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Summary

This on-demand teaching session is a comprehensive guide on chest pain for medical professionals, with a special focus on cardiac causes such as angina and acute coronary syndrome (ACS). The session talks in-depth about various types of chest pains, from stable angina to myocardial infarction and unstable angina, as well as diagnostic procedures, including blood tests and ECGs. The instructor also delves into pharmacology, covering nitrate tolerance and effective treatments including GTN spray, aspirin, beta blockers, and statins. Finally, the teaching session is interactive, featuring a case scenario and MCQ to provide participants an opportunity to apply knowledge. Whether you're new to the field or a seasoned pro, this session offers practical insights to enhance your clinical decision-making process.
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🎓 Join us for an electrifying journey through the world of ECGs based on AC Syndrome 📚✨

Our ECG Lecture Series continues with another insightful session on electrocardiography with a insight on AC Syndrome! 🧠💡

This will be conducted by Dr. Lee and Dr. Lisseter

Learning objectives

1. Understand the different types of chest pain and their potential causes, with a particular focus on cardiac-related chest pain. 2. Learn about the presenting symptoms, risk factors, and potential investigations for stable angina. 3. Understand the treatment options for stable angina, including both immediate symptomatic relief and secondary prevention strategies. 4. Recognize the signs and symptoms of Acute Coronary Syndrome (ACS) and understand how it is differentiated from stable angina. 5. Understand the principles of patient education and counseling in relation to angina and ACS, including instruction on the use of medications such as GTN spray.
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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

You fill out our feedback form. Um When it says, please put your email in, please put your email in and don't say yes. Er, last time some of you guys said yes, but I don't know where your emails are because it's anonymous. So, um yeah, just keep that in mind when, when, if you do want the powerpoint slides. Um So today we'll be presenting er chest pain or A CS um and just a bit of an outline. So we'll just be going um we're gonna be talking about cardiac causes of chest pain. So that includes stable angina um A CS. Um And then that subsection is about unstable Angina stemi ente. And then, because this is an E CG teaching series, um I'll also be going through some EC GS as well. So just to start off with, um I'm just gonna put out this sort of my map of chest pain. Um This teaching is on cardiac causes of chest pain, but I think it's important to begin thinking of chest pain, sort of in the wider sense um as well as sort of the obvious uh cardiac problem because in an M CQ or in real life. Um, the vignette or the patient coming to you isn't going to say that they got chest pain and it's gonna be a cardiac question. They could be coming in with chest pain, but it might be, um, you know, it might be respiratory related. So it might be a pneumothorax that they're coming in with or they might have lifted something heavy and I don't think that it's, you know, a heart attack, but actually it's just like costochondritis when they've just sort of strained their chest wall muscles. Um, so I thought I would just pop this up to, to help sort of see where, um, cardiac chest pain might sort of fall into your differentials of chest pain. So, moving on to what we're actually gonna be talking about today. So, um, so this is stable angina. Um, so it is uh the narrowing of coronary arteries which is precipitated by exertion but relieved by rest or GTN. Er, so risk factors could be hypertension, uh hypercholesterolemia, diabetes, smoking, et cetera, and often patients, uh will come in, they'll be complaining of constricting, um, sort of discomfort in the chest, it might radiate to the neck or the jaw or sort of like left arm pain and in stable angina, characteristically, it's precipitated by physical exertion, um, relieved by rest or nitrates within five minutes. Um, and having that relieved by rest or relieved by nitrates is very important in its differential. So, um sort of to start off with the investigations. I often go, you do the least invasive to the m most invasive. So you start with your bedside tests like an E CG. Um, the ECG in stable angina will be normal. Um And then I'd say go on to do blood. So that would be a lipid profile. And a HBA1C. Again, those are looking at the risk factors as well of stable angina or any coronary artery disease. And later on will help management in terms of having secondary prevention. And then the more specialized test that you'd want to do is an exercise tolerance test, um or a CT Coronary angiogram. Um I don't know if you have seen a exercise test before, but essentially you do an E CG at rest at baseline and then they get on a treadmill and then you sort of ramp up the exercise. Um and you look for any E CG changes um or until or what they sort of can tolerate. Um And then a CT angio uh CT Coronary angio is um injecting dye into the sort of coronary arteries and having a look at the degree of sort of stenosis or or occlusion um or narrowing. So, in terms of the aims of treatment, there are sort of two main ones, first being the immediate symptomatic relief during episodes of angina. So then that would be with GTN spray. Um And then you've also got the secondary prevention of cardiovascular disease. So that would be with antiplatelet therapy like an aspirin, um a statin. So, if you've got hyperlipidemia, you'd have the statin to reduce that. Um And then you'd want a beta blocker or a rate limiting um calcium channel blocker. Um The nice guidelines which I'll show in a couple of slides, uh recommends using a beta blocker or a rate limiting calcium channel blocker as a first line. Um And if the patient is still symptomatic after monotherapy, so, after using a beta blocker or a rate channeling rate limiting channel calcium channel blocker, um then you'd wanna give both and then if not, then you'd wanna consider adding something like isosorbide mononitrate, um Nicorandil or um Rana, Rana. Um and just as a bit of a counseling point and something that often crops up in MC QS is nitrate tolerance. So often a patient will come in with symptoms of taking um sorry, the side effects of nitrates. Um and they'll say what can you do to, you know, help this or, you know, what would you prescribe instead? Um And it's just um ensuring that patients who take standard release, isosorbide mononitrate um have er they, it has a asymmetric ace, yeah, dosing interval. Um So you need to maintain a daily nitrate free time between 10 to 14 hours. But if it's modified release, then that's not really a problem, you don't have those peaks and troughs. Um So then just moving on to another sort of scenario. Often in an osk situation, you might have something like this. So you an F one, Mr Jones or blogs or whatever has come into the rapid assessment chest pain clinic or A&E or whatever you'd like for central chest pain on exertion. Um He has undergone a series of investigations, has had a provisional diagnosis of angina, um explained the diagnosis. So just have a moment to think about what counseling points you might want to think about or how you might explain Angina. And then I'll go on to the next slide to sort of explain what, what's sort of the key points to, to keep in mind. Ok. So in terms of the key point, it's, um, teaching the patient how to take the GTN spray. Um, sometimes in osk stations they'll, they'll be the vignette and then it'll say counsel them how to take the medication. So it's really important to say you have to spray it under the tongue. Um, and if they don't feel any effect, not to keep spraying it because it's, it causes, um, drops in BP cos it's a vasodilator. So you need to tell them to be patient with it. Take it, wait five minutes, if it doesn't relieve the pain, take it again. Um, and then safety netting. So if the pain continues, er, for more than 15 minutes, despite using the spray twice, then to go to A&E, um, and then in the important side effects are dizziness or fainting. So, like I explained, if you take too much, it can cause um vasodilation, which can cause a drop in BP because there isn't the arterial er the venous um resistance. And then you could also have headaches as well. And then just in terms of information giving in an ay, I guess this could be um sort of spoken about any type of counseling station in any OSK. But you wanna have a structured approach, you wanna chunk and check, explore the patient's ideas and concerns um safety net. And then at the end, it's always good to say II would give them a patient information leaflet. Um OK, so um moving on to sort of an M CQ. So if we could launch a pole, um and then you guys can sort of pick whichever option you think is best. Um So if I just read it out whilst everyone can fill out the pole. Um So you are seeing John a 50 year old man who um comes in uh with central constricting chest pain, walking upstairs, triggers the pain, the pain goes away with resting. He suffers with hypertension diabetes and he takes verapamil for migraine prophylaxis. Um His other medications include GTN spray, aspirin, atorvastatin, Ramipril, and Metformin. And on examination, his rhythm seems to be uh irregular, there is no murmur on auscultation of the heart and there is no tenderness on chest wall palpation. He is asking for medication that would be most helpful to preventing the chest pain from occurring. What is the most appropriate treatment? So, I've got a Bisoprolol B, Digoxin C, metoprolol D, Nicorandil and then E Ibuprofen. Um So I'll just give that sort of 10 more seconds. Um Before we close the pole, uh looks like we've got some um answers. It's good that we've got a split of answers which is really good. Um And then I'll go through it in a second. Um So I'm hoping that my animations work. Um So, and that's how this works. So the answer is, um, Nicorandil. So if I just go through it all, yeah. Ok. So beta blockers would be first line. However, um, the patient's on verapamil. So having a Bisoprolol, um having a Bisoprolol, having a beta blocker and the calcium channel blocker would cause bradycardia which increases the risk of heart block or congestive cardiac failure. Um And then we'll see Ibuprofen. So that might help with the immediate pain. Um, although G 10 will be better, but it doesn't reduce the frequency of angina and none of you uh picked um, digoxin. So that's great because, um, yeah, that wouldn't, that would also slow down your heart rate and it doesn't reduce the frequency of angina. So that's why all through process of elimination, we get to Nicorandil, which is, if you remember, um, one of the, one of the medications that you would use if um monotherapy doesn't work or contra intubated. Um So then moving on to A CS. Um So this is acute Coronary syndrome. Um broadly speaking, it's a thrombus from an atherosclerotic plaque which blocks a coronary artery. Um So the presentation of A CS is crushing, chest pain, um radiating to the left arm, neck or jaw, it's associated with nausea and vomiting. Um They can come out in cold sweats and they can also experience palpitations. Um So my next slide is basically a, a summary, well, sort of a summary or overview slide of what A CS is. So this is um a acute Coronary syndrome is broken up into sort of two broad categories, one of them unstable angina and the other category myocardial infarction. And then as you know, it, the stem and ends STM. Um So I just use this to help sort of illustrate um the different branches when someone says that it's A CS, it's sort of this, it does not include stable angina, stable angina is completely different. Um because there is no injury um to the to the tissue, there's no sort of um yeah, lasting damage or um yeah, no necrosis. Um So, and then, yeah, so then you've got the A CS that's unstable vagina and you've got a myocardial infarction. Um So I'll go on to explain uh se and ST me later as well. Um So just moving on to unstable Angina so unstable angina is myo myocardial ischemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury or necrosis. Um So there isn't actually any acute injury to the heart cells itself. Um It is an imminent precursor to an M I. So it is an imminent precursor to a myocardial infarction. Um around 50% of N semis will progress to an M I within 30 days if left untreated. So it is very important to treat this. Um when they do have unstable Angina and the management will be the same as an NSTEMI, which I will go to explain in a moment. So in terms of the things that characterize unstable angina, it's prolonged. So it's greater than 20 minutes of chest pain at rest or new onset slash severe angina. Um So if you remember what stable Angina is, it's within five M, it's rest, it's not relieved, it's pain that is relieved within five minutes um or with the use of GTN spray. And then in terms of the ECG, it may be normal or there may be ST wave depression or transient T wave inversion. And then um you have a normal troponin and that's really key because that's sort of what differentiates between unstable angina and an and an M I. So moving on to an end tey, so this is a non ST elevated myocardial infarction. Um This is often referred to as a partial M I or for exams sake cos this often comes up in an M CQ. Um It's called a subendocardial M I. Um So this is characterized by ST segment depression in a region, deep T wave inversion and pathological Q waves. I'll go on to the next slide to show you some EC GS of NSTEMI to, to see what those sort of E CG features look like. And the management for NSTEMI and Unstable Angina is um people use the Batman analogy er sort of acronym, sorry. Um So it's like B for beta blocker, A for Aspirin, T for teg TEGretol, M for morphine, A for anticoagulants such as Fondaparinux and then N for nitrate or like a GTN. Um The other thing that people say is oxygen but the guidelines r show that you only give oxygen when someone's oxygen sats are below their um sort of scale. So for example, 96% and above or 88 to 92 of your CO PD. So going through um the E CG changes. So in A N semi, you see this inverted T wave. So the red line I've drawn here is the isometric line. Um So any, so the T wave inversion, if you have a look is below the isometric line and then if you also have a look at the ST depression, um it's also below the isometric line. So I don't know if you can see my precursor. Um But if I just draw it like this, that's where the isometric line would be. And then this sort of J point is below the isometric line. So that would be ST depression. So often STP depression can be quite hard to pick up. Or people think that things are ST depression when it's not, it's really important to get a ruler. Um and sort of draw the line um where it's sort of the baseline where the E CG sits and then you can see clearly whether there is ST depression or not. So this is an E CG, I'll just let you guys take uh a moment to see if you can spot um spot what's wrong with it or the s the tey um sort of features. No. So, um here you can see that there is if I sort of use my cursor, I'm really hoping you can see it um to sort of drag an imaginary line so you can see that here there. I can't see the cast on, ah Cheers Alex. Thanks. Um Fun. How do II can see it? I think it's just, it's a white person against the background. I can see you can see it. Ok, thanks. Perfect. Um So yeah, if we imagine that, well, I'm gonna try and move my cursor kind of crazily. Um So yeah, this is the isometric line here and you can see that if I draw if I keep sort of squiggling my mouse back and forth, there is some um ST depression here and then the isometric line is here. Um And so and so forth. So you can see that there is some ST depression. Um And I'm also gonna go through the rest of the E CG. So I don't know if that's super convincing. There is some ST depression here in the Leeds one. It's just not as prominent as it is in Leeds two in these three. It's quite hard to see um, in a VR um I mean, it's, it's negative anyway. Um, it's not really in a VLA VF not really convincing. And then if you have a look at the chest leads. So V one, there isn't any noticeable depression there neither and V two neither and V three, but if we have a look at V four to V six, there's quite prominent. So if we have a look at the isometric line here, there's very prominent ST uh depression. So we can see that it's most prominent, I think in V four. So hopefully that's clear. Um for, for the E CG. Um Here's another one. So if you just take another moment to have a look at this E CG, so here you can see um sort of more obviously because it's the, the, the pattern of the, of the E CG. Um but there is some T wave inversion. Um So in Leeds one, so normally the er, the P wave, sorry, not the P wave the, er, T wave should be up. Um, it's not really prominent in lead two, or in the three. and then in a VR it's not there but in a VL you can see that the T wave is inverted so it should be up. Um, and not really in a VF, I mean, maybe, but it's not very convincing and then if we have a look at V one, it's not there because they're all in the correct direction for the T waves. Um But then in V four, you can sort of just about maybe see it, but it's more prominent in V five and V six. So this is at wave inversion. Um So just going back to the nice guidelines. Um So this is the management of Anstey or unstable Angina. So it's the same management for both of them. Um And, you know, you can see that you've got the uh antiplatelet therapy. So that's the loading dose of aspirin. You've got your Fondaparinux. Um And essentially this is, this is the guideline that's used. Um The link to this will be in the powerpoint slides or if you just simply Google and there you want unstable Angina treatment, my C KS that gives you the, the guidelines. So anything C KS is the guidelines just as a heads up. So now I'm gonna move on to semi, so that's ST elevated myocardial function. This refers to full thickness or for the sake of MC QS, it's transmural M I. This is characterized by new left bundle branch block or persistent or new ST segment elevation in at least two contiguous leads of greater than one millimeter in all leads. So what I mean by contiguous um contiguous E CG leads refer to those that lie next to each other anatomically and indicate a specific myocardial territory. So my next couple of slides will sort of clear up what I mean by a contiguous E CG. Um I put the little asterisk here just if you wanna be um you know finicky about it. Um So it is ST segment elevation um of greater than one millimeter in all leads or for leads V two to V three. These are the chest leads, they're nearest to the heart. Um These are greater than uh 2.5 millimeter ST elevation in men, younger than 40 greater than two millimeter in men, over 40 or greater than 1.5 millimeter in women. Um But for the sake of sort of simplicity because this is quite um I don't know in like very in depth detail. It's essentially a stemi er sorry stemi is characterized on an E CG with the new left bundle branch blocks or ST elevation um hence stemi. Um And the management is immediate discussion and transfer to a local cardiac center for an angiogram. Um and then Batman. So that's the same management as the stable, unstable Angina. And the um Antemi. Um And the reason why I say um they need immediate transfer to local cardiac center for angiogram is that not all hospitals have PCI. So that stands for primary coronary intervention. Um So, for example, the hospital that I'm working at is a district hospital. We don't have PCI. So we need to, as soon as someone has a semi on their E CG, we need to immediately call up our neighboring hospital which does have facilities for a PCI um and transfer them across blue lighted. Um So what is a PCI? Um So essentially a catheter that goes through the radial artery. Well, it's m most often the radial artery. Um but it can be the brachial artery or the femoral artery. It is time sensitive. So, um so you can either categorize it as door to door from diagnosis of stemi. So if they're coming through the doors of A&E and you look at the E CG and make the diagnosis of a stemi, they need to be treated or transferred to a PCI center within two hours or 100 and 20 minutes or um you know, if they're at home lying in bed and they eventually come to A&E um they need to go to a PCI center or have a PCI within 12 hours of onset of symptoms. So that, that's the criteria. It's either 100 and 20 minutes from diagnosis, from walking into the hospital or 12 hours from onset of symptoms if they are beyond that time. Um or there is no Cath lab available. So say you're in the middle of, I don't know, I somewhere in the middle of the UK that has no access to any PCI or all the PCI labs are completely fill up. Then your second line treatment is thrombolysis. Um but it's not really ideal. Uh The other thing is if there is evidence for more than two coronary arteries, artery disease on the angio, then you need to fix the most pertinent blockage with a PCI and then you need to refer them to the MDT for consideration of a cabbage. So that's a coronary artery bypass graft. Um So like for example, if you see that E CG and it's all like there's stemi everywhere and there's like signs of necrosis in the heart everywhere. Um And it's not gonna be just one artery that's causing the problem. There might be two arter, two sort of coronary arteries, er then you need to fix the one that's causing the biggest problem or the or the biggest blockage. And then once they're treated with that, let them sort of recover from that and then refer to have a bypass. So, so this is what I mean by er contiguous leads. E CG leads. Um I think a lot of you might have seen this before. Um And it basically shows the territories of um of the E CG. So which parts of the E CG correspond to which coronary arteries that may be blocked. I always found this really difficult to remember. Some people say this is like a booze. Er, and then this is sort of like an upside down. I basically, I, you could memorize it like this. Um, some people it works for them. Um, and you know, when they look at an E CG, they can see the pattern. Um I'm not very good at this. Er So I have a different way. Um But for the sake, I'll just go through this picture. So this is your normal E CG. You can see that leads one ABL. So that's the foot. Uh Sorry, that's not, that's the A leads one, the left and V five and V six, the lateral leads um might be easy to remember lateral because V five and V six are right at the edge of the um like heart board if you think about the E CG. So if you remember Alex's teaching last month, um it was like where to put the E CG stickers and most lateral are V five and V six. You've got the inferior leads. So that's leads 23 and a VF that one to the foot. So that's how you might remember inferior. Um And then you've got your anterior or septal. Um M I and um yeah, so those are the chest leads because it's right in front of the heart. That's how I remember or yeah, just right in front of the heart. Um The, so that, that works for a lot of people. Um I think I'm a little bit more. Um I guess the way that I remember things um makes sense, it needs to make sense for me so I can draw the picture out. So what I need to do is draw this triangle out. Um So in the middle, I've drawn a picture of a heart and I've got the leads like an E CG. So if you just cast your mind back to Alex's teaching on EC GS, so, um when you look at the person, you've got your A VR, so that's your right, you've got your left and you've got your foot. So that's where you're putting your E CG stickers and then V one to V six that's across your chest. So it's just like an E CG and then I draw a triangle around it. So lead one goes towards ABL and then leads two and these three goes towards the feet. So it's important that you keep the direction of the triangle the way that I've drawn the arrows. Um And I'll show you why. So, um here, um I've highlighted it in yellow. Um So you've got an inferior M I, so anything going to the bottom because it's inferior heart. So you can see that the leads two and leads three lead to the bottom and then it's to the foot. So that's how I remember. Inferior M I and then that's the right coronary artery. And then you've got your anterior lateral M I. So then the way that I do it is ok, anterior lateral. So the most lateral part, if you think about a person having an E CG, it would be their left side, not their right, because it goes towards, if you think about the heart, it's on your left hand side. So if it's more left, then it's more lateral. If it goes towards the middle, then it's medial. So an anti lateral M I is towards your left hand side. And then if you draw towards the left hand side, you've got leads one coming this way and then you've got a uh A VL itself and you've got leads one to lead six. So this is the main stem of the left uh coronary artery. So if you actually have an M I in that place, it will be a massive blockage. So then the left coronary artery branches into two. So sort of smaller branches. Um So that's the circumflex or the right left coronary artery and the de um descending one. So if we just take the co uh circumflex, so it's a lateral MRI. So you need to think about what the most lateral positions of the ECG leads are. So if we think about that, it's a V uh sorry, it's leads one and then ABL, so that's the most lateral. And then you can ignore the middle chest leads because that's not as lateral as V five and V six. And then you've got the anteroseptal M I so that the left descending branch of the left coronary artery and that's a V one to V six because that's right in the septum. So just to recap, you've got the left coronary artery. Um and then that branches into the left descending branch of the left coronary artery and the circumflex. And um the left descending branch of the coronary artery is the anterior septal M I. So that's right in the septum. Um And then the um left circumflex is the most lateral because if you think about the heart anatomically, that's its most lateral. So you wanna think of the most lateral leads. Um Yeah. So hopefully, that wasn't too confusing. This is just the way that I like to remember it. I just throw out this triangle and think about um what leads makes sense um in terms of its position really. So if we launch another pole um for this M CQ and A CS, just to put things into practice, um I'll read it out whilst we launch the poll. Um So I've got a 59 year old man um presenting to A&E with a nine hour history of severe crushing, chest pain, sweating and nausea. Um An E CG is forward which shows ST elevation in leads two to leads four. He is hemodynamically stable. He's given, he's given the loading dose of 300 mg of aspirin. He's given sublingual nitrates IV morphine. What is the next most appropriate step in his management? I'll give you sort of another 20 seconds to um answer. Oh, maybe I'll read out the options. So A it's um offer fibrinolysis. So that's the thrombolysis B calculate the grace score. So that's the global Registry of Coronary artery events. Er C is immediate transfer to a PCI center. Er D is transferred to a PCI center within four days. E is to continue to administer 75 mg of aspirin U TNA. Good pay relief and then f is transfer for a cabbage. So it looks like um everyone's gone for immediate transfer to PC. Oh, not everyone. Sorry, my bad. Er most of you have gone for immediate transfer for a PCI center and uh some people have gone for er fibrinolysis. Um So if we have a look at the spin yet, um this is very typical of a sty um you know that you've got your ST elevation, he's got this crushing chest pain, he's got that associated sweating and nausea. Um So we've started the initial steps whilst he's in uh A&E he's given the loading dose of aspirin, he's given the pain relief, et cetera. Um What do you do next? Some of you might have written a fibro fibrinolysis because it's nine hours and like I said, when you come into A&E, it's within 100 and 20 minutes, but he's just come to A&E with a nine hour history. So he's just step through the door. So that's within our 12 hour time frame of being able to do a PCI fibrinolysis is offered to patients who, um, so if this patient had come in with a 13 hour or history of central, er, chest pain, he, he wouldn't be for a PCI to have to have fibrin lysis or if he's been sitting in A&E because it's busy and he's somehow been missed and he's been sitting there for, you know, goodness knows, how long will the transport takes ages to transfer him over then that needs to be within the 120 minutes. Um And then you could calculate the grade score but you're wasting precious time doing that. Um So it's not, it's not B uh and then it's uh not d because that it's an emergency. He's got chest pain, it's got ST elevation um E considered to administer, administer aspirin. He tell good pain relief. That's not wrong. You do wanna do that. Um but not at the expense of trying to get him to a PCI center ASAP and then transfer for a cabbage. Um Well, if there's evidence for more than two coronary artery diseases on the angiogram, um then you would eventually want to do a cabbage. But here you can see the E CG shows that there's just se in, in B2 to B four. So there aren't two sort of um areas of infarction. It's sort of limited to the, to the one area. So hopefully, uh that makes a little bit of sense. So going on to a little bit of quiz. So just putting things into practice, um I'll give about 30 to 40 seconds um per E CG. Um So if we could launch some more poles, please. Um So for this E CG, I'll give you guys about, I'll give you guys 30 seconds to do that. OK? So hopefully that was enough time. Maybe I'll just give it another, I'll give it a little bit longer. OK? So if we just go over this, so I've sort of highlighted where I can see um the, the I irregularities of this E CG. So if we look at sort of lead one, that looks pretty nice and normal leads two, maybe I would, I would actually be slightly suspicious of lead two of having some um ST elevation um these three maybe as well. Um A but I II don't know, II would say that's so of just about, but it's not particularly clear. Also, I know that this um image is blurry. So you can't like count how many blocks it is, how many squares, sorry. Um A V ri mean that's normal for a VR and then there's none in a VL and none, maybe some in a VF I think it's quite hard to say. Um But I think it's most prominent in the chest leads. So I'm looking at where it's most prominent. Um So you've got that, um It's very definitive here. So if you had the Isometric line, um you can see some very obvious jump here. Um Again, in V two, it's massive. Um So that's the isometric line and you can see this again, massive jump here. Um And then you can also uh see it again in B3. Um It's again, very obviously there. Um And then, um and then you can also see it in 45 and not really six. So if you just think about sort of the approximate uh location of this infarction, um it's looking at all the chest leads. So it is the um anteroseptal M I and that's the left descending uh branch of the left coronary artery. So moving on to this one, I'll give a, I'll give a minute cos it is very difficult. Oh If we could launch the next poll. Sorry. Cheers. OK. Bye. OK, perfect. Um So this is a bit mean because I've just been talking about sties and looking at the areas. Um but this is an Nstemi so you can see that there is T wave inversion most er prominently in V two and V three, you can see it elsewhere. Um The reason why I put this one up is this is Wellans syndrome. So this is a deep t inversion in V two and V three. and it shows uh it's essentially a high risk G. So you wanna treat this one very quickly. Um It's high grade stenosis in the er left anterior descending coronary artery. Um So you, so this is a high risk and semi but good job guys, you, you look like you've, you've cut, cut out the end semi, which I chucked in. So just moving on to the next one. So we get the pole for the next E CG again, I'll give another minute. OK. So if we have a look here um with this sort of scribble that I've done, this is an inferior M I, it looks at leads 23. So I've very scr tried to draw the isometric line here and where I can see the elevation. So that's two leads an aVF. Um And then if you think about my little triangle or whatever way that you like to look at it or the boot, whatever it is, um You can see that this is an inferior M I, some of you have put anterior lateral. Um If you're looking at an anterior lateral M I, you're looking at um lead to one um which I'm not very convinced of any er elevation here. Um And you're looking at um A VL, I guess I can understand why you might see that, but it's, it's more it's a brilliant version um if anything and then uh the chest leads as well. Um And I'm not massively convinced of any uh ST innervation. There we go. Yeah. So that's why this is an inferior M I. Um And then that's the le the right coronary artery. Um And then our last E CG here. So, uh one last minute, thanks for the next poll. Thanks. OK. So I've said that this is a lateral M I um I mean, I can see actually looking back at this, I can sort of see that it, that it is um anterior lateral one. If I look very, I don't know if I can convince myself um for some um if I look at the isometric line, I dunno, I'm not massively convinced, but um I dunno, you can beg to differ um because these things aren't necessarily er sort of set in stone or, or concrete, may I say? But it's most obvious if we have a look at lead one. So there's the isometric line and you can see that there is a very prominent um se elevation again in abl, very obvious. And then I'd say it's most obvious in V five and V six. If I just draw the isometric line, you can see that this jump here is um se innervation. Um and then again in V six. So this junction here, although I guess it's less prominent, but this junction from here uh I'm hoping that you can see my moss but, um, is almost two. It is about two blocks if I look closely at V one. I mean, it's not really, um, because if we have a look at where the T wave starts again in V two, uh, if we draw that here, it sort of starts below it. Er, V three, I'm gonna draw another isometric line right here. Um, and it's not particularly er elevated and then V four, I would call that like very mildly, but again, it needs to be sort of uh 1 to 2 and like here, it's not really that prominent. Um Here ma no, not really, but maybe on this one. Yes. Um So hopefully that, that explains it. Um Oh I see a question. Uh A V is it just lateral? So um leads one A VL and then V five and V six is er lateral? Um Yeah. Yeah, that's lateral. Um If it's including all of the chest leads, then it's the anterial lateral. Um Yeah. Am I saying that? Right? Yeah. So if it's just the hang on, let me go onto this. Oh no, I haven't got, where is my, so I'm just gonna get to the right slide. Um There we go. So if we have a look at this, um you've got your, there we go. So that's the inferior one. Let me just try and click here. So here we've got the anterior lateral, it's leads one. So if you have a look this way, it's leads one, it's towards the ABL and then it's all of the chest leads because that's the main anterior lateral is the left coronary artery. So it's the one that affects most of the regions because the left coronary artery di um divides uh into the um descending and the circumflex. And then if I go onto the lateral M I um that's the circumflex branch of the left coronary artery. So then it's, it's less leads because it's less sort of area affected. Um So then it's just the leads one ABL and then V five and V six. Thanks Alex for writing that there. Um Just going back to this E CG. Um So, yeah, hopefully it uh yeah, it, it takes a lot of practice I think also having a minute to, to quickly look at an E CG is also very difficult. Um But again, it's just looking at them and then eventually, um it'll come a bit quicker and then this is just a, a summary slide at the end um of what we've sort of gone through today in terms of you've got your chest pain, you've got your stable angina, which I didn't write there and you've got your umbrella of A CS. So that's essentially like heart attack. Um You've got your unstable angina, your mis that split to stemi and ends Demi and then we've also had a look at some of the EC GS and practice the reading them, um, or interpreting them. So, er, yeah, that's, thank you. That's all from, er, me today and me and Alex today. Um, we've got our, some, our feedback form. We'd be really grateful if you could fee, er, fill that out and you'll get the powerpoints at the end. Um, yeah. And any questions, er, yeah, please put them in the chat or? Yeah, thank you, Ja, I think you're on mute. Yeah. Um I'll stay around and uh see if there's any other questions to, to answer. Um, but yeah, please fla still on mute. How you can hear me now? Yeah. Ok. Thanks. Thank you very much, Doctor Lee and uh Lister Alex and Lauren. It was a very informative or wonderful ac sym um, a syndromes, good lecture. Thank you very much. Er, we appreciate you taking your time out and lecturing on Meath platform. Lauren's just posted on the, on the chat guys. Your, the link for the feedback form. Please do fill that out for your certificates. We'll send a feedback form automatically to your emails. Please fill that feedback form in too and you'll receive your certificate. Like I said, please join us again for our next series next month. 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