopics. So all that means is this is arising from the ventricle and these normal ones are coming through your normal electrical system. And if there are two normal ones followed up by an abnormal one, it's called trigemini. So all this means is it's an irregular rhythm that puts you at a higher risk of having things like heart attacks and BT S and cardiac arrests and the most commonest of all presentations, your irregularly irregular rhythm, just by saying, irregularly irregular. What do you think this might be? Yeah. Yeah. Brilliant. So, the chat I can see people are putting down af so this is af essentially you've got no P waves whatsoever. And as you can see, there's no pattern to those QR S complexes at all. They're just sort of randomly coming in and going out. So it's one of these rhythms where you would be counting the number of QR S complexes and timing them by six, because there's just no way you'd be able to calculate a rate without doing that, you'd have to take an average over 10 seconds. So the next thing after rate rhythm is your axis, axis is basically the general direction in which your electrical depolarization is happening across the heart. So in a normal person, it's going to start the sa node and just work its way down and a little bit, it's going to go up, back up your walls of your ventricle. So when you take the average, the majority of your signal is going down and left, essentially what this means in an ECG is always look at lead one and vs and if the QRS complexes are both positive, in other words, they're both pointing upwards, you've got normal access, left axis deviation is when your majority of your signals are going up and left as opposed to down. And left, the way it translates in an ECG is if you look at lead one, the QR S complexes would be positive. So pointing upwards and lead A VF is going to be negative. So pointing downwards and the way I tend to remember is leaving, starts with an L. So left axis deviation. So lead one is at the top of your ECG and aVF is at the bottom. So if they're pointing away from each other, they're leaving each other. And that means left axis deviation, this can sometimes be normal with increased age just because your heart gets chunkier as you age with hypertension and all those comorbidities. And that can cause a bit of left axis deviation. The other thing is if you have left bundle branch block. So remember this is your left bundle. If you knock this out, the majority of your signals will have to travel through the heart to reach your left ventricle. So from your right side, they will have to travel up and left to reach your left ventricle. And as a consequence, you'll have your majority of your signals going this way, causing a left axis deviation with the left bundle branch pattern. The other thing is ventricular pacing. We'll go through that in an in a later slide because it's a little bit more complicated if you've got inferior mis and they cause arrhythmias like VT S to come from there, inferior mis affect this area. And if an arrhythmia is coming from here. It's going to spread to the rest of your heart in that direction. And therefore you'll have a left axis deviation. So left axis deviation is the main things you want to remember is if your left ventricle is chunky, you're going to have it. If you have a left bundle branch block, you're going to have it. And if you have a ventricular pacing, you will have it right axis deviation is the opposite. So you have a returning pattern. So lead one is going to be negative, pointing downwards the R wave and your aVF is going to be positive, pointing upwards. So they're going to be pointing towards each other returning starting with an R and therefore denoting that it's a right axis deviation. So the things you tend to see it in is if your right ventricle is chunky. So if you have a huge right ventricle, right heart strain from things like PE or CO PD causing Cor Pulmonale, all of those things are going to cause a larger mass on the right side, which means the majority of your signal is going to be traveling towards that right side and downwards, which is why you'll have a right axis deviation pattern. If you have an an lateral A and arrhythmias are arising from there, your and interlateral a affect this area. So if there is an arrhythmia that affects this area, it's going to be traveling down and right, causing a right axis, deviation, extreme axis is not something you would be seeing very often. It's when the deter is on the exact opposite direction to normal. So if you've got something that's coming out of the bottom of your heart, it will cause an extreme axis deviation. So you'd only see it after something like an M or if they've got conditions where there are deposits in the heart like cancer, sarcoidosis, amyloidosis, all of those things that causes arrhythmias to arise from the lower part of the ventricles will travel upwards and towards the right. So these, you don't see very often at all and for these, you'd have both negative. So normal axis is both positive left axis deviation is leaving. So lead one will be up. AVF will be done, right? Axis deviation is returning. So lead one will be done. AVF would be up and your extreme axis deviation is both of them are negative. So moving on to P waves, P waves represent your atrial depolarization. This should be about three boxes in with just the P wave, not the pr interval and it should be positive in your lead two. So if your P wave is tall and peaky like this, does anyone know what that is caused by, if you pop in the chat atrial dilation? Yeah. So it's going to be something that affects the atria, isn't it? So very correctly pointed out, it's going to be something that affects the atria in the sense that that signal is bigger. So the atria itself must be bigger. The out of the two atria, the one that causes all of those signals to be produced is your right atrium. So if that one is bigger, you're going to have a bigger signal, a taller signal. So this particular pattern is called P Pulmonale where you have right heart strain causing right atrial hypertrophy. So if your right atrium is chunky, you're gonna have a tall P wave and it's called P Pulmonale Pul. The way I remember is pulmonary is always related to the right side. And therefore P wave P Pulmonale must be the right and it's taller because that's where all of the signals start, excuse the disgustingly drawn drawing there. But if your P wave is split up like that, it's also caused by atrial hypertrophy, but it's the left side. So as you can see, the signals will have to travel through the Bachman bundle to reach your left side. So if this side is bigger, there's going to be a delay peak of your P wave. So you're going to have a normal peak of your P wave, which is going to be your right side and a delayed second peak, which denotes your left side. So this is called P mitrale mitral valve is on the left side. So that's a good way to remember. This is your left sided atrial hypertrophy that causes this anything that causes left atrial hypertrophy. So things like mitral stenosis causing more strain on your left side. From things like rheumatic heart disease can cause P mitrale. So tall and peaky is going to be ap pulmonale caused by your right ventricular hypertrophy split is going to be P mitrale from your left side. Now, pr interval which is more important um denotes the amount of time your atria take to depolarize and for that depolarization to reach all of your both atrium and reach your AV node. This is normally between 3 to 5 boxes. It shouldn't be longer than five boxes in a normal heart. But if it's longer than five boxes, then you need to start thinking about things like heart blocks. So can anyone tell me what this particular pr interval changes? You can see that going upwards. Yes. So someone's put delta wave in the um comments. So basically, you've got a shortened pr interval here where you've got an upwards going wave reaching into the QR S complex. So it's caused by preexcitation of your ventricles. So instead of going through the normal, slowed down a V node and then downwards into your ventricles and then depolarizing your ventricles, got a random extra pathway that deters your ventricles prematurely. So instead of having that pr interval, you end up having an upslope from that P preexcitation. So conditions like Wolff Parkinson White disease can cause this and this if you count from the beginning of the P RP wave and to the end of the PR interval, you've got about 123456 boxes. So you've got a prolonged pr interval with normal QR S complexes. So what do you think this is? So it's the pr interval that's prolonged from the P wave up until the Q wave, first degree heart block. Yes. So if you've got a prolonged pr interval with regular QR S complexes, and it looks like sinus rhythm. And the only abnormality is the fact that the pr interval is prolonged, it's going to be a first degree heart blocks. So we'll go through the heart blocks in general. So this is going to be your second degree heart block. We saw an example of this earlier where you have a short pr interval, slowly getting longer and then you drop a beat and then slowly getting longer and longer to drop a beat. So when your pr interval progressively lengthens until a QR S complex is dropped. And then for that pattern to repeat again, it will be called your first sorry Mobitz type one, Wey Bag heart block. So it's your type two heart block, second degrees. Anyone know what this is? It's a little bit more sq out of the heart blocks. So this is your Mobitz type two. So essentially the way you know if it's Mobitz type one or type two is to look at your pr interval and see if it's consistent. So you can see that the pr interval isn't really changing. It's the same throughout what's different is occasionally you have a dropped beat. So you've got a normal pr interval with a dropped beat here and there. Meaning this is a Mobitz type two heart block and the last one, if I annotate the P waves and the R waves, can anyone tell me in the comments what type of heart block this is? Yeah. So it's third degree heart block. The way you can tell a third degree heart block is to look at the P waves and R waves separately. As you can see, the R waves are equally distant from each other and the P waves are equally distant from each other. But the thing is they're not talking to each other at all. They're just doing their own thing. So your Atria just pumping in accordance with your P waves and your ventricles are pumping in accordance with your S complexes. So there is just no connect between the top and the bottom. In other words, there is a complete block between the atria and the ventricles. So a complete heart block. The other thing to look at when you're looking at complete hub blocks is the width of your QR S complex. If it's broad, then you say it's a ventricular escape rhythm. In other words, the escape rhythm that escapes death is coming from the ventricles or if it's narrow like here is going to be called a junctional escape rhythm. So that originates from either your A V node or your bundle of his. So anything above the bifurcation is going to be safe. It's above the level of the atrioventricular septum. Anything below is going to be a ventricular escape rhythm. So this would be a complete heart block with your junctional escape rhythm. Now, moving on to QR S complex, I never understood this when I was a medical student, but going through it with a very simple aspect, your first Q wave is represented by your septal depolarization. As you can see the bundles are closer to your left side rather than your right. So the initial depolarization happens from left to right. And if you remember the normal axis, it's right to left. So you're going in the opposite to the normal axis, which is why Q waves are downwards. So you get a downwards initial spike due to septal depolarization. And then you got your R wave which is your predominant downward depolarization down deception to reach your apex. And then you've got your S waves which are basically the upward depolarization up the ventricular walls. There are loads of different pathological reasons who'd have QR S differences. So some parts with Q wave problems would include pathology in V one and V three. So you should not be able to see AQ wave in your V one V two and V three leads. So if you see those, that means that there is pathology and in terms of your S waves, if you see an S wave in your lead, one, then think along the S one Q three T three pathway that generates pe. So QR S complexes can be split into broad and narrow. So the narrow QR S complex is when the QR S itself is three boxes or smaller, this doesn't mean it's necessarily normal. So normal can be narrow but abnormal can be narrow as well. So things like SVT um normal sinus rhythm, af flutter, all of those things will have a narrow narrow complex. All this means is whatever is coming down to the ventricles is arising from the atrial area. So above the septum, so a bundle of his V node, sa node, any parts of the atria. If your signal is coming from those regions, you're gonna have a normal QR S complex. Broad QR S complex is when your QR S itself is 33 longer than three boxes, three small boxes. So if it's wider than three small boxes, that the rhythm is arising from below the bifurcation. In other words, if it's coming from the right bundle, it will have to go all the way across the heart to reach the other side, taking longer to depolarize the ventricle. And therefore, you would end up with a wide QRS complex. So this is when you have your ventricular problems. So VT VF, complete heart block with ventricular escape rhythms, bundle branch blocks. So right bundle branch, left bundle branch, all of those things will give you a broad QRS complex. So anything atrial is going to cause a narrow QR S complex, anything ventricular is going to cause a broad QR S complex. So to simplify it from sort of conditions, you have your atrial tachycardia, atrial flutter fibrillation, normal sinus rhythm. All of these things will come from your top atrial area. So narrow QR S complex, your ventricular rhythms like VT VF and complete heart block with ventricular escape rhythm is going to come from your ventricles and therefore broad QR S complex. And the only exception is if you have an SVT, which is AAA rhythm that arises from the top area, which is your Atria, but you would need to have aberrancy. So all that means is have a bundle branch block on top of your SVT to cause that. So can every like, can everyone see this E CG? OK. If you can, can you tell me what these basically mean? These little lines here? You've got your little spikes and the ECG here, can anyone tell me what those are? Yes. So someone's put down pacing. So this person has a dual chamber pacemaker, which is the most common type of pacemaker that we tend to put in people. So you've got one lead in your right atrium sensing what's happening in your atria. And you've got a second lead that's in your right ventricle. This is the one that paces. So essentially what you've done is you've got one lead in your heart in your ventricle in your right side, that actually tells the whole of the heart to pump whole of your ventricles. In other words, you've given yourself a left bundle branch block because your l left, right ventricular lead, sorry, your right ventricular lead essentially acts as a right bundle giving you a left bundle branch block. So as you can see here, the QR S complexes are going to be wide because the only thing that tells the entire heart to be is on the right. And therefore, we'll have to go across the heart to deter the other side taking longer. So you end up with a broad QRS complex with a left bundle branch block pattern. And the only way you know, this is not pathological is because you've got those pacing spikes. If you've got a left bundle branch block pattern with no pacing spikes, then you panic. But the fact that you've got those pacing spikes here would mean that that's normal. You've got that left under branch block precisely because you've got pacemaker in. Let me zoom into this. So now if you look at this pattern just at this region, this is essentially the same rhythm, same pattern as the the previous ECG that showed pacemaker without those pacing spikes. So essentially what this is, is your left bundle branch block go through the reasons. So the first thing you wanna look at is your QR S complex and how broad it is. So you've got broad QR S complex, which means whatever rhythm this is is coming from below the level of the atrioventricular septum. Sorry. It's just, I think lots of time. There we go. So essentially because you've got a broad cis complex, all of that rhythm is coming from below the atrioventricular septum. So it's got to be either a bundle branch block or anything below that. The way I remember left under branch blocks is through William W is going to be the pattern you see in V one and you're going to see an M shape to the QR S complex in your V six. Now, this doesn't usually happen in your right bundle branch blog. So you tend to see it more often. But with left bundles, you don't see a classic W and a classic M, what you tend to see is the loss of Q waves that as you can see, usually in a normal heart, you're going to have the Q waves going this way left to right in the left bundle branch block, most of your depolarization is happening in the opposite direction. So in your V one to V six, you shouldn't have any Q waves at all. So if you don't have AQ wave at all, that's an indication that it could be a left bundle branch with broad QR s complex and look at the R waves in V five to V six. It should be positive and sometimes you can see a little notch at the top. So if in your iski, if they're giving you a left bundle branch, they're most likely gonna give you one with the VII pattern in it. They won't give you a more difficult one without that. The other thing you're going to have in your left bundle is your left axis deviation, as we said, because your left bundle is knocked out and the only functioning bundle is your right bundle. The majority of your depolarization is happening from the right to the left causing left axis deviation. You also have this thing called appropriate discordance. So all that means is if your depolarization is abnormal, your rep polarization is also going to be abnormal. So you've got this sort of ST elevation that you can see here with T waves that follow it as well. So this ST elevation in context of the left bundle branch block makes sense because you've got abnormal depolarization followed by abnormal repolarization. So this would fit with just a left bundle branch block, but that's not going to be something you're going to say as an F one or a medical student, you see ST elevation with left bundle branch block, you always treat it as a stemmy. If you see tall ST segments in two or more contiguous leads. You always say it's a stemmy, get serial ecgs and your troponins going and then you can investigate later on and say this is a left underground block. Nothing more. The important thing to remember is left under branch block is not normal. It's very rarely just normal in people. So there's always a pathological reason why you have it, whether it be a stemmy, most common cause or dilated cardiomyopathy, left ventricular hypertrophy. So if your left ventricle is chunky, you're going to have this pattern. And if you have an mi you're going to have this pattern. So if you have a left bundle branch block pattern, always think stemmy because it's better for you to rule it out rather than miss it and then regret later on. Now, if I tell you this is the opposite of the left branch block, what do you think this is any ideas as to what type of E CG this is? Yeah. So a few people have texted on the chat saying it's right on the bra pattern. You've got the bunny ears M here and you can somewhat appreciate a tiny, little downward spike here up and then down again showing a W pattern here. So M and A W. So marrow is the way I tend to remember M at the top V one and W in V six with marrow R in the middle, right bundle branch block. Uh Let me zoom out. So again, you're going to have a broad QR S complex because we're at the ventricular level below the atrioventricular septum, you're going to have a marrow pattern and a wide slurred S wave. So that comes with a W so as you can see here that s wave is wider than the rest of the QR S complex. So this is going to be a right bundle branch block pattern. This can be normal in, in about 5 to 10% of the population. You can see this um in the elderly population to be normal. But at the same time, you don't want to be missing pathology. So there is growing evidence to suggest right under branch block can be an uh an idea of inferior stemmy as well. So if you're ever in doubt if the patient comes in with chest pain or sweating and all of the symptoms that makes you think of a heart attack regardless of the ECG always do troponins and go through that procedure and get Sarah Ac GS. Again, you can see some appropriate discordance. In this case, some ST depressions and T wave inversions and these are normal in the context of a right bundle branch block. But again, if you see ST depression think and semi first and then you can rule it out afterwards, these are course majorly normal and then you've got your right ventricular hypertrophy. So if your right ventricle is chunky, you're going to have a right bundle branch block. And the more common sort of acute presentations with right bundle branch blocks are going to be your pe because you've got your right heart to do a lot of work. Meaning you end up with a right bundle branch block and your core pulmonale following your COPD patients. If they've worked and worked and worked their lungs over years and years, you're going to have core pulmonale right ventricular hypertrophy causing a right bundle branch block. The key thing to note in your right bundles is that your axis is usually normal. As you can see here, this one is sort of neutral, not positive, not negative, but this one is positive. So they're not really leaving or returning, they're not doing anything. In other words, this is normal axis. If you have left axis deviation with right bundle branch block. So if these two are leaving and you've got this pattern, your V one to V six, then you would consider anterior fascicular block with the right bundle branch block. So your right bundle is knocked out and your anterior fascicle is knocked out if you've got a right axis deviation with the right one branch block. So if these two are returning, so this downwards and this upwards with this pattern in VV one to V six, then you would think of posterior fascicular block. So this one is knocked out. The other thing to sort of note is your pseudo right bundles. So this is just one condition. You've got something called Brugada syndrome, which is an electrolyte channel problem that's inherited. And as a consequence, you end up with some ST elevation in your V one area with an M shape and your V one as well tends to be V one to V three sometimes and you get a bibasic T wave as well. So M shape and your V one to V three with ST elevation and at wave inversion can be Brugada syndrome as well. Next thing to think about is amplitude. We don't really consider this much in an acute setting because if your, if your patient is acutely unwell, you don't really need to think about conditions that would cause the sort of tallness or shortness left ventricular hypertrophy would obviously cause your V one to be two R wave to be taller. So because your, your left ventricle is so chunky, the amount of depolarization that gets to the leads to cause that amplitude is going to be higher and same thing with your right ventricle, but essentially the flip of it. So S wave is going to be taller in your left ventricular hypertrophy R wave is going to be taller in your right ventricular hypertrophy. So RR is a good way to remember in V one and V two and the opposite in your vsi V five to V six one. Key thing you can potentially have is electrical alternatives So all this means is you got one tall QR S complex, one short QR s tall, short, tall, short. So your electrics, your amplitude is alternating electrical alters. So this happens when you've got your heart pumping forward and then backwards. And the condition this tends to happen in is if your heart itself is surrounded by so much fluid with every pump, it ends up shooting forward and then backwards and then forward and backwards. So essentially your heart swings towards your leads and then away from your leads causing a tall QR S when it's towards your leads out of your chest, and then a short QR s when it's away from the leads back into your chest. And the condition you tend to see this is in T or severe pericardial effusion and moving on to the ST segment, the most likely thing to turn up in your sy, you've got elevation and depression, which are the most important ones, elevation in your limb leads. So that's going to be your 123 A V once as well. Um If it's one small box or a box, if it's any taller than one small box, then that's considered elevation in your precordial leads, it's going to be two small boxes. If it's anything more than that, it's ST elevation, the most common thing or the thing that you should always mention in your is cases is the fact that it's caused by stemmy. If there are two contiguous leads with that elevation, we'll go through what contiguous leads are in a second. Other causes as we've already discussed would be left under branch block that causes ST elevation. Brugada can cause it as well. Prinzmetal Angina. So if, if, if you haven't heard of Prinzmetal Angina, it's basically your coronary vessels going into vasospasm. So they start going like this, meaning you're not getting much oxygen and blood flow to that sort of ventricular ventricular area that follows that spasm. So you get transient ischemia causing ST elevation. And once that spasm sort of resolves itself, you won't have ST elevation anymore. So that would also cause you ST elevation, other causes you've got pericarditis. So pericarditis, ST elevations is going to be throughout all of your leads. So you're going to not have just one contiguous set. Instead, you're just going to see ST elevations across all of your leads B1 to B6 A VRA VL. Everything's going to have your ST elevation. If you see an everything, think pericarditis, perimyocarditis is very similar as the same thing as pericarditis, but you've got your myocardium involved as well. So both of those things is going to cause your saddle shaped ST elevation throughout your ecg Takotsubo. If you haven't heard of it, it's called also the broken heart syndrome where your uh your heart sort of balloons out in the end, essentially causing a lot of ischemia, a lot of bruising and all of those things, which is also going to cause your ST elevation. Other things that can cause ST elevation pe if you end up with a pe massive enough to cause right heart strain and raised ICP as well. So if you've got a patient that's come in with a brain bleed, they're going to have an abnormal ECG. The pattern tends to vary patient to patient. But if you've got a patient with a brain bleed, always do an ECG as well. And they tend to have ST elevation, not necessarily mean that they've got stemi, it could just be that they've got a brain bleed. Now, moving on to depression, that sound sad, moving on to SD depression. You want to look at your V one to V two leads. And if it's anywhere more than half a box, half a small box, then that's depression and all of the leads anywhere bigger than one small box of lowering is going to be your ST depression. These are just for extra information. Essentially, you don't really need to know down sloping and up sloping and sagging. If it's depression, ST depression, then it is ST depression. And the first thing you want to think about is if there are two contiguous leads involved, it's going to be uns stemmy and you want to rule it out, which means do your troponins, do your serial ecgs and then you can think about everything else. You can also have ST depression as a part of reciprocal change. So if you have a stemi, you've got ST elevations in some of the leads and leads that come opposite to it will have your ST depressions. Other things that can cause it is includes tachycardia. So if you're exercising and you do an ECG at the same time, you'll see those ST depressions because your heart is going so fast and you're causing ischemia because it's beating so fast. And as a consequence, you'll have ST depression and that should resolve as soon as your heart returns to normal rate. Other causes include hypokalemia, right or left bundle branch blocks as we've already talked about before and right, ventricular hypertrophy and left ventricular hypertrophy just because your heart is so chunky, it's struggling to get the amount of sort of blood supply and oxygen that it needs. And as a consequence, you end up with some ischemia that causes ST depressions J point is essentially this area. So right at the end of your QR S complex, and if there is a positive deflection at your J point here, it's quite suggestive of these conditions. So firstly, you've got your Brugada syndrome. So if you see that J point deflection in your V one, think br Brugada hypothermia can cause J point deflection as well. But at the same time, if you think about it, hypothermic patients are going to be cold and shivering. So the trace you tend to get on these patients, you can't really identify J point and all the rest essentially because you're going to be so filled with artifact that you can't see all of those things. Another thing that can cause it is hypercalcemia rather than an ECG your history is going to give you that picture. So if you see AJ point in your V one, that's high digestive gata, everything else can be ascertained from better from history examination and blood tests. Now contiguous leads. In terms of the E CG, you've got lead 123 in the first three A VRA VL and A VF in the next two. And then B1 to 6 organized in this way, the way I tend to remember which region comes, where is the, is stand for inferiors. L stand for laterals, A stands for septal and A stands for anterior. So the way I remember is the inferiors are in the inferior corner, sort of pushed away in the bottom, your laterals or on the lateral ends. So on the outside and your septal and anterior are in the middle. So inferior in the corner, bottom corner, laterals in the lateral septal in the middle and the anterior just sort of leaks away from the septal and VR is useless. That's how I used to remember the ECG S. There's also the big lie, little eye and all as well. LAC is denoted by the circumflex artery. So if you can see that's the circumflex artery there coming around the left ventricle. So it's on the lateral side and therefore, it is the lateral circumflex artery is on the lateral side and denotes the lateral sections. Inferior artery, inferior section is denoted by the right coronary artery. So you can see this is the right coronary artery going on the inferior aspect of the heart. And therefore, it's the inferior anterior and anteroseptal is the left anterior descending. So the artery that comes down here supplies the middle of your heart to the septal region and the front of your heart. So, anteroseptal is your LD and it's donated by B1 to B four. Finally, we've got the out of the waves, we've got T waves, T waves can be inverted, flattened, peaked or biphasic. The first thing you wanna see is if it's inverted the wrong way around, if it's pointing downwards as opposed to upwards, then you think Nstemi that should be a top one. The other thing is if it's invested in V one, it can be normal in most people including adults. But as you age, it should flip, essentially, it is normal in lead three in everyone and AVR as well, you can have some T wave inversions in pe. So the S one Q three T three pattern, you've also got your left bundle branch blocks and right bundle branch blocks that can cause T wave inversions as a part of that appropriate discordance and other causes include digoxin toxicity. And raised ICP. So raised ICP can cause anything and everything flattened. So your T wave, instead of being a nice up and down pattern, if it's sort of flat, it can be caused by your hypokalemia. So hypo falling to the ground potassium. So T waves are affected mostly by the potassium because it's repolarization. So if you think potassium affects T wave, if it's flat, it's on the ground hypokalemia. If it's peaked, it's going up hyperkalemia. So T waves equals potassium, low hypokalemia, high hyperkalemia. If it's biphasic, it means that it's up and down. So as opposed to starting and ending in the same plane, it will go up and go below the level, it started in and come back up. So this will be a bibasic T wave here. So if it's initially positive, it can be something called Wellens. It's essentially a fancy stemmy and Brugada, which we've already discussed causing ST elevation. So essentially, you've caused an ST elevation which sort of merges into an inverted T wave causing a biphasic T wave. If you've got ST elevations, you can get that sort of positive to negative bibasic T. If it's initially negative, it's hypokalemia just think negative equals on the floor hypo. Now, finally QT intervals. So this is when this begins at your QR S complex. So from the beginning of your QR S complex Q wave to the end of your T wave and it's a little bit longer and normal in women than men. So men, it's normal range should be below 440 milliseconds. So that's about 11 small boxes and in women it's 460. So 11.5 small boxes, it is affected by rate. So if someone is going extremely bratty, you QT interval is going to be prolonged just because they're going very slow and equally if they're going very, very fast, if they're in tachycardia or AF or, or whatever, it's going to cause your QT interval to shorten artificially just because the rate is so fast. So always look at the calculated QT interval. So QTC will come up at the top of your ECG S unlikely that it would be that easy. In your, in your case, you won't, you won't be expected to calculate a QT interval. But if it, if their rate is around 60 BPM, you don't need to calculate a QT co it's the corrected QT interval is calculated according to a rate of 60 BPM. But if they're going at 60 you don't need to calculate it anything above or below, then you would need to calculate. The calculation is very complicated and therefore, you will not be expected to do it in your ache prolongation is caused by loads of things. So the way I remember it is the hypos, hypokalemia, hypomagnesemia, hypocalcemia, hypothermia. So the first three are all of the electrolytes, any of the electrolytes that go down will cause your QT to be prolonged and hypothermia again, your QT interval to be appreciated in a shivering patient giving you an ECG is going to be quite difficult and whether that's going to be useful in you treating the hypothermic patient, I'm not too sure, but it can also cause your QT to be prolonged. There are congenital conditions that cause long QT syndrome. So long QT 12 and three, as well as the congenital conditions, Rama Romano Ward, and Gerbil Lange Nielsen. So Romano Ward is autosomally dominant. So if only one of the parent of your, your patient has it and it's seen in every generation of the family, then you would think it's more Romano Ward and ger gerbil lounge. N is the autosomal recess recessive one and it's also associated with sensory neural hearing loss as well. So if you've got a person with hard of hearing as one of the symptoms with a Long Qt syndrome, then you would think more on the J Ln condition as opposed to Romana Ward. The other one is your drugs. A lot of drugs cause your QT uh interval to be prolonged. I remember it as the anti. So you've got your antiarrhythmic. So the more common ones are your amiodarone and Cetalol. Both of these prolong your QT interval. Then your antidepressants, antipsychotics, antihistamines and antibiotics. All of those things cause your QT to be prolonged. There are particular antibiotics, antihistamines anti, well, most antipsychotics and some antidepressants that cause it so have a read of the specific drugs that cause QT prolongations. It's not an exhaustive list. It's not very long. So if you just remember the anti being the way you remember, it can help and the hypos being another way to remember as well. Shortening is only caused by one thing hypocalcemia. So if you think about it, having loads of calcium would mean that you'd be able to pump your muscles a lot faster. In other words, your kids intervals is going to be shorter. So in summary, the way we interpret an E CG, just say what you think because you're going to be looking at the rate. If you're calculating the rate in your head, just say it out loud because it will tell the examiner that you have a systematic approach. It always go through your systematic approach of identification looking at what you're interpreting, having something to compare it against and then your rate after checking your speed rate, rhythm access P waves, pr interval, QRS complex ST segment T waves and QT interval. If you have that, even if you don't come to a diagnosis at the end, at least you've interpreted your ECG appropriately, always offer differentials at the end of your interpretation. It doesn't matter if it's an E CG doesn't matter if it's a chest X ray offer a differential at the end. It means that you're interpreting and not just looking at it and see what you're seeing. So it's good to say what you see, but also make sure you tell your examiner you've thought about what you've seen and you're telling them what you think it means, familiarize yourself with the Tachycardia and Bradycardia guidelines. So there's a really good tachycardia guideline or a pathway where you see whether it's narrow or broad complex. And there are very specific things you do depending on those the sort of values and flow chat. So if you familiarize yourself with those, a lot of the acute stations can cover that. So things like someone who's come in with very hard, very fast heart rate and then you do a cardiac monitor on them and you see narrow complex tachycardia, it's quite easy to just flow through if you know the um guidelines and the pathways used. So familiarize yourself with the tachycardia and bradycardia pathways and also your cardiac arrest guidelines as well, right? If we go through cases now, Missus Lucas is a 27 year old woman who's pregnant G one P ZERO. Since this is her first ever child, she's 20 weeks pregnant and she's come in for her 20 week scan. Her observations are done when she arrives and her heart rate is seen to be 100 and 80 BPM. So the poor healthcare panics and does a BP which comes back 100 and seven bet. 100 and 7/68. She is otherwise completely fine. She just says her heart is going a little bit fast. She's alert and responsive and is talking to you. So she's slowly moved into a bed and an a toy assessment is done to obtain a 12 lead ECG Interpret this ECG What do you think is happening? You pop in the chat, I give you a couple of months. Yeah. So someone's popped in the chat S VT narrow complex tachycardia S VT. Yeah, so brilliant. So this is a narrow complex tachycardia. Someone has very rightly pointed out which one of the differentials is going to be your S VT. So all you need to think about here is it's regular. As you can see here, it's the QR S complexes are equidistant from each other. You can't really appreciate ap wave anywhere because it's all buried. But you can see that it's nice and regular and you can see that the rate is very, very fast. The axis is normal, both pointing positive and looking at the P waves not there. QR s complexes are narrow, you can't really appreciate any of the ST segments. The T waves are not necessarily tall in all of the leads. So this is going to be a narrow complex tachycardia or S VT. So appropriately, she is now on a cardiac monitor and vagal maneuvers are performed. So this woman is asked to blow into a 20 mL syringe very hard, very quickly, carotid sinus massage is performed. None of this is successful. So, following the tachycardia guidelines, you go on and give to her 6 mg of IV Aena, you notice that her rhythm on the monitor is very different to what it was before. So you obtain another 12 lead E CG, she's still awake but starting to feel more funny and more drowsy interpret her E CG. What do you think is happening here? Ventricular fibrillation? Yeah. The third point. Yes. How would you describe this? Because ventricular fibrillation and to de pointes are sort of diagnoses, aren't they? So if you had to describe this ecg, what would you say? We said narrow complex tachycardia for the last one, what would this one be polymorphic tachycardia? Yeah, that's good as well. So you've got broad complex, don't you? So last one, if we can see the QR S complexes are very, very narrow. So this one is the opposite side. You've got your broad complex QR S complexes we're growing still very, very, very tacky. And as someone has very correctly pointed out, it looks very fibrillatory. So it looks, especially if you look at the rhythm strip here, just looks very, very, very fibrillatory. So the way to sort of distinguish between sa de pointes and ventricular fibrillation is to look at the rhythm strip because if you look at RV three and V six, the amplitude is going to be different in each of those. So if you look at the rhythm strip, it's fairly consistent. It's just looking very fibrillatory as opposed to going up and down. And you don't see that sort of classic turning of the points. So this could very well be do at the point and I could be very, very wrong. But all we can say is it is polymorphic in that it's coming from different parts of the ventricle and is fibrillating and the ventricle is basically going like this so well done for identifying that. This is a scary, scary rhythm. So, can anyone in the chat tell me why, what condition when given adenosine can cause this? So if we remember the lady had S VT in the beginning and we've given her adenosine and she's gone into this rhythm. So, w what condition when given adenosine causes ventricular fibrillation or the cyto point or anything that causes broad complex tachycardia? It's a very, very tricky question. So if I say it's actually no, it's a very, very mean question. So I'll just give you the answer. So there's one condition where you have SVT, but it's contraindicated to give adenosine to if you know that they have that condition. And that's Wolf Parkinson white. So essentially heart block. Yes, someone's foot, maybe wolf Parkinson white, well done. So wolf Parkinson white is a condition where you have an accessory pathway from your atria to your ventricle. So you don't have the normal break of your A V node. So your A V node prevents your heart from going at rates above around 100 and 80 to 200 sometimes 220 you don't go very, very, very, dangerously fast and you don't destabilize your ventricles from it. Whereas your accessory pathway bundle of Kent has none of that breakage. So it doesn't, you know, stop your heart from going above a certain rate. So if you have bundle of Kent and your A V node is completely knocked out by adenosine, so the way adenosine works is by completely shutting down your A V node, all you have left is that bundle of Kent which has no breaks. So essentially you put your ventricles into overdrive, pushing them into ventricular tachycardia, ventricular fibrillation, do the point. Any of those conditions can be caused by just giving adenosine, which is why if you're thinking of giving adenosine always have defibrillator pads on them. So this patient having gone into BF, you can just shock them back. Whereas if he didn't have pads on them and he gave them adenosine, he would have pushed them into ventricular fibrillation. And there would have been a delay until when the patient gets the first shock. So if you're giving adenosine, always get your pads on because when they're in this kind of rhythm, you can't tell if it's caused by Wolf Parkinson white unless they give you a history of wolf. Parkinson white, unless you're a cardiology consultant or whatever. It's impossible to tell whether they actually have Wolf Parkinson White when they're going this fast. So follow the guideline, give them adenosine, that's completely fine. But if they go into this rhythm, shock them back. Adenosine has a half life of about 15 seconds. So it's going to run out and you're going to go back to your normal rhythm anyway. So it's fine. So long as you have the pads on. Now, case two, Mr Collins is an 86 year old gentleman with a background of hypertension and persistent af on Ramipril 5 mg and Bisoprolol 5 mg OD. He has been taking these medications for over five years. He's completely compliant with them. He's happy with those medications he presented to A&E with three episodes of transient loss of consciousness over the last three months. Please interpret his 12 ladies fee. What do you think is happening here? This is a slightly tricky one, but go through that process of rate rhythm access and then P waves complexes. T waves and then your intervals. All right, if we go through it sort of systematically, let's look at the rate first. So there are about 12345676 to 7 because it starts at a QR s and it ends at a QR. So I feel a bit mean, including both. So we'll say 6 to 76 would mean 36 BPM and seven would mean 42. So something between, so let's say 38 BPM, very, very bright. And you can see the QR S complexes are regular equidistant from each other. So it's a regular bradycardia and the axis, they've got a bit of a left axis deviation here, not, not very relevant, but we'll move on. I can't really appreciate any P waves in the lead two. So that should already give you an idea of what this condition might be in your background. No P waves in lead two, always think atrial fibrillation. So no P waves that I can appreciate and lead to looking at the QR S complexes. Now, I can see that they're quite broad, about four little boxes. So we've got a broad QRS complex and a normalish T wave pattern. So essentially what we have here is regular QR S complexes with the background of atrial fibrillation, which shouldn't really fit. So if you have atrial fibrillation, your QR S complexes should be irregular, especially if you're just rate controlled and not rhythm controlled. So if your QR S complexes suddenly revert to regular, then always think there is a block. A patient with persistent atrial fibrillation only rate controlled reverting to regular QRS complexes should always make you think heart block and the fact that the patient has a heart rate in the boots of about 38 BPM should also make you think this is a hot block of sorts. The fact that the QRS complex is broad and not narrow should make you think it's a ventricular escape rhythm making this an emergency. So complete hub blocks with an escape rhythm that arises from the ventricular level is an emergency because this has a potential to then go into VTV F type of picture. Whereas if the QR S complex is narrow, then you have a little bit of time to fiddle around with, this would be an emergency. This is a complete heart block in a patient with af case three, a little bit simpler, Miss Heads is a 76 year old gentleman that does not make sense. Who presented with shortness of breath, palpitations, jaw ache and feeling very dizzy and sweaty. He has vomited twice in the last hour. Please interpret his 12 lead ECG. So just from the history, have some idea of what you think this E CG might show. And then if this is what it shows, what do you think it is and give me a territory as to what you think it is as well. This is the kind of E CG you're going to be getting on your excuse. It's very straightforward. It's on your face. You should be able to read this one. Lovely. Yeah, well done. So I've got a few common things. It's an inferior semi RCA, semi well done. You're giving me the arteries as well. ST elevations in 23 A VF inferior, semi brilliant, well done. So you've got your inferior corner, you've got your SD elevations here. So that denotes the fact that it's an inferior stemmy. And as someone has rightly pointed out in the comments, it's caused by an RCA infact case four MD. Long is a 65 year old gentleman with a background of previous anterior stemi and liver cirrhosis who has been started on solo for hemodynamically stable current fe. So all the MBO aside, this man had a previous heart attack has a background of liver cirrhosis has been started on solo for some arrhythmias of his heart. Here's the 12 LE CG. What do you think? He's just been started on SOTOL yesterday? I'm sorry, someone has written, what was the last one? I'll go back to it in a second. If we just try and figure out what this ECG is, I'll, I'll go back to the last one if you remember sotalol is an antiarrhythmic and it has a certain effect on one of the segments. Yeah. QT prolongation. So, as you can see here, this is your Q region and this is where your T wave ends. Essentially the whole of the cycle is basically taken over by the QT interval. It's so prolonged and it's caused by the fact that we've started the patient on sotalol. So SOL is one of those drugs that's really good at suppressing a lot of arrhythmias that's not really taken care of by other medications. But at the same time, it's three times more likely to cause a QT prolongation than amiodarone. So, always think in your mind if someone's been started on sotalol, they should have repeat ECG S every day just to make sure their QT interval is not going over a certain limit. Stopping. The medication should make them revert back to their normal QT interval, just go back to the previous. So essentially what I've said here is the fact that you've got lead two, lead three and F this corner is the inferior corner. So it denotes the inferior region of the heart. And that's how I tend to remember it. And the fact that you've got ST elevations here here and here should mean that you've got an inferior Demi ST elevation, myocardial infarction, ST elevation in your inferior regions, giving you myocardial infarction. And therefore, it's an inferior stemi and inferior stemmy are caused by an infarct of your right coronary artery. And you can see here, you've got some SD depressions that are reciprocal to that. And you can see some of that m pattern here as well, which gives you a little bit of an incomplete right bundle branch pattern ugly. Most of my examples from this um presentation are from these two sites. So if you're practicing with your friends, just pick a random ecg out of the sites, ask them to interpret it. Some of them are more difficult than the others start with your easy conditions like atrial fibrillation, semi and N semis and then work your way up from there. There are things that you should be able to see. So P ES pericarditis sties, NSTEMI and atrial fibrillation, atrial flutter and SVT S. These are the things that tend to be the commonest ECG S that come up in exams because they have a recurring pattern that you can think of and easily say very quickly. So familiarize yourself with those and your heart blocks as well. And after that, you can learn the more fancier stuff and these have really good libraries of PCG S on there. So have a look at those. Um Thank you. That's the QR code for the feedback for this session. So if you could fill that out, that would be very, very kind. And I'm happy to answer any questions. Yes. This session is recorded and the recording will be available on meal later on. I'll stop sharing in a second and, oh, no worries. You're welcome. I'll stop sharing for a second so I can return to this stage. Oh, my gosh, it was terrifying. There you go. Thank you very much guys. Thank you for coming. If you have any questions, I'm gonna stick around for a little while so you can pop them in the chat and now I can see the chat very properly. So ask me any questions you have about ecgs. I'm not an expert, but I can answer to the best of my knowledge. You're welcome. And please, please please fill out the feedback form. If you can. It would be much appreciated. I'll put the link of the feedback form in the chat as well if you can. Thank you. Oh, thank you guys. That was very kind. What does P look like, please on an EG? Let me get up an EG actually, so I can actually show you guys. Mm 1232. Yes, I'm trying to find an E CG with the, the good pattern. There we go. That's a good one. Let me share my screen. So you can see it. That's crazy. There we go. So S one Q three T three. So S one lead one, you would be able to see an S wave. So the downward deflection, this deep S wave, you see an S one Q three. So you'd see AQ wave. So always remember S and Q are both downward deflection. Q is the first one before a positive deflection. So Q is down first and then up for an R wave and then S for a down downward wave. So if there is a first downward deflection that's going to be AQ wave seen in the lead three here. And if it's a second downward deflection here, that's going to be a S wave. So S one in lead one, Q in your lead three and at wave inversion in your lead three as well. You'd see these in massive massive pieces like it has to be huge for you to be able to appreciate an S one Q three T three. By that time, the patient is already like breathless, coughing up blood, all of the symptoms you'd see with that, you can also see a sort of m pattern in your V one here. So a little bit of a right bundle type uh pattern which you also see in PPE S. So right bundle branch block pattern can be seen in Pe as well. So it is a really good ECG actually, you can see the M and the sort of slurred S wave here. I'm trying to zoom out, right? Let me, you can see the sled S wave in V six here and an M shape here in V one. So that Dennos a right bundle branch block pattern, which can be seen in P ES as well as AQ sorry S wave in lead one, Q wave in lead three and T wave inversion in lead three as well. Now, these are all fancy versions of what happens in a pe the more common presentation ecg wise you're going to get is going to be sinus tachycardia pe patients come in and the first thing you see is a heart rate of around 100 and 20 100 and 30 BPM and they're in sinus. So sinus tachycardia with shortness of breath, cough hemoptysis. All of those should be pointing those red flags in your mind. This is a pe your S one Q three T three and right bundle branch block patterns are your fancier things. You can potentially see that in your eye ski. Maybe they'll, they'll throw one of those at you. But the more common version is going to be a sign of tachycardia. Hope that helps any other questions. What are precordial leads? Could you explain the bigeminy and Trigeminy? Yes, of course. Let me try and we share my size. Yeah. Sorry, I closed my presentation. I'll bring it back up in a sec. There you go. Share a slide. Mhm By. So your precordial leads actually let's go through that one first. So your precordial leads are essentially your V one to V six. Your chest leads are your precordial leads and your limb leads are 123 V RVF and BL. So Precordial are the chest ones, V one to V six. So the second half of your E CG and the first half of your E CG where you have 123 VRA VL and aVF, they're your limb leads. So that's the two different aspects of leads essentially. So your limb leads are usually a direction between one lead and the second lead. So usually your one is between the one you put on your right arm and your left arm. So it's sort of measuring the, the difference between one and the other. Whereas your precordial are basically just independent leads. You've got V one as its own lead coming out from your heart towards the lead V two is its own V three is its own. There are no two lead associations. So those are your pre cordial leads and your limb leads are always associated with another. So if we go through by Germany, there we go. So these broad QR S complexes here, these broad ones with T wave inversions are basically impulses that are coming from the ventricle. If I bring up a picture of a heart. So instead of your normal depolarization down from the sa node down into your ventricles and up the purkinje fibers, you've got a random place in your ventricle that's just firing. So this could be from scarring from a pre previous m or um things like sarcoidosis where you've got deposits in your heart that causes changes and fibrosis. And therefore, you've got firing from there. So if you've got areas in your ventricle that just fires off randomly, you're gonna get a broad QRS complex that just comes up, that's called a ventricular ectopic ectopic, meaning it's outside of the normal depolarization of your heart ectopic. So if you've got a ventricular ectopic, it's coming from the ventricle and it's outside of your normal depolarization. Now, if it's coming from just occasionally, every now and then maybe every 25 beats, 30 beats, you get a random ventricular topic that can sometimes be normal. But if you're getting it very, very regularly, for example, in your ventricular bigeminies. So here those narrow curious complexes denotes your normal, top to bottom depolarization. Whereas these are those random ventricular firing. So these are more likely to be caused by something permanent in your ventricle, like scarring from a previous M or depositions from sarcoidosis or amyloidosis or something like that. So if you've got something random in your ventricle firing regularly like this, then you're more likely to go into a ventricular rhythm. That's aberrant. So if you've got a random ventricular rhythm that just decides to go rogue, you could go into things like ventricular tachycardia. So instead of having those normal QRS complexes in the middle, you'd just go broad complex, curs fast, fast, fast VT or you could just completely destabilize a ventricular wall causing ventricular fibrillation outside the point. All of those ventricular tachycardias could be caused by having by Germany. This increases your risk of having those um arrhythmias. Same thing with Tri Germany. So Bigeminy two by as in two, you've got one and 21 and two trimon is when you have two narrow complexes, narrow, narrow, wide, narrow, narrow, wide, tri as in three, narrow, narrow, wide, narrow, narrow, wide. So that would be your Tri Germany, same thing with quadra Germany. So if you have regular random QR S complexes that are broad, that are just coming up. So pvcs, um ventricular ectopics that's just randomly coming up very regularly. Then you need to have a cardiologist. Look at your ecg very closely and think about interventions, including suppressing the heart rate or ablating the area that's firing off and causing these essentially. Does that make sense? I know it's a little bit complicated and more nuanced any other questions at all? No worries. Easy to fun. It's difficult, but it's fun if you have any other questions at all. Guys, just pop us an email, we'll have access to the email, so we'll, we'll eventually get back to you. The session is recorded, so we'll put up the recording in metal, so you'll have access to it if you want to go back and have a look. Um But otherwise good luck with your EC GS are fun. So don't be too daunted by them. Once you start understanding them, they will be very, very fun and good luck. Thank you.